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Titolo:
ACTIVATION OF JUNB AND C-MYC PRIMARY RESPONSE GENES BY INTERLEUKIN-9 IN A HUMAN FACTOR-DEPENDENT CELL-LINE
Autore:
KANG LY; YANG YC;
Indirizzi:
INDIANA UNIV,SCH MED,WALTHER ONCOL CTR,DEPT BIOCHEM MOLEC BIOL,975 WALNUT ST,IB 540 INDIANAPOLIS IN 46202 INDIANA UNIV,SCH MED,WALTHER ONCOL CTR,DEPT BIOCHEM MOLEC BIOL INDIANAPOLIS IN 46202 INDIANA UNIV,SCH MED,DEPT MED HEMATOL ONCOL INDIANAPOLIS IN 46202
Titolo Testata:
Journal of cellular physiology
fascicolo: 3, volume: 163, anno: 1995,
pagine: 623 - 630
SICI:
0021-9541(1995)163:3<623:AOJACP>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-ENHANCING ACTIVITY; COLONY-STIMULATING FACTOR; PROTEIN-TYROSINE KINASE; SIGNAL TRANSDUCTION; BONE-MARROW; EXPRESSION CLONING; IL-2 RECEPTOR; MURINE; TRANSCRIPTION; PROLIFERATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
53
Recensione:
Indirizzi per estratti:
Citazione:
L.Y. Kang e Y.C. Yang, "ACTIVATION OF JUNB AND C-MYC PRIMARY RESPONSE GENES BY INTERLEUKIN-9 IN A HUMAN FACTOR-DEPENDENT CELL-LINE", Journal of cellular physiology, 163(3), 1995, pp. 623-630

Abstract

Interleukin 9 (IL-9) stimulates the proliferation of various hematopoietic cell types. To elucidate the molecular mechanisms underlying thecell proliferation action, immediate-early gene expression elicited by IL-9 in a human factor-dependent cell line, MO7e, was studied. IL-9 stimulation resulted in a rapid and transient elevation of primary response genes including junB and c-myc. The differential effects of protein kinase inhibitors, herbimycin A, genistein, and H-7 on the steady-state mRNA level and the transcription rate of junB and c-myc genes triggered by IL-9 were also investigated. Herbimycin A, but not genistein, specifically inhibited the expression of junB steady-state mRNA andthe in vitro transcription of the junB gene. IL-9-enhanced c-myc geneexpression was completely inhibited by both herbimycin A and genistein at the level of transcriptional initiation. H-7 failed to inhibit c-myc, but partially abolished junB mRNA induction. The role of protein kinase C in IL-9-mediated junB induction was also examined. The different responses of junB and c-myc messages to protein kinase inhibitors suggested that more than one pathway may be involved in IL-9-mediated signal transduction which leads to the expression of junB and c-myc genes. (C) 1995 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/10/20 alle ore 00:23:51