Multiple roles of the DSCR1 (Adapt78 or RCAN1) gene and its protein product Calcipressin 1 (or RCAN1) in disease

被引：98
作者：
Harris, CD [1 ]
Ermak, G [1 ]
Davies, KJA [1 ]
机构：
[1] Univ So Calif, Ethel Percy Andrus Gerontol Ctr, Los Angeles, CA 90089 USA
来源：
CELLULAR AND MOLECULAR LIFE SCIENCES | 2005年 / 62卷 / 21期
关键词：
Down syndrome; Alzheimer's disease; cardiac hypertrophy; calcineurin; calcipressin; 1; MCIP1; DSCR1; Adapt78; RCAN1;
D O I：
10.1007/s00018-005-5085-4
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：
The DSCR1 (Adapt78) gene(1) is transiently induced by stresses to temporarily protect cells against further potentially lethal challenges. However, chronic expression of the DSCR1 (Adapt78) gene has now been implicated in several pathological conditions including Alzheimer's disease, Down syndrome and cardiac hypertrophy. Calcipressin 1 has been shown to function through direct binding and inhibition of the serine threonine protein phosphatase Calcineurin. Pharmacological inhibition of calcineurin, by the immunosuppressive drugs cyclosporin A and FK506, affects a wide variety of diseases. It is, therefore, likely that this endogenous calcineurin inhibitor, calcipressin 1, may also play a role in a variety of human diseases.
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收藏
页码：2477 / 2486
页数：10
相关论文
共 90 条
[11]  
Cho ML, 2002, ARTHRITIS RHEUM-US, V46, P42, DOI 10.1002/1529-0131(200201)46:1<42::AID-ART10026>3.0.CO
[12]  
2-A
[13]  
Chu ZL, 1996, MOL CELL BIOL, V16, P5974
[14]  
CRAIN BJ, 1988, NEUROSCIENCE, V27, P387
[15]   Hamster adapt78 mRNA is a Down syndrome critical region homologue that is inducible by oxidative stress [J].
Crawford, DR ;
Leahy, KP ;
Abramova, N ;
Lan, L ;
Wang, YH ;
Davies, KJA .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1997, 342 (01) :6-12
[16]   The essential role of calcium in induction of the DSCR1 (ADAPT78) gene [J].
Davies, KJA ;
Harris, CD ;
Ermak, G .
BIOFACTORS, 2001, 15 (2-4) :91-93
[17]   IMMUNOSUPPRESSANT FK506 ENHANCES PHOSPHORYLATION OF NITRIC-OXIDE SYNTHASE AND PROTECTS AGAINST GLUTAMATE NEUROTOXICITY [J].
DAWSON, TM ;
STEINER, JP ;
DAWSON, VL ;
DINERMAN, JL ;
UHL, GR ;
SNYDER, SH .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (21) :9808-9812
[18]   Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo [J].
De Windt, LJ ;
Lim, HW ;
Bueno, OF ;
Liang, QR ;
Delling, U ;
Braz, JC ;
Glascock, BJ ;
Kimball, TF ;
del Monte, F ;
Hajjar, RJ ;
Molkentin, JD .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (06) :3322-3327
[19]   Amyloid beta peptide formation in cell-free preparations - Regulation by protein kinase C, calmodulin, and calcineurin [J].
Desdouits, F ;
Buxbaum, JD ;
DesdouitsMagnen, J ;
Nairn, AC ;
Greengard, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (40) :24670-24674
[20]   Pressure overload induces severe hypertrophy in mice treated with cyclosporine, an inhibitor of calcineurin [J].
Ding, B ;
Price, RL ;
Borg, TK ;
Weinberg, EO ;
Halloran, PF ;
Lorell, BH .
CIRCULATION RESEARCH, 1999, 84 (06) :729-734
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