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Titolo:
An important role of CDK inhibitor p18(INK4c) in modulating antigen receptor-mediated T cell proliferation
Autore:
Kovalev, GI; Franklin, DS; Coffield, VM; Xiong, Y; Su, L;
Indirizzi:
Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Microbiol & Immunol,Sch Med, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 h Med, Chapel Hill, NC 27599 USA Univ N Carolina, Sch Med, Dept Biochem & Biophys, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 ophys, Chapel Hill, NC 27599 USA
Titolo Testata:
JOURNAL OF IMMUNOLOGY
fascicolo: 6, volume: 167, anno: 2001,
pagine: 3285 - 3292
SICI:
0022-1767(20010915)167:6<3285:AIROCI>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT KINASE INHIBITOR; CYCLE PROGRESSION; MICE LACKING; INK4 FAMILY; P27(KIP1) EXPRESSION; MOUSE DEVELOPMENT; TUMOR-SUPPRESSOR; LYMPHOCYTES-T; PROTEIN; ACTIVATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
65
Recensione:
Indirizzi per estratti:
Indirizzo: Su, L Univ N Carolina, Lineberger Comprehens Canc Ctr, Dept Microbiol & Immunol,Sch Med, Chapel Hill, NC 27599 USA Univ N Carolina Chapel Hill NC USA 27599 Chapel Hill, NC 27599 USA
Citazione:
G.I. Kovalev et al., "An important role of CDK inhibitor p18(INK4c) in modulating antigen receptor-mediated T cell proliferation", J IMMUNOL, 167(6), 2001, pp. 3285-3292

Abstract

The inhibitors of cyclin-dependent kinase (CDK) 4 (INK4) bind CDK4/6 to prevent their association with D-cyclins and G, cell cycle initiation and progression. We report here that among the seven CDK inhibitors, p18(INK4c) played an important role in modulating TCR-mediated T cell proliferation. Loss of p18(INK4c) in T cells led to hyperproliferation in response to CD3 stimulation. p18(INK4c)-null mice developed lymphoproliferative disorder and Tcell lymphomas. Expression of IL-2, IL-2R-alpha, and the major G, cell cycle regulatory proteins was not altered in p18-null T cells. Both FK506 and rapamycin efficiently inhibited proliferation of p18-null T cells. In activated T cells, p18(INK4c) remained constant, and preferentially associated with and inhibited CDK6 but not CDK4. We propose that p18(INK4c) sets an inhibitory threshold in T cells and one function of CD28 costimulation is to counteract the p18(INK4c) inhibitory activity on CDK6-cyclin D complexes. The p18(INK4c) protein may provide a novel target to modulate T cell immunity.

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Documento generato il 30/11/20 alle ore 07:04:32