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Titolo:
ACTIVATION OF SRF-REGULATED CHROMOSOMAL TEMPLATES BY RHO-FAMILY GTPASES REQUIRES A SIGNAL THAT ALSO INDUCES H4 HYPERACETYLATION
Autore:
ALBERTS AS; GENESTE O; TREISMAN R;
Indirizzi:
IMPERIAL CANC RES FUND,TRANSCRIPT LAB,44 LINCOLNS INN FIELDS LONDON WC2A 3PX ENGLAND IMPERIAL CANC RES FUND,TRANSCRIPT LAB LONDON WC2A 3PX ENGLAND
Titolo Testata:
Cell
fascicolo: 4, volume: 92, anno: 1998,
pagine: 475 - 487
SICI:
0092-8674(1998)92:4<475:AOSCTB>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORE HISTONE HYPERACETYLATION; PROTEIN-SYNTHESIS INHIBITORS; SERUM RESPONSE ELEMENT; TUMOR VIRUS PROMOTER; C-FOS PROMOTER; TERNARY COMPLEX; TRANSCRIPTIONAL ACTIVATION; NUCLEOSOME STRUCTURE; CHROMATIN STRUCTURE; GENE-EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
57
Recensione:
Indirizzi per estratti:
Citazione:
A.S. Alberts et al., "ACTIVATION OF SRF-REGULATED CHROMOSOMAL TEMPLATES BY RHO-FAMILY GTPASES REQUIRES A SIGNAL THAT ALSO INDUCES H4 HYPERACETYLATION", Cell, 92(4), 1998, pp. 475-487

Abstract

Constitutively active forms of the small GTPases RhoA (RhoA.V14) and Cdc42 (Cdc42.V12) induce expression of extrachromosomal SRF reporter genes in microinjection experiments, but only Cdc42.V12 can efficientlyactivate a chromosomal template. Both SAPK/JNK-dependent or -independent signals can cooperate with RhoA.V14 to activate chromosomal SRF reporters, and it is SAPK/JNK activation by Cdc42.V12 that allows it to activate chromosomal templates. Cooperating signals can be bypassed bydeacetylase inhibitors. Three findings show that histone H4 hyperacetylation is one target for cooperating signals, although it alone is not sufficient: (1) Cdc42.V12, but not RhoA.V14, induces H4 hyperacetylation; (2) cooperating signals use the same SAPK/JNK-dependent or -independent pathways to induce H4 hyperacetylation; (3) growth factor and stress stimuli induce substantial H4 hyperacetylation, detectable in reporter gene chromatin. These data establish a link between signal-regulated acetylation events and gene transcription.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 07/04/20 alle ore 22:59:44