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Titolo:
Altered regulation of cell cycle machinery involved in interleukin-1-induced G(1) and G(2) phase growth arrest of A375S2 human melanoma cells
Autore:
Murai, T; Nakagawa, Y; Maeda, H; Terada, K;
Indirizzi:
Natl Inst Hlth Sci, Dept Bbiol Evaluat, Osaka Branch, Div Biol Evaluat,Chuo Ku, Osaka 5400006, Japan Natl Inst Hlth Sci Osaka Japan 5400006 uat,Chuo Ku, Osaka 5400006, Japan
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 9, volume: 276, anno: 2001,
pagine: 6797 - 6806
SICI:
0021-9258(20010302)276:9<6797:AROCCM>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR NECROSIS FACTOR; RETINOBLASTOMA PROTEIN; DEPENDENT KINASES; GENE-EXPRESSION; CDK INHIBITORS; CYTO-TOXICITY; DNA-DAMAGE; HUMAN MYT1; I TRIAL; P21;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
79
Recensione:
Indirizzi per estratti:
Indirizzo: Murai, T Natl Inst Hlth Sci, Dept Bbiol Evaluat, Osaka Branch, Div Biol Evaluat,Chuo Ku, Hoenzaka 1-1-43, Osaka 5400006, Japan Natl Inst Hlth Sci Hoenzaka 1-1-43 Osaka Japan 5400006 06, Japan
Citazione:
T. Murai et al., "Altered regulation of cell cycle machinery involved in interleukin-1-induced G(1) and G(2) phase growth arrest of A375S2 human melanoma cells", J BIOL CHEM, 276(9), 2001, pp. 6797-6806

Abstract

Interleukin-1 (IL-1) inhibits the growth of A375S2 human melanoma cells byarresting them at G(1) and G(2) phases of the cell cycle. The arrests are preceded by a rapid decrease in kinase activities of cyclin E-Cdk2 and cyclin B1-Cdc2, which are critical for G(1)-S and G(2)-M progression, respectively. IL-1 quickly enhances the protein expression of the CDK inhibitor p21(cip1). The induced p21 binds preferentially to cyclin E-Cdk2, and the increase in pal binding parallels the decrease in cyclin E-Cdk2 activity. Thus, p21 is likely to be responsible for the inhibition of cyclin E-Cdk2 activity and G(1) arrest. Coinciding with the decrease in cyclin B1-Cdc2 activity,there is an increase in tyrosine phosphorylation of Cdc2, suggesting that an increase in the inactive Tyr-15-phosphorylated form of Cdc2 is involved in the decrease in cyclin B1-Cdc2 activity and G(2) arrest. Furthermore, wefound that IL-1 causes rapid dephosphorylation of p107, but not of pRb or p130, while the total protein levels of p130 are increased. Thus, IL-1 may exert its growth arresting effects via p107 and p130 pathways rather than through pRb.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/05/20 alle ore 14:58:54