Holdings: Red cell membrane transport in health and disease

Red cell membrane transport in health and disease: with 31 tables

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Bibliographic Details
Format:	Book
Language:	English
Published:	Berlin [u.a.] Springer 2003
Subjects:	Erythrozytenmembran - Membrantransport - Physiologie - Aufsatzsammlung Erythrozytopathie - Pathophysiologie - Aufsatzsammlung Physiologie Membrantransport Pathophysiologie Erythrozytenmembran Erythrozytopathie Aufsatzsammlung
Online Access:	Inhaltsverzeichnis
Item Description:	Literaturangaben
Physical Description:	XXVIII, 748 S. graph. Darst.
ISBN:	3540442278

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adam_text	CONTENTS CONTRIBUTING AUTHORS....................................................................................XXIII 1 DISTRIBUTION AND MOVEMENT OF MEMBRANE LIPIDS...........................................1 1.1 INTRODUCTION..................................................................................................1 1.1.1 LIPID COMPOSITION, STRUCTURE AND MOTIONS ..........................................1 1.1.2 MEASUREMENTS OF DISTRIBUTION AND MOVEMENT OF LIPIDS BETWEEN THE MEMBRANE BILAYER LEAFLETS..............................................3 1.1.3 STEADY STATE DISTRIBUTION OF LIPIDS BETWEEN THE MEMBRANE BILAYER LEAFLETS.................................................................................................4 1.1.4 LIPID DOMAINS......................................................................................5 1.2 NON-MEDIATED PASSIVE TRANSBILAYER MOVEMENTS OF LIPIDS.........................6 1.2.1 PHOSPHOLIPIDS .......................................................................................6 1.2.2 CHOLESTEROL AND OTHER NEUTRAL LIPIDS...................................................7 1.2.3 FATTY ACIDS: MEDIATED OR NON-MEDIATED MOVEMENT?..........................8 1.3 MEDIATED PASSIVE TRANSBILAYER MOVEMENTS OF LIPIDS .................................9 1.3.1 CA 2+ -ACTIVATED BIDIRECTIONAL MOVEMENT OF LIPIDS VIA THE PHOSPHO- LIPID SCRAMBLASE...................................................................................9 1.3.2 MOVEMENT OF ANIONIC LIPIDS VIA THE ANION EXCHANGER AE1 ............11 1.4 MEDIATED OUTWARD MOVEMENT OF NEWLY SYNTHESIZED PHOSPHATIDYL- CHOLINE .......................................................................................................12 1.5 ACTIVE TRANSBILAYER MOVEMENTS OF LIPIDS ................................................13 1.5.1 INWARD MOVEMENTS OF PHOSPHATIDYLSERINE AND PHOSPHATIDYL- ETHANOLAMINE VIA THE AMINOPHOSPHOLIPID TRANSLOCASE (APLT) ........13 1.5.2 OUTWARD MOVEMENTS OF LIPIDS VIA THE MULTIDRUG RESISTANCE PROTEIN MRP1 (ABCC1) ....................................................................14 1.6 DISTURBANCE OF DISTRIBUTION AND TRANSBILAYER MOVEMENTS OF MEMBRANE PHOSPHOLIPIDS IN PATHOLOGY .......................................................................15 1.7 SUMMARY....................................................................................................16 REFERENCES........................................................................................................17 2 MEMBRANE LIPIDS AND PROTEINS AS A BASIS OF RED CELL SHAPE AND ITS ALTERATIONS ............................................................................................27 2.1 INTRODUCTION................................................................................................27 2.2 EARLY HISTORY..............................................................................................28 2.3 EXPERIMENTAL CHANGES OF RESTING SHAPE ...................................................28 2.3.1 OUTLINE OF OBSERVATIONS......................................................................28 2.3.2 OUTLINE OF THE POSSIBLE ORIGINS OF SHAPE CHANGES.............................30 2.4 A ROLE FOR THE LIPID BILAYER: THE BILAYER COUPLE CONCEPT OF SHAPE CHANGES .....................................................................................................33 2.4.1 UNDERLYING OBSERVATIONS AND DEFINITION............................................33 2.4.2 SHAPE CHANGES FOLLOWING ALTERATIONS OF THE TRANSBILAYER BALANCE OF MEMBRANE LIPIDS...........................................................................36 VIII CONTENTS 2.4.3 SHAPE CHANGES FOLLOWING IN SITU MODIFICATION OF PHOSPHOLIPID PATTERNS...............................................................................................37 2.4.4 SHAPE CHANGES ARISING FROM EXPERIMENTALLY INDUCED TRANSBILAYER REDISTRIBUTION OF ENDOGENOUS PHOSPHOLIPIDS ....................................38 2.5 SHAPE CHANGES OF UNRESOLVED ORIGIN........................................................40 2.5.1 DEPLETION OF ATP OR MAGNESIUM AND EXPOSURE TO VANADATE ............40 2.5.2 LIGANDS OF BAND 3 PROTEIN..................................................................40 2.5.3 EFFECTS OF GLASS CONTACT AND OF SERUM ALBUMIN ...............................41 2.5.4 PHOSPHOLIPID SYMMETRIZATION FOLLOWING FIELD PULSE EXPOSURE: A TOOL FOR TESTING THE REQUIREMENT OF BILAYER ASYMMETRY FOR SHAPE CHANGES OF UNRESOLVED ORIGIN ..........................................41 2.6 FROM THE BILAYER TO A QUADRILAMINAR MEMBRANE.......................................43 2.6.1 CONSTITUENTS OF THE EXO- AND THE ENDOFACIAL MEMBRANE SURFACE COAT.......................................................................................43 2.6.2 INFLUENCE OF THE EXOFACIAL LAMINA: SHAPE EFFECTS OF ENZYME TREATMENT...........................................................................................45 2.6.3 INFLUENCE OF THE ENDOFACIAL LAMINA: THE ROLE OF THE MEMBRANE SKELETON IN SHAPE TRANSFORMATIONS ...................................................45 2.6.4 SHAPE EFFECTS OF CYTOPLASMIC PH ......................................................46 2.6.5 INFLUENCE OF ION GRADIENTS AND TRANSMEMBRANE POTENTIAL.................47 2.6.6 LIMITATION OF SHAPE CHANGES BY THE MEMBRANE SKELETON .................48 2.6.7 MEMBRANE STABILIZATION BY THE SKELETAL NETWORK AND ITS ALTERATIONS ..............................................................................49 2.7 PATHOLOGICAL ALTERATIONS OF RED CELL SHAPE IN VIVO ...................................49 2.7.1 STOMATOCYTOSIS GOING ALONG WITH ALTERATIONS OF CELL VOLUME .........50 2.7.2 SHAPE CHANGES DUE TO ALTERED PROPERTIES OF HAEMOGLOBIN...............50 2.7.3 LIPID-BASED ALTERATIONS OF CELL SHAPE...............................................50 2.7.4 PROTEIN-BASED ALTERATIONS OF RED CELL SHAPE.....................................51 2.8 OUTLOOK ......................................................................................................52 REFERENCES .......................................................................................................52 3 HUMAN RED CELL SHAPE AND THE MECHANICAL CHARACTERISTICS OF THE MEMBRANE......................................................................................................... 61 3.1 INTRODUCTION ...............................................................................................61 3.2 CONTINUUM MECHANICS VS. MEMBRANE COMPOSITION ..................................62 3.3 MODES OF MEMBRANE DEFORMATION.............................................................63 3.3.1 GENERAL REMARKS................................................................................63 3.3.2 ISOTROPIC OR BIAXIAL DEFORMATION .......................................................63 3.3.3 SHEAR OR UNIAXIAL DEFORMATION ..........................................................63 3.3.4 BENDING DEFORMATION.........................................................................63 3.4 RESTING SHAPE OF MEMBRANE PATCHES.........................................................64 3.4.1 GENERAL REMARKS................................................................................64 3.4.2 SURFACE AREA.......................................................................................64 3.4.3 ASPECT RATIO.......................................................................................65 3.4.4 SPONTANEOUS CURVATURE ......................................................................65 3.5 MEMBRANE STIFFNESS...................................................................................66 3.5.1 GENERAL REMARKS................................................................................66 CONTENTS IX 3.5.2 ISOTROPIC STIFFNESS...............................................................................66 3.5.3 SHEAR STIFFNESS....................................................................................67 3.5.4 BENDING STIFFNESS ...............................................................................67 3.6 UNIFORMITY OF THE MEMBRANE.....................................................................69 3.6.1 GENERAL REMARKS................................................................................69 3.6.2 SURFACE AREA.......................................................................................69 3.6.3 ASPECT RATIO .......................................................................................69 3.6.4 SINGLE-LAYER BASED SPONTANEOUS CURVATURE ......................................69 3.6.5 DOUBLE-LAYER BASED SPONTANEOUS CURVATURE.....................................70 3.7 RESTING SHAPES OF RED CELLS......................................................................70 3.7.1 GENERAL REMARKS................................................................................70 3.7.2 THE BICONCAVE DISCOCYTE...................................................................70 3.7.3 ECHINOCYTES AND STOMATOCYTES ...........................................................71 3.7.4 CONCLUSIONS ........................................................................................72 3.8 RELATIVE IMPORTANCE OF SINGLE-LAYER AND DOUBLE-LAYER BASED SPONTANEOUS CURVATURE..............................................................................72 3.9 NON-UNIFORM MECHANICAL PROPERTIES OF THE MEMBRANE ............................73 3.9.1 SPHERICAL ECHINOCYTES AND STOMATOCYTES ...........................................73 3.9.2 EFFECTS OF RAISING THE CYTOPLASMIC CONCENTRATION OF CALCIUM..........74 APPENDIX .........................................................................................................74 REFERENCES........................................................................................................80 4 PASSIVE MEMBRANE PERMEABILITY FOR IONS AND THE MEMBRANE POTENTIAL.....83 4.1 INTRODUCTION................................................................................................83 4.2 SPECIFIC TRANSPORT SYSTEMS FOR MONOVALENT CATIONS IN THE MAMMALIAN RED CELL MEMBRANE...................................................................................83 4.3 THE LOW IONIC STRENGTH (LIS) EFFECT.........................................................87 4.4 THE K + (NA + )/H + EXCHANGER..................................................................... ....91 4.5 GENERAL CONSIDERATION OF THE RESIDUAL AND LEAK CATION FLUXES................95 4.6 THE TRANSMEMBRANE POTENTIAL, SURFACE POTENTIAL, AND THE ELECTRIC FIELD IN THE MEMBRANE........................................................................................97 4.7 CONCLUSION ...............................................................................................103 REFERENCES......................................................................................................103 5 NA + /K + PUMP ...................................................................................................111 5.1 INTRODUCTION..............................................................................................111 5.2 DEVELOPMENT OF THE CONCEPT OF ACTIVE TRANSPORT ...................................111 5.3 EARLY CHARACTERIZATION OF THE NA + /K + PUMP IN RED CELLS.........................112 5.4 THE ENZYMATIC BASIS OF THE NA + /K + PUMP ...............................................114 5.5 RED CELL CHARACTERISTICS FAVOURABLE FOR THE STUDY OF THE NA + /K + PUMP..115 5.6 TRANSPORT OF NA + AND K + AND THE REACTION MECHANISM OF THE NA + /K + PUMP.......................................................................... ........117 5.6.1 NA + /K + EXCHANGE ..............................................................................118 5.6.2 NA + /NA + EXCHANGE ............................................................................120 5.6.3 K + /K + EXCHANGE...................................................................... ..........121 5.6.4 THE REACTION MECHANISM OF THE NA + /K + PUMP.................................123 5.7 THE QUATERNARY STRUCTURE OF THE RED CELL NA + /K + PUMP .........................127 X CONTENTS 5.8 UNRESOLVED ISSUES ....................................................................................129 5.8.1 PROPERTIES OF THE THIRD NA + SITE........................................................129 5.8.2 SELECTIVITY OF THE CATION BINDING SITES ............................................131 5.8.3 NA + I /H + O EXCHANGE AND K + O /H + I EXCHANGE.........................................132 5.8.4 NA + TRANSPORT COUPLED WITH ANION TRANSPORT..................................132 5.9 CONCLUSION...............................................................................................133 REFERENCES .....................................................................................................133 6 ION CHANNELS ................................................................................................... 139 6.1 INTRODUCTION .............................................................................................139 6.2 THE CA 2+ -ACTIVATED K + CHANNEL ...............................................................139 6.3 THE VOLTAGE-DEPENDENT NON-SELECTIVE CATION CHANNEL.........................144 6.4 THE LOW CONDUCTANCE K + CHANNEL..........................................................146 6.5 THE ANION-SELECTIVE CHANNEL..................................................................146 6.6 WHOLE CELL PATCH-CLAMP RECORDINGS ......................................................147 6.7 CONCLUSION...............................................................................................147 REFERENCES .....................................................................................................148 7 THE SWELLING-SENSITIVE OSMOLYTE CHANNEL ................................................... 153 7.1 INTRODUCTION .............................................................................................153 7.2 SWOLLEN TO THE SAME EXTENT, RED CELLS CAN ADOPT DIFFERENT REGULATORY PATTERNS....................................................................................................154 7.3 RED CELLS WILL ADOPT THE REGULATORY PATTERN THAT MAINTAINS CELL HOMEOSTASIS ............................................................................................156 7.4 REGULATION OF SWELLING-SENSITIVE, OSMOLYTE PATHWAYS...........................158 7.4.1 THE OPENING OF OSMOLYTE PATHWAYS IS CONTROLLED BY IONIC STRENGTH AND IS INSENSITIVE TO CELL VOLUME EXPANSION ....................159 7.4.2 A SINGLE OR SEVERAL OSMOLYTE TRANSPORT PATHWAYS?........................161 7.4.3 OPENING OF THE OSMOLYTE CHANNEL IN RESPONSE TO A GRADUAL AND SLOW DECREASE IN MEDIUM OSMOLALITY......................................162 7.5 SWELLING-SENSITIVE OSMOLYTE PATHWAYS: ASSOCIATION WITH BAND 3 PROTEIN .....................................................................................................162 7.5.1 THE ORGANIC OSMOLYTE PATHWAY HAS THE FUNCTIONAL CHARACTERISTICS OF AN ANION CHANNEL ........................................................................162 7.5.2 THE ORGANIC OSMOLYTE CHANNEL: A PATHWAY FOR CATIONS..................163 7.5.3 THE SWELLING-SENSITIVE OSMOLYTE CHANNEL IS ASSOCIATED WITH BAND 3 PROTEIN (AE1)...............................................................164 7.6 MOLECULAR IDENTIFICATION OF THE SWELLING-SENSITIVE OSMOLYTE CHANNEL...165 7.7 CONCLUSION...............................................................................................167 REFERENCES .....................................................................................................168 8 NA + -K + -2CL - COTRANSPORT ................................................................................ 173 8.1 INTRODUCTION .............................................................................................173 8.2 THE NKCC1 PROTEIN ................................................................................174 8.3 NKCC1 ANTIBODIES..................................................................................176 8.4 THE NKCC1 REACTION CYCLE....................................................................176 8.5 BREADTH OF PHYSIOLOGICAL FUNCTIONS.........................................................181 CONTENTS XI 8.6 COORDINATE REGULATION OF VOLUME-REGULATORY TRANSPORTERS ...................182 8.7 CELL VOLUME DETECTION ............................................................................183 8.8 REGULATION OF NKCC ...............................................................................185 8.9 THERMODYNAMIC CONSIDERATIONS ..............................................................186 8.10 FUNCTION OF NKCC IN RED CELLS ............................................................186 REFERENCES......................................................................................................190 9 K + -CL - COTRANSPORT IN VERTEBRATE RED CELLS.................................................197 9.1 INTRODUCTION..............................................................................................197 9.1.1 HISTORICAL PERSPECTIVE.......................................................................197 9.1.2 THE LK SHEEP RED CELL....................................................................198 9.1.3 IONIC REQUIREMENTS AND TRANSPORTER KINETICS..................................198 9.1.4 MOLECULAR IDENTITY OF THE K + -CL - COTRANSPORTER ................................199 9.2 PHYSIOLOGICAL CHARACTERISTICS ...................................................................200 9.2.1 VOLUME DEPENDENCE ........................................................................200 9.2.2 H + DEPENDENCE .................................................................................202 9.2.3 UREA..................................................................................................203 9.2.4 OXYGEN .............................................................................................203 9.2.5 HYDROSTATIC PRESSURE.........................................................................204 9.2.6 TEMPERATURE .....................................................................................204 9.2.7 BICARBONATE.......................................................................................205 9.3 MECHANISM OF REGULATION........................................................................205 9.3.1 PROTEIN PHOSPHORYLATION ...................................................................205 9.3.2 MACROMOLECULAR CROWDING, ION CONCENTRATION OR MECHANO- RECEPTION?.........................................................................................207 9.3.3 MAGNESIUM AND ORGANIC PHOSPHATES................................................208 9.3.4 KCC AND REDOX POTENTIAL ................................................................209 9.4 FUTURE PERSPECTIVES..................................................................................210 9.4.1 THE CYTOSKELETON AND REGULATION OF KCC .......................................210 9.4.2 DIVERSE FUNCTIONS OF KCC IN RED CELLS AND OTHER TISSUES.............211 REFERENCES......................................................................................................212 10 THE BAND 3 PROTEIN: ANION EXCHANGER AND ANION-PROTON COTRANSPORTER ...............................................................................................221 10.1 INTRODUCTION............................................................................................221 10.2 MEASURING ANION-PROTON COTRANSPORT....................................................222 10.3 H + -CL - COTRANSPORT AND ITS RELATIONSHIP TO CL - /CL - EXCHANGE..................225 10.4 MOLECULAR BASIS OF THE RELATIONSHIP BETWEEN ANION EXCHANGE AND ANION-PROTON COTRANSPORT...............................................................229 10.5 CHLORIDE EQUILIBRIUM EXCHANGE AND CHLORIDE-PROTON COTRANSPORT: COMPARISON OF EXPERIMENTAL EVIDENCE WITH THEORETICAL PREDICTIONS ...231 10.6 H + -SO 4 2- COTRANSPORT AND ITS RELATIONSHIP TO H + -CL - COTRANSPORT: GENERAL FEATURES ....................................................................................237 10.7 THE RELATIONSHIP BETWEEN H + -CL - AND H + -SO 4 2- COTRANSPORT: SPECIFIC FEATURES....................................................................................239 10.8 H + -SO 4 2- COTRANSPORT VS. H + -CL - COTRANSPORT: DISCUSSION .......................242 XII CONTENTS 10.9 CHEMICAL MODIFICATION OF THE COTRANSPORT PROCESS ...............................244 10.10 SUMMARY..............................................................................................247 APPENDIX .......................................................................................................248 REFERENCES .....................................................................................................250 11 BAND 3 MEDIATED TRANSPORT ........................................................................ 253 11.1 FUNCTIONS OF BAND 3 AND RELATED PROTEINS.............................................253 11.2 BASIC CHARACTERISTICS..............................................................................254 11.2.1 ONE-FOR-ONE EXCHANGE ..................................................................254 11.2.2 DIVALENT VS. MONOVALENT ANION TRANSPORT .....................................255 11.2.3 BASIC TRANSPORT MECHANISM * PING-PONG MODEL...........................255 11.2.4 EVIDENCE FOR THE PING-PONG MODEL ................................................259 11.3 ASYMMETRY OF THE SYSTEM......................................................................260 11.3.1 SIDEDNESS OF UNLOADED TRANSPORT SITES..........................................260 11.3.2 EFFECTS OF CHLORIDE ON SIDEDNESS OF TRANSPORT SITES......................261 11.3.3 EFFECTS OF BICARBONATE ON SIDEDNESS OF TRANSPORT SITES.................261 11.3.4 CONSEQUENCES OF ASYMMETRY FOR FLUXES UNDER PHYSIOLOGICAL CONDITIONS......................................................................................262 11.4 STRUCTURE OF AE1....................................................................................263 11.4.1 THE CYTOPLASMIC DOMAIN (CDAE1)................................................263 11.4.2 STRUCTURE OF THE MEMBRANE DOMAIN REVEALED BY ELECTRON MICROSCOPY ....................................................................................264 11.4.3 TOPOLOGY OF THE AE1 MEMBRANE DOMAIN......................................264 11.4.4 THE FIRST EIGHT TM SEGMENTS ........................................................265 11.4.5 REMAINING C-TERMINAL SEGMENTS; CONTROVERSIAL TOPOLOGIES........267 11.5 FROM STRUCTURE TO FUNCTION: INFORMATION FROM MUTATIONS AND CHEMICAL LABELLING.........................................................................268 11.5.1 INTERPRETATION OF MUTATION AND CHEMICAL MODIFICATION DATA .........270 11.5.2 CARBOXYL GROUP MODIFICATION: PUTATIVE IDENTIFICATION OF PROTON BINDING SITES..................................................................................271 11.5.3 AMINO GROUP MODIFICATION BY DISULPHONIC STILBENES...................272 11.5.4 OTHER AMINO-REACTIVE PROBES........................................................275 11.5.5 HISTIDINE MODIFICATION ...................................................................275 11.5.6 ARGININE MODIFICATION....................................................................276 11.5.7 CYSTEINE MODIFICATION....................................................................277 11.5.8 FUNCTIONAL IMPORTANCE OF SERINE AND THREONINE ............................277 11.5.9 PROTEIN FLEXIBILITY AND CROSS-LINKING............................................277 11.5.10 SENSING OF CHANGES IN AE1 CONFORMATION BY CHEMICAL PROBES..278 11.6 MODEL FOR ANION EXCHANGE....................................................................280 11.6.1 RESIDUES THAT CROSS THE PERMEABILITY BARRIER (PB) AND/OR BIND SUBSTRATES.......................................................................................280 11.6.2 EVIDENCE FOR ANION ACCESS CHANNELS IN AE1 ................................283 11.6.3 SEPARATE BINDING SITES FOR HALIDES AND OXYANIONS........................284 11.6.4 STRUCTURAL NATURE OF THE TRANSPORTING CONFORMATIONAL CHANGE (TCC)................................................................................286 11.6.5 RELATION TO AE1 STRUCTURE ..............................................................287 CONTENTS XIII 11.6.6 RELATION TO STRUCTURE AND MECHANISM OF OTHER MEMBRANE TRANSPORT PROTEINS..........................................................................288 REFERENCES......................................................................................................289 12 AMINO ACID TRANSPORT .................................................................................303 12.1 INTRODUCTION............................................................................................303 12.2 WHY DO RED CELLS NEED AMINO ACID TRANSPORTERS? .............................304 12.3 A COMMENT ON METHODOLOGY ................................................................306 12.4 TRANSPORT SYSTEM NOMENCLATURE............................................................306 12.5 IDENTIFICATION OF RED CELL AMINO ACID TRANSPORT SYSTEMS ...................307 12.6 KINETIC STUDIES.......................................................................................307 12.7 SYSTEM GLY .............................................................................................309 12.8 BAND 3....................................................................................................309 12.9 THE HETERODIMERIC AMINO ACID TRANSPORTERS (L, ASC, Y + L)...................309 12.9.1 SYSTEM L.........................................................................................310 12.9.2 SYSTEM Y + L .....................................................................................311 12.10 SYSTEM ASC.........................................................................................312 12.11 SYSTEM Y + .............................................................................................312 12.12 SYSTEM N..............................................................................................312 12.13 SYSTEM T ..............................................................................................313 12.14 SYSTEM GLU ...........................................................................................313 12.15 PHYSIOLOGICAL TRANSPORT RATES FOR AMINO ACIDS .................................313 12.16 ALTERATIONS OF AMINO ACID TRANSPORT IN DISEASE STATES ......................315 12.17 CONCLUSION ...........................................................................................316 REFERENCES.................................................................... ..................................316 13 EQUILIBRATIVE NUCLEOSIDE TRANSPORT PROTEINS.............................................321 13.1 INTRODUCTION............................................................................................321 13.2 BIOCHEMICAL STUDIES OF RED CELL NUCLEOSIDE TRANSPORT PROTEINS..........322 13.2.1 IDENTIFICATION OF THE RED CELL NUCLEOSIDE TRANSPORTER AS A BAND 4.5 PROTEIN......................................................................322 13.2.2 PRODUCTION OF NUCLEOSIDE TRANSPORTER ANTIBODIES .........................324 13.2.3 PURIFICATION OF THE HUMAN AND PIG RED CELL NUCLEOSIDE TRANSPORTERS ...................................................................................324 13.2.4 TRYPTIC CLEAVAGE STUDIES................................................................325 13.3 CDNA CLONING OF ENT NUCLEOSIDE TRANSPORT PROTEINS.........................325 13.3.1 CDNA CLONING AND HETEROLOGOUS EXPRESSION OF RECOMBINANT HUMAN AND RAT ENT1....................................................................325 13.3.2 CDNA CLONING AND HETEROLOGOUS EXPRESSION OF RECOMBINANT HUMAN AND RAT ENT2....................................................................327 13.3.3 OTHER ENT FAMILY MEMBERS..........................................................328 13.4 MOLECULAR PROPERTIES OF RECOMBINANT MAMMALIAN ENT PROTEINS ........329 13.4.1 ENT MEMBRANE TOPOLOGY .............................................................329 13.4.2 CHIMERIC STUDIES ............................................................................330 13.4.3 IDENTIFICATION OF AN EXOFACIAL CYSTEINE RESIDUE WITHIN THE RAT ENT2 TRANSLOCATION PORE...............................................................330 XIV CONTENTS 13.5 CONCLUSIONS ...........................................................................................332 REFERENCES .....................................................................................................333 14 GLUCOSE TRANSPORT........................................................................................ 339 14.1 INTRODUCTION ...........................................................................................339 14.2 SPECIFICITY OF SUGAR TRANSPORTERS ..........................................................339 14.3 NET VS. EXCHANGE TRANSPORT OF GLUCOSE.................................................340 14.4 MEMBRANE TOPOLOGY OF GLUTS ............................................................342 14.5 EVIDENCE FOR THE 12 TM HELIX MODEL FOR GLUTS .................................342 14.5.1 TRYPSINOLYSIS..................................................................................342 14.5.2 ANTIBODY STUDIES............................................................................343 14.5.3 SCANNING MUTAGENESIS STUDIES .......................................................344 14.5.4 CYSTEINE SCANNING MUTAGENESIS OF TMS 7, 10 AND 11 EVIDENCE FOR TWO HYDROPHILIC PORES TRAVERSING GLUT1.............................345 14.5.5 COVALENT LINKAGE OF INHIBITORS.......................................................346 14.5.6 CONFORMATIONAL CHANGE RESULTING FROM LIGAND INTERACTIONS.........347 14.5.7 BIOPHYSICAL STUDIES SHOWING HELICITY OF THE TRANSMEMBRANE STRANDS ...........................................................................................348 14.6 STRUCTURAL-FUNCTIONAL STUDIES ON GLUTS ..............................................349 14.6.1 FUNCTIONAL DIFFERENCES BETWEEN THE ISOFORMS GLUT1 AND GLUT4....................................................................................349 14.6.2 STRUCTURE-FUNCTIONAL COMPARISONS OF GLUTS 1 AND 4...................350 14.6.3 STRUCTURAL BASIS OF SPECIFICITY DIFFERENCES BETWEEN GLUTS .........351 14.7 PROBLEMS RELATING TO GLUCOSE TRANSPORT ...............................................352 14.7.1 PROBLEM 1: IS THE CARRIER A ONE MOBILE OR TWO FIXED SITE TRANSPORTER?...................................................................................352 14.7.2 PROBLEM 2: CAN LIGANDS BIND TO INSIDE AND OUTSIDE SITES SIMULTANEOUSLY?.............................................................................356 14.7.3 PROBLEM 3: IS GLUT1 AN ASYMMETRIC TRANSPORTER?......................356 14.8 ATP INTERACTIONS WITH SUGAR TRANSPORT .................................................358 14.8.1 ATP EFFECTS ON HUMAN GLUT1.....................................................358 14.8.2 ATP ON GLUCOSE TRANSPORT IN AVIAN RED CELLS .............................360 14.8.3 STRUCTURAL BASIS FOR ATP INTERACTION WITH GLUT1 ........................360 14.9 DRUG INTERACTIONS WITH GLUCOSE TRANSPORT.............................................361 14.9.1 BARBITURATES ....................................................................................361 14.9.2 GLUCOSE TRANSPORTER DEFICIENCY SYNDROME (GTDS) IN RELATION TO DRUG ACTION ...............................................................................362 14.9.3 STEROIDS, FLAVONES AND ISOFLAVONES ................................................362 14.9.4 THE L-TYPE CHANNEL ANTAGONISTS ..................................................363 14.9.5 ANTIPSYCHOTIC DRUGS........................................................................363 14.9.6 ACTIONS OF HIV PROTEASE INHIBITORS ON GLUTS..............................363 14.10 CONCLUSIONS..........................................................................................364 REFERENCES .....................................................................................................365 15 CALCIUM HOMEOSTASIS IN NORMAL AND ABNORMAL HUMAN RED CELLS ........ 373 15.1 INTRODUCTION ...........................................................................................373 15.2 METHODOLOGICAL CONSIDERATIONS .............................................................374 CONTENTS XV 15.3 USE OF INCORPORATED CA 2+ CHELATORS........................................................375 15.4 USE OF CA 2+ IONOPHORES ..........................................................................376 15.5 INHIBITION OF THE CA 2+ PUMP....................................................................376 15.6 CALCIUM HOMEOSTASIS IN PHYSIOLOGICAL CONDITIONS ...............................377 15.6.1 TOTAL AND TOTAL EXCHANGEABLE CALCIUM CONTENT OF RED CELLS .......377 15.6.2 THE PHYSIOLOGICAL [CA 2+ ] I LEVEL ......................................................378 15.6.3 CYTOPLASMIC CA 2+ BUFFERING............................................................379 15.7 PASSIVE CA 2+ TRANSPORT ...........................................................................380 15.8 THE CA 2+ PUMP AND THE PHYSIOLOGICAL PUMP-LEAK TURNOVER OF CA 2+ .....381 15.9 THE V MAX OF THE CA 2+ PUMP......................................................................381 15.10 EFFECTS OF DEOXYGENATION AND PH I ON THE V MAX OF THE CA 2+ PUMP .........382 15.11 ELEVATED CELL CA 2+ IN EXPERIMENTAL CONDITIONS ...................................383 15.11.1 SECONDARY EFFECTS OF ELEVATED [CA 2+ ] I...........................................383 15.11.2 EFFECTS OF PHYSIOLOGICAL AGENTS ON THE PERFORMANCE OF THE CA 2+ PUMP IN INTACT RED CELLS............................................385 15.11.3 POPULATION RESPONSE TO INCREASED CA 2+ INFLUX..............................386 15.12 ELEVATED CELL CA 2+ IN PATHOLOGICAL CONDITIONS.....................................388 15.12.1 MALARIA .........................................................................................389 15.12.2 SICKLE CELL ANAEMIA.....................................................................392 15.12.3 THALASSAEMIA ................................................................................395 REFERENCES......................................................................................................396 16 MAGNESIUM TRANSPORT..................................................................................407 16.1 INTRODUCTION............................................................................................407 16.2 MAGNESIUM HOMEOSTASIS IN RED CELLS...................................................407 16.3 RED CELL MAGNESIUM CONTENT................................................................408 16.3.1 DISTRIBUTION OF MAGNESIUM BETWEEN BOUND AND FREE FORMS.........408 16.3.2 LEVELS OF FREE IONIZED MAGNESIUM ................................................410 16.3.3 CHANGES IN MAGNESIUM CONTENT WITH CELL AGE .............................410 16.4 RED CELL MEMBRANE MAGNESIUM PERMEABILITY ......................................412 16.5 IS ACTIVE MAGNESIUM TRANSPORT NEEDED?..............................................413 16.6 MAGNESIUM TRANSPORT MECHANISMS.......................................................413 16.7 METHODS FOR INVESTIGATING MAGNESIUM TRANSPORT IN RED CELLS .............414 16.8 MAGNESIUM TRANSPORT IN HUMAN RED CELLS...........................................415 16.8.1 SODIUM-DEPENDENT MAGNESIUM TRANSPORT.....................................415 16.8.2 INHIBITORS OF SODIUM-DEPENDENT MAGNESIUM TRANSPORT................416 16.8.3 INTERACTIONS BETWEEN SODIUM AND MAGNESIUM ACROSS THE MEMBRANE ......................................................................................416 16.8.4 HOW MANY SODIUM IONS ARE EXCHANGED WITH EACH MAGNESIUM ION?.............................................................................417 16.8.5 CAN MAGNESIUM EFFLUX OCCUR AGAINST AN ELECTROCHEMICAL GRADIENT?..................................................................... ...................417 16.8.6 ROLE OF ATP ...................................................................................418 16.8.7 SODIUM-INDEPENDENT MAGNESIUM EFFLUX........................................418 16.8.8 CHANGES IN MAGNESIUM TRANSPORT IN DISEASE ................................419 16.9 MAGNESIUM TRANSPORT IN FERRET RED CELLS.............................................420 16.9.1 MAGNESIUM EFFLUX FROM FERRET RED CELLS ......................................420 XVI CONTENTS 16.9.2 MAGNESIUM UPTAKE ........................................................................422 16.9.3 TRANSPORT IN MAGNESIUM-LOADED CELLS ..........................................423 16.10 MAGNESIUM TRANSPORT IN RODENT RED CELLS.........................................423 16.10.1 RAT RED CELLS................................................................................424 16.10.2 HAMSTER AND GUINEA-PIG RED CELLS..............................................425 16.11 MAGNESIUM TRANSPORT IN AVIAN RED CELLS...........................................426 16.12 CONCLUSIONS..........................................................................................427 REFERENCES .....................................................................................................429 17 TRACE METAL TRANSPORT ................................................................................ 435 17.1 INTRODUCTION ...........................................................................................435 17.2 TRANSPORT SYSTEMS .................................................................................437 17.2.1 AS FREE METAL (HYDRATED IONS).......................................................437 17.2.2 TRANSPORT BY BAND 3 AS AN ANIONIC COMPLEX.................................442 17.2.3 UPTAKE DEPENDENT ON FORMATION OF METAL-AMINO ACID COMPLEXES .....................................................................................443 17.3 CONCLUSIONS ...........................................................................................446 REFERENCES .....................................................................................................447 18 MONOCARBOXYLATE AND OTHER ORGANIC ANION TRANSPORT............................ 451 18.1 INTRODUCTION ...........................................................................................451 18.2 THREE PATHWAYS FOR MONOCARBOXYLATE TRANSPORT ACROSS THE PLASMA MEMBRANE OF RED CELLS.........................................................................452 18.3 NON-IONIC DIFFUSION OF MONOCARBOXYLATES............................................452 18.4 BAND 3-MEDIATED TRANSPORT OF MONOCARBOXYLATES ................................453 18.5 THE SPECIFIC MONOCARBOXYLATE TRANSPORTER (MCT1) ............................454 18.5.1 KINETICS PROPERTIES .........................................................................454 18.5.2 SUBSTRATE SPECIFICITY.......................................................................456 18.5.3 INHIBITORS ........................................................................................459 18.6 IDENTIFICATION, CLONING AND SEQUENCING OF THE RED CELL MONOCARBOXYLATE CARRIER.......................................................................461 18.7 MCT1 IS A MEMBER OF A FAMILY OF PROTON-LINKED MONOCARBOXYLATE TRANSPORTERS...........................................................................................463 18.8 TOPOLOGY OF MCT1 AND OTHER MEMBERS OF THE MCT FAMILY ...............464 18.9 STRUCTURE FUNCTION RELATIONSHIPS IN MCT1 ...........................................465 18.10 MCT1 IS TIGHTLY ASSOCIATED WITH THE CELL SURFACE GLYCOPROTEINS GP70 (EMBIGIN) AND CD147 (BASIGIN) ...............................................466 18.11 MONOCARBOXYLATE TRANSPORT INTO MALARIA INFECTED RED CELLS..............468 18.12 CONCLUSIONS..........................................................................................469 REFERENCES .....................................................................................................470 19 WATER PERMEABILITY....................................................................................... 477 19.1 INTRODUCTION ...........................................................................................477 19.2 WATER DIFFUSION THROUGH LIPIDS.............................................................477 19.3 EVIDENCE FOR DISCRETE PERMEABILITY PATHWAYS .......................................478 19.4 MOLECULAR IDENTIFICATION OF WATER CHANNELS..........................................479 19.5 THE AQUAPORIN FAMILY...........................................................................480 CONTENTS XVII 19.6 STRUCTURE-FUNCTION RELATIONSHIPS...........................................................481 19.7 AQUAPORINS AND RED CELLS .....................................................................484 19.8 SUMMARY................................................................................................485 REFERENCES......................................................................................................485 20 GAS TRANSPORT...............................................................................................489 20.1 INTRODUCTION............................................................................................489 20.2 BASIC PRINCIPLES OF GAS TRANSPORT..........................................................489 20.2.1 OXYGEN TRANSPORT: FACTORS AFFECTING HAEMOGLOBIN FUNCTION .......489 20.2.2 FACTORS AFFECTING CARBON DIOXIDE TRANSPORT AND EXCRETION IN BLOOD..........................................................................................491 20.3 CONTROL OF RED CELL PH..........................................................................493 20.3.1 CONTROL OF RED CELL PH IN THE ABSENCE OF SIGNIFICANT SECONDARILY ACTIVE CATION OR PROTON TRANSPORT.............................493 20.3.2 EFFECT OF NA + /H + EXCHANGE ON RED CELL PH ...................................494 20.3.3 EFFECT OF K + -CL - COTRANSPORT ON RED CELL PH .................................497 20.4 ROLES OF PH CHANGES IN REGULATION OF OXYGEN TRANSPORT.....................498 20.5 RED CELL VOLUME AND HAEMOGLOBIN OXYGEN AFFINITY...........................499 20.6 INTERACTIONS BETWEEN MEMBRANE TRANSPORT AND REGULATION OF HAEMOGLOBIN OXYGEN AFFINITY BY ORGANIC PHOSPHATES ....................500 20.7 PATTERNS OF CARBON DIOXIDE TRANSPORT AND EXCRETION IN VERTEBRATES.....500 REFERENCES......................................................................................................504 21 THE HEREDITARY STOMATOCYTOSES AND ALLIED CONDITIONS: INHERITED DISORDERS NA + AND K + TRANSPORT .................................................................511 21.1 INTRODUCTION............................................................................................511 21.2 NORMAL RED CELL CATION TRANSPORT ........................................................511 21.3 HISTORY; NOSOLOGY..................................................................................512 21.4 TEMPERATURE EFFECTS...............................................................................513 21.5 CLINICAL ASPECTS .....................................................................................515 21.6 GENETIC MAPPING....................................................................................516 21.7 THE STOMATOCYTIC RED CELL ....................................................................516 21.8 THE STOMATIN PROTEIN .............................................................................517 21.9 POSSIBLE PATHOGENIC MECHANISMS FOR THE STOMATOCYTOSES.....................518 REFERENCES......................................................................................................520 22 METABOLIC DISORDERS .....................................................................................525 22.1 INTRODUCTION............................................................................................525 22.2 TO LIVE PERILOUSLY: THE LIFE OF A NORMAL RED CELL................................527 22.3 THE DAMAGING ROLE OF HEMICHROMES, FREE HAEM AND FREE IRON..........528 22.4 PATHOPHYSIOLOGICAL CONSEQUENCES OF OXIDANT DAMAGE.........................532 22.5 G6PD DEFICIENCY...................................................................................533 22.5.1 STRUCTURE OF NORMAL AND MUTANT G6PD..........................................533 22.5.2 INTRACELLULAR REGULATION OF G6PD IN NORMAL AND G6PD- DEFICIENT RED CELLS ........................................................................534 22.5.3 OXIDANT-INDUCED HAEMOLYSIS .........................................................535 22.5.4 THE FAVIC CRISIS .............................................................................535 XVIII CONTENTS 22.5.5 TOXIC COMPONENTS OF FAVA BEANS AND THEIR HAEMOLYTIC ACTIVITY ..........................................................................................536 22.5.6 OXIDANT STRESS AND CALCIUM HOMEOSTASIS......................................538 22.5.7 PREDOMINANTLY EXTRAVASCULAR HAEMOLYSIS IN OXIDATIVELY STRESSED G6PD-DEFICIENT RED CELLS...............................................539 22.6 RED CELL ALTERATIONS IN DIABETES MELLITUS .............................................540 22.6.1 GLYCATION OF PROTEINS IN DIABETES...................................................541 22.6.2 FUNCTIONAL EFFECTS OF RED CELL PROTEIN GLYCATION ..........................542 22.6.3 INCREASED PHAGOCYTOSIS OF DIABETIC RED CELLS: POSSIBLE MECHANISMS ...................................................................................543 22.6.4 ROLE OF RED CELL ALTERATIONS IN DIABETES COMPLICATIONS ...............544 22.7 CONCLUDING REMARKS .............................................................................544 REFERENCES .....................................................................................................545 23 SICKLE CELL DISEASE ........................................................................................ 549 23.1 INTRODUCTION ...........................................................................................549 23.2 MECHANISMS OF SICKLE RED CELL MEMBRANE DAMAGE ............................549 23.2.1 OXIDATION........................................................................................549 23.2.2 LOSS OF MEMBRANE..........................................................................550 23.2.3 BINDING OF HB S TO THE INNER MEMBRANE........................................550 23.3 RED CELL MEMBRANE STRUCTURAL ABNORMALITIES IN SICKLE CELL DISEASE...550 23.3.1 ALTERED CYTOSKELETON......................................................................550 23.3.2 ALTERED MEMBRANE LIPID COMPOSITION ..........................................551 23.4 RED CELL MEMBRANE TRANSPORT ABNORMALITIES IN SICKLE CELL DISEASE...551 23.4.1 K + -CL - COTRANSPORT ..........................................................................553 23.4.2 CA 2+ -ACTIVATED K + CHANNEL (GARDOS PATHWAY) ...............................554 23.4.3 DEOXYGENATION-INDUCED CATION FLUXES ..........................................555 23.5 THERAPEUTIC APPROACHES BASED ON INHIBITION OF SICKLE CELL DEHYDRATION ...........................................................................................556 23.5.1 INHIBITION OF GARDOS CHANNEL.........................................................556 23.5.2 INHIBITION OF K + -CL - COTRANSPORT .....................................................557 23.5.3 INHIBITION OF ANION PERMEABILITY ...................................................558 23.5.4 INHIBITION OF DEOXYGENATION-INDUCED FLUXES.................................558 REFERENCES .....................................................................................................558 24 THE MEMBRANE PHYSIOLOGY OF THE MALARIA-INFECTED RED CELL ............... 569 24.1 INTRODUCTION ...........................................................................................569 24.2 THE INTRAERYTHROCYTIC PHASE OF THE PARASITE LIFE CYCLE .........................570 24.3 TRANSPORT CHARACTERISTICS OF THE PARASITISED RED CELL MEMBRANE..........572 24.4 ELECTROPHYSIOLOGICAL CHARACTERISTICS OF THE PARASITISED RED CELL MEMBRANE..............................................................................................574 24.5 ROLES AND CONSEQUENCES OF THE ALTERED PERMEABILITY OF THE INFECTED RED CELL MEMBRANE...............................................................................576 24.6 THE PARASITOPHOROUS VACUOLE AND PARASITE MEMBRANES ........................578 24.7 CHEMOTHERAPEUTIC OPPORTUNITIES ...........................................................580 REFERENCES .....................................................................................................581 CONTENTS XIX 25 HYPERTENSION.................................................................................................587 25.1 INTRODUCTION............................................................................................587 25.2 TRANSPORTERS INVOLVED IN ABNORMAL MONOVALENT ION HANDLING IN EXPERIMENTAL MODELS OF PRIMARY HYPERTENSION ................................588 25.2.1 NA + /K + PUMP.......................................................................... .........588 25.2.2 NA + -K + -2CL - COTRANSPORT .................................................................589 25.2.3 NA + /H + EXCHANGE ............................................................................589 25.2.4 OTHER ION TRANSPORT PATHWAYS........................................................590 25.3 ION TRANSPORTERS IN ESSENTIAL HYPERTENSION ...........................................590 25.3.1 NA + -K + -2CL - COTRANSPORT .................................................................591 25.3.2 NA + /LI + COUNTERTRANSPORT VS. NA + /H + EXCHANGE...............................591 25.4 ARE ABNORMALITIES OF RED CELL ION TRANSPORTERS IN PRIMARY HYPERTENSION GENETICALLY DETERMINED?.................................................592 25.5 ROLE OF ION TRANSPORTERS EXPRESSED IN RED CELLS IN BLOOD PRESSURE REGULATION..............................................................................................593 25.6 EVIDENCE FOR THE INVOLVEMENT OF ION TRANSPORT ABNORMALITIES IN THE PATHOGENESIS OF HYPERTENSION......................................................594 25.7 MOLECULAR DETERMINANTS OF ABNORMAL ION TRANSPORT IN HYPERTENSION..595 25.8 CONCLUSION AND FUTURE DIRECTIONS..........................................................597 REFERENCES......................................................................................................598 26 DISORDERS OF BAND 3......................................................................................603 26.1 INTRODUCTION............................................................................................603 26.2 ERYTHROID PHENOTYPES WITH PARTIAL DEFICIENCY OF BAND 3 ......................603 26.2.1 AUTOSOMAL DOMINANT SPHEROCYTOSIS WITH BAND 3 DEFICIENCY .......603 26.2.2 AUTOSOMAL DOMINANT SPHEROCYTOSIS WITH PROTEIN 4.2 DEFICIENCY......................................................................................605 26.2.3 AUTOSOMAL RECESSIVE SPHEROCYTOSIS WITH PROTEIN 4.2 DEFICIENCY......................................................................................605 26.3 ERYTHROID PHENOTYPES WITH COMPLETE ABSENCE OF BAND 3.....................606 26.3.1 SEVERE HUMAN AUTOSOMAL RECESSIVE HAEMOLYTIC ANAEMIA ..........606 26.3.2 MOUSE BAND 3 MUTANTS AND KNOCKOUTS..........................................606 26.3.3 SEVERE SPHEROCYTIC HAEMOLYTIC ANAEMIA IN A STEER ......................607 26.3.4 PHENOTYPE OF CONGENITAL DYSERYTHROPOIETIC ANAEMIA IN ZEBRAFISH ....................................................................................607 26.4 OTHER ERYTHROID PHENOTYPES CAUSED BY BAND 3 MUTATIONS....................608 26.4.1 SOUTHEAST ASIAN OVALOCYTOSIS ........................................................608 26.4.2 HEREDITARY ACANTHOCYTOSIS .............................................................609 26.4.3 BLOOD GROUP ANTIGENS CARRIED BY BAND 3 .....................................609 26.5 NON-ERYTHROID PHENOTYPES CAUSED BY BAND 3 MUTATIONS .....................610 26.5.1 AUTOSOMAL DOMINANT DISTAL RENAL TUBULAR ACIDOSIS ....................610 26.5.2 AUTOSOMAL RECESSIVE DISTAL RENAL TUBULAR ACIDOSIS ....................612 26.6 CONCLUSION .............................................................................................613 REFERENCES......................................................................................................613 27 AMINO ACID TRANSPORT IN DISEASE ...............................................................621 27.1 INTRODUCTION............................................................................................621 XX CONTENTS 27.2 MEASUREMENT OF TRANSPORT KINETICS IN RED CELLS ..................................622 27.2.1 TRANSPORT SYSTEMS AND TRANSPORTERS ..............................................622 27.2.2 ROLE OF L-ARGININE TRANSPORT IN NITRIC OXIDE PRODUCTION .............622 27.3 URAEMIA, PATHOPHYSIOLOGY AND TREATMENT.............................................623 27.3.1 TRANSPORT ALTERATIONS IN URAEMIA...................................................624 27.3.2 L-ARGININE TRANSPORT AND URAEMIA................................................624 27.3.3 POSSIBLE MECHANISMS EXPLAINING THE INCREASED Y + TRANSPORT ACTIVITY IN URAEMIA........................................................................627 27.4 CHRONIC HEART FAILURE ............................................................................629 27.4.1 L-ARGININE-NO PATHWAY AND HEART FAILURE ...................................629 27.4.2 AMINO ACID PLASMA PROFILE IN CHRONIC HEART FAILURE....................630 27.4.3 ALTERATIONS ON L-ARGININE TRANSPORT IN CHRONIC HEART FAILURE......631 27.5 POSSIBLE OVERLAPPING OF MECHANISMS PRESENT IN BOTH CHRONIC HEART FAILURE AND URAEMIA ..............................................................................632 27.6 L-ARGININE TRANSPORT ALTERATIONS IN DIABETES .......................................633 27.7 L-ARGININE TRANSPORT AND SEPSIS...........................................................634 27.8 AMINO ACID TRANSPORT ALTERATIONS IN SICKLE CELL DISEASE ....................634 REFERENCES .....................................................................................................635 28 TRANSGENIC MODELS OF RED CELL DISORDERS.................................................. 643 28.1 INTRODUCTION ...........................................................................................643 28.2 PRODUCTION OF GENETICALLY MODIFIED ANIMALS........................................643 28.2.1 CONVENTIONAL TRANSGENESIS.............................................................644 28.2.2 GENE TARGETING...............................................................................645 28.2.3 TISSUE-SPECIFIC GENE TARGETING .....................................................649 28.3 TRANSGENIC MODELS OF RED CELL MEMBRANE DISORDERS...........................649 28.3.1 HEREDITARY SPHEROCYTOSIS ...............................................................650 28.3.2 HEREDITARY ELLIPTOCYTOSIS/PYROPOIKILOCYTOSIS.................................653 28.4 TRANSGENIC MODELS OF RED CELL TRANSPORT DISORDERS ............................654 28.4.1 GRADIENT-DRIVEN SYSTEMS ...............................................................655 28.4.2 STOMATOCYTOSIS ...............................................................................656 28.5 TRANSGENIC MODELS OF OTHER RED CELL DISORDERS...................................656 28.5.1 SICKLE CELL DISEASE.........................................................................657 28.5.2 HAEMOGLOBINOPATHIES.....................................................................658 28.5.3 THE HAEMOPHILIAS ..........................................................................659 28.5.4 METABOLIC DISORDERS .......................................................................660 28.6 GROWTH AND DIFFERENTIATION DEFECTS.......................................................661 28.6.1 THE ERYTHROPOIETIN AND THE ERYTHROPOIETIN RECEPTOR .....................662 28.6.2 THE ERYTHROID-SPECIFIC GATA TRANSCRIPTION FACTORS....................663 28.6.3 ERYTHROID KRUPPEL-LIKE FACTOR.......................................................665 REFERENCES .....................................................................................................666 29 RED CELL AGEING ............................................................................................ 673 29.1 INTRODUCTION: THE PROPERTIES OF MAMMALIAN RED CELLS ..........................673 29.2 RED CELL AGEING IN MAMMALS................................................................675 29.3 PROPERTIES OF HUMAN RED CELLS OF DIFFERENT DENSITY ............................677 29.4 PREPARATION OF RED CELLS OF WELL-DEFINED CELL AGE..............................680 CONTENTS XXI 29.5 THE AGEING OF RED CELLS REINVESTIGATED...............................................683 29.6 RED CELL STORAGE IN BLOOD BANKS ..........................................................685 REFERENCES......................................................................................................687 30 ACTIVE AND PASSIVE MONOVALENT ION TRANSPORT ASSOCIATION WITH MEMBRANE ANTIGENS IN SHEEP RED CELLS: A MOLECULAR RIDDLE.........691 30.1 INTRODUCTION: A WELL-ESTABLISHED CELLULAR MODEL ..................................691 30.2 CATION POLYMORPHISM THROUGH PUMPS AND LEAKS ..............................692 30.2.1 NA + /K + PUMPS .................................................................................693 30.2.2 LEAKS...........................................................................................694 30.2.3 AN INTEGRATED VIEW ........................................................................701 30.3 M AND L MEMBRANE ANTIGEN/ANTIBODY POLYMORPHISM .........................701 30.3.1 GENETIC BASIS..................................................................................701 30.3.2 MOLECULAR PROPERTIES OF THE M/L ANTIGENS.....................................702 30.3.3 THE M/L ANTIBODIES .......................................................................705 30.4 FUNCTIONAL ASSOCIATION OF ANTIGENS WITH PUMPS AND LEAKS ..............706 30.4.1 NA + /K + PUMP ACTIVATION BY THE L P ANTIBODY..................................706 30.4.2 K + -CL - COTRANSPORT INHIBITION BY THE L L ANTIBODY...........................707 30.4.3 COMPLEMENT-MEDIATED HAEMOLYSIS BY ANTI-M AND ANTI-L...........708 30.5 CLONAL VS. MATURATIONAL CHANGES OF TRANSPORTERSAND ANTIGENS.............709 30.5.1 CLONAL CELLULAR CHANGES IN LAMBS.................................................709 30.5.2 RETICULOCYTE MATURATION IN ANAEMIC SHEEP...................................710 30.6 OVERALL PHYSIOLOGICAL CONSEQUENCES AND THE HK/LK DIMORPHISM ......711 30.7 MEMBRANE ANTIGENS AND TRANSPORT IN SPECIES OTHER THAN RUMINANTS ..711 REFERENCES.................................................................... ..................................712 31 COMPARATIVE PHYSIOLOGY OF RED CELL MEMBRANE TRANSPORT ....................721 31.1 INTRODUCTION............................................................................................721 31.2 CARNIVORES * DOG AND CAT......................................................................722 31.3 HERBIVORES * HORSE AND DEER.................................................................724 31.4 RODENTS * MOUSE AND RAT ......................................................................725 31.5 LOWER VERTEBRATES..................................................................................726 31.5.1 BIRDS ...............................................................................................726 31.5.2 AMPHIUMA......................................................................................727 31.6 CONCLUSION .............................................................................................728 REFERENCES......................................................................................................729 INDEX ...................................................................................................................735
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genre	(DE-588)4143413-4 Aufsatzsammlung gnd-content
genre_facet	Aufsatzsammlung
id	DE-604.BV017350351
illustrated	Illustrated
indexdate	2024-07-09T19:16:57Z
institution	BVB
isbn	3540442278
language	English
oai_aleph_id	oai:aleph.bib-bvb.de:BVB01-010457034
oclc_num	249003045
open_access_boolean
owner	DE-355 DE-BY-UBR DE-11
owner_facet	DE-355 DE-BY-UBR DE-11
physical	XXVIII, 748 S. graph. Darst.
publishDate	2003
publishDateSearch	2003
publishDateSort	2003
publisher	Springer
record_format	marc
spelling	Red cell membrane transport in health and disease with 31 tables I. Bernhardt ... (eds.) Berlin [u.a.] Springer 2003 XXVIII, 748 S. graph. Darst. txt rdacontent n rdamedia nc rdacarrier Literaturangaben Erythrozytenmembran - Membrantransport - Physiologie - Aufsatzsammlung Erythrozytopathie - Pathophysiologie - Aufsatzsammlung Physiologie (DE-588)4045981-0 gnd rswk-swf Membrantransport (DE-588)4038575-9 gnd rswk-swf Pathophysiologie (DE-588)4044898-8 gnd rswk-swf Erythrozytenmembran (DE-588)4152965-0 gnd rswk-swf Erythrozytopathie (DE-588)4277002-6 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Erythrozytenmembran (DE-588)4152965-0 s Membrantransport (DE-588)4038575-9 s Physiologie (DE-588)4045981-0 s DE-604 Erythrozytopathie (DE-588)4277002-6 s Pathophysiologie (DE-588)4044898-8 s Bernhardt, Ingolf Sonstige oth SWB Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010457034&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis
spellingShingle	Red cell membrane transport in health and disease with 31 tables Erythrozytenmembran - Membrantransport - Physiologie - Aufsatzsammlung Erythrozytopathie - Pathophysiologie - Aufsatzsammlung Physiologie (DE-588)4045981-0 gnd Membrantransport (DE-588)4038575-9 gnd Pathophysiologie (DE-588)4044898-8 gnd Erythrozytenmembran (DE-588)4152965-0 gnd Erythrozytopathie (DE-588)4277002-6 gnd
subject_GND	(DE-588)4045981-0 (DE-588)4038575-9 (DE-588)4044898-8 (DE-588)4152965-0 (DE-588)4277002-6 (DE-588)4143413-4
title	Red cell membrane transport in health and disease with 31 tables
title_auth	Red cell membrane transport in health and disease with 31 tables
title_exact_search	Red cell membrane transport in health and disease with 31 tables
title_full	Red cell membrane transport in health and disease with 31 tables I. Bernhardt ... (eds.)
title_fullStr	Red cell membrane transport in health and disease with 31 tables I. Bernhardt ... (eds.)
title_full_unstemmed	Red cell membrane transport in health and disease with 31 tables I. Bernhardt ... (eds.)
title_short	Red cell membrane transport in health and disease
title_sort	red cell membrane transport in health and disease with 31 tables
title_sub	with 31 tables
topic	Erythrozytenmembran - Membrantransport - Physiologie - Aufsatzsammlung Erythrozytopathie - Pathophysiologie - Aufsatzsammlung Physiologie (DE-588)4045981-0 gnd Membrantransport (DE-588)4038575-9 gnd Pathophysiologie (DE-588)4044898-8 gnd Erythrozytenmembran (DE-588)4152965-0 gnd Erythrozytopathie (DE-588)4277002-6 gnd
topic_facet	Erythrozytenmembran - Membrantransport - Physiologie - Aufsatzsammlung Erythrozytopathie - Pathophysiologie - Aufsatzsammlung Physiologie Membrantransport Pathophysiologie Erythrozytenmembran Erythrozytopathie Aufsatzsammlung
url	http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010457034&sequence=000001&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA
work_keys_str_mv	AT bernhardtingolf redcellmembranetransportinhealthanddiseasewith31tables

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