CYCLOSPORINE AND MITOCHONDRIAL DYSFUNCTION

被引：9

作者：

MCGUINNESS, O ^{[1
]}

CROMPTON, M ^{[1
]}

机构：

[1] UNIV LONDON UNIV COLL,DEPT BIOCHEM,LONDON WC1E 6BT,ENGLAND

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 1990年 / 18卷 / 05期

关键词：

D O I：

10.1042/bst0180883

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

引用

页码：883 / 884

页数：2

共 10 条

[1] CYTOSOLIC FREE CA-2+ IN SINGLE-RAT HEART-CELLS DURING ANOXIA AND REOXYGENATION
ALLSHIRE, A
PIPER, HM
CUTHBERTSON, KSR
COBBOLD, PH
[J]. BIOCHEMICAL JOURNAL, 1987, 244 (02) : 381 - 385
[2] THE REVERSIBLE CA-2+-INDUCED PERMEABILIZATION OF RAT-LIVER MITOCHONDRIA
ALNASSER, I
CROMPTON, M
[J]. BIOCHEMICAL JOURNAL, 1986, 239 (01) : 19 - 29
[3] BROEKEMEIER KM, 1985, J BIOL CHEM, V260, P105
[4] KINETIC EVIDENCE FOR A HEART MITOCHONDRIAL PORE ACTIVATED BY CA-2+, INORGANIC-PHOSPHATE AND OXIDATIVE STRESS - A POTENTIAL MECHANISM FOR MITOCHONDRIAL DYSFUNCTION DURING CELLULAR CA-2+ OVERLOAD
CROMPTON, M
COSTI, A
[J]. EUROPEAN JOURNAL OF BIOCHEMISTRY, 1988, 178 (02): : 489 - 501
[5] CROMPTON M, 1988, BIOCHEM J, V255, P357
[6] A HEART MITOCHONDRIAL CA-2+-DEPENDENT PORE OF POSSIBLE RELEVANCE TO RE-PERFUSION-INDUCED INJURY - EVIDENCE THAT ADP FACILITATES PORE INTERCONVERSION BETWEEN THE CLOSED AND OPEN STATES
CROMPTON, M
COSTI, A
[J]. BIOCHEMICAL JOURNAL, 1990, 266 (01) : 33 - 39
[7] ALLOSTERIC INHIBITION OF THE CA2+-ACTIVATED HYDROPHILIC CHANNEL OF THE MITOCHONDRIAL INNER MEMBRANE BY NUCLEOTIDES
HAWORTH, RA
HUNTER, DR
[J]. JOURNAL OF MEMBRANE BIOLOGY, 1980, 54 (03) : 231 - 236
[8] MYOCARDIAL ADENINE POOL DEPLETION AND RECOVERY OF MECHANICAL FUNCTION FOLLOWING ISCHEMIA
HUMPHREY, SM
HOLLISS, DG
SEELYE, RN
[J]. AMERICAN JOURNAL OF PHYSIOLOGY, 1985, 248 (05): : H644 - H651
[9] REGULATION OF BRAIN MITOCHONDRIAL CALCIUM-ION TRANSPORT - ROLE OF ATP IN THE DISCRIMINATION BETWEEN KINETIC AND MEMBRANE-POTENTIAL-DEPENDENT CALCIUM-ION EFFLUX MECHANISMS
NICHOLLS, DG
SCOTT, ID
[J]. BIOCHEMICAL JOURNAL, 1980, 186 (03) : 833 - 839
[10] TURRENS JF, 1982, ARCH BIOCHEM BIOPHYS, V217, P401, DOI 10.1016/0003-9861(82)90518-5

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