Molecular cloning and characterization of RGC-32, a novel gene induced by complement activation in oligodendrocytes

被引:88
作者
Badea, TC [1 ]
Niculescu, FI [1 ]
Soane, L [1 ]
Shin, ML [1 ]
Rus, H [1 ]
机构
[1] Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA
关键词
D O I
10.1074/jbc.273.41.26977
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
Sublytic complement activation on oligodendrocytes (OLG) down-regulates expression of myelin genes and induces cell cycle in culture. Differential display (DD) was used to search for new genes whose expression is altered in response to complement and that may be involved in cell cycle activation. DD bands showing either increased or decreased mRNA expression in response to complement were identified and designated Response Genes to Complement (RGC) 1-32, RGC-1 is identical with heat shock protein 105, RGC-2 with poly(ADP-ribose) polymerase, and RGC-10 with IP-10, A new gene, RGC-32, that encodes a protein of 137 amino acids was cloned. RGC-32 has no homology with other known proteins, and contains no motif that would indicate its function. In OLG, the mRNA expression was increased by complement activation and by terminal complement complex assembly. RGC-32 protein was localized in the cytoplasm and co-immunoprecipitated with cdc2 kinase. Overexpression of RGC-32 increased DNA synthesis in OLGxC6 glioma cell hybrids. These results suggest that RGC-32 may play a role in cell cycle activation.
引用
收藏
页码:26977 / 26981
页数:5
相关论文
共 24 条
[1]   TERMINAL COMPLEMENT PROTEINS C5B-9 RELEASE BASIC FIBROBLAST GROWTH-FACTOR AND PLATELET-DERIVED GROWTH-FACTOR FROM ENDOTHELIAL-CELLS [J].
BENZAQUEN, LR ;
NICHOLSONWELLER, A ;
HALPERIN, JA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 179 (03) :985-992
[2]  
CARNEY DF, 1990, J IMMUNOL, V145, P623
[3]   IMMUNOCYTOCHEMICAL LOCALIZATION OF THE TERMINAL COMPLEMENT COMPLEX IN MULTIPLE-SCLEROSIS [J].
COMPSTON, DAS ;
MORGAN, BP ;
CAMPBELL, AK ;
WILKINS, P ;
COLE, G ;
THOMAS, ND ;
JASANI, B .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 1989, 15 (04) :307-316
[4]   CEREBROSPINAL-FLUID C9 IN DEMYELINATING DISEASE [J].
COMPSTON, DAS ;
MORGAN, BP ;
OLEESKY, D ;
FIFIELD, R ;
CAMPBELL, AK .
NEUROLOGY, 1986, 36 (11) :1503-1506
[5]   TERMINAL COMPLEMENT COMPLEX C5B-9 STIMULATES MITOGENESIS IN 3T3 CELLS [J].
HALPERIN, JA ;
TARATUSKA, A ;
NICHOLSONWELLER, A .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 91 (05) :1974-1978
[6]  
Lang TJ, 1997, J NEUROCHEM, V68, P1581
[7]   THE ROLE OF COMPLEMENT IN THE PATHOGENESIS OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS [J].
LININGTON, C ;
MORGAN, BP ;
SCOLDING, NJ ;
WILKINS, P ;
PIDDLESDEN, S ;
COMPSTON, DAS .
BRAIN, 1989, 112 :895-911
[8]   IMMUNOHISTOCHEMICAL LOCALIZATION OF TERMINAL COMPLEMENT COMPONENT-C9 IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS [J].
LININGTON, C ;
LASSMANN, H ;
MORGAN, BP ;
COMPSTON, DAS .
ACTA NEUROPATHOLOGICA, 1989, 79 (01) :78-85
[9]  
LIU WT, 1983, J IMMUNOL, V131, P778
[10]  
NICULESCU F, 1994, J BIOL CHEM, V269, P4417