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Titolo:
THE GABP-RESPONSIVE ELEMENT OF THE INTERLEUKIN-2 ENHANCER IS REGULATED BY JNK SAPK-ACTIVATING PATHWAYS IN T-LYMPHOCYTES/
Autore:
HOFFMEYER A; AVOTS A; FLORY E; WEBER CK; SERFLING E; RAPP UR;
Indirizzi:
UNIV WURZBURG,INST MED STRAHLENKUNDE & ZELLFORSCH,MSZ,VERSBACHER STR 5 D-97078 WURZBURG GERMANY UNIV WURZBURG,INST MED STRAHLENKUNDE & ZELLFORSCH,MSZ D-97078 WURZBURG GERMANY UNIV WURZBURG,INST PATHOL D-97080 WURZBURG GERMANY
Titolo Testata:
The Journal of biological chemistry
fascicolo: 17, volume: 273, anno: 1998,
pagine: 10112 - 10119
SICI:
0021-9258(1998)273:17<10112:TGEOTI>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-TRANSDUCTION PATHWAYS; OXIDASE SUBUNIT-IV; PROTEIN-KINASE; TRANSCRIPTION FACTORS; BINDING-PROTEIN; C-JUN; GENE-TRANSCRIPTION; E4TF1 SUBUNITS; ETS; CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
58
Recensione:
Indirizzi per estratti:
Citazione:
A. Hoffmeyer et al., "THE GABP-RESPONSIVE ELEMENT OF THE INTERLEUKIN-2 ENHANCER IS REGULATED BY JNK SAPK-ACTIVATING PATHWAYS IN T-LYMPHOCYTES/", The Journal of biological chemistry, 273(17), 1998, pp. 10112-10119

Abstract

T cell activation leads via multiple intracellular signaling pathwaysto rapid induction of interleukin-a (IL-2) expression, which can be mimicked by costimulation with 12-O-tetradecanoylphorbol-13-acetate (TPA) and ionomycin. We have identified a distal IL-2 enhancer regulated by the Raf-MEK-ERK signaling pathway, which can be induced by TPA/ionomycin treatment. It contains a dyad symmetry element (DSE) controlled by the Ets-like transcription factor GA-binding protein (GABP), a target of activated ERK. TPA/ionomycin treatment of T cells stimulates both mitogen-activated ERK, as well as the stress-activated mitogen-activated protein kinase family members JNK/SAPK and p38. In this study, weinvestigated the contribution of the stress-activated pathways to theinduction of the distal IL-2 enhancer. We show that JNK- but not p38-activating pathways regulate the DSE activity. Furthermore, the JNK/SAPK signaling pathway cooperates with the Raf-MEK-ERK cascade in TPA/ionomycin-induced DSE activity. In T cells, overexpression of SPRK/MLK3,an activator of JNR/SAPK, strongly induces DSE-dependent transcription and dominant negative kinases of SEK and SAPK impair TPA/ionomycin-induced DSE activity. Blocking both ERK and JNK/SAPK pathways abolishesthe DSE induction. The inducibility of the DSE is strongly dependent on the Ets-core motifs, which are bound by GABP. Both subunits of GABPare phosphorylated upon JNK activation in vivo and three different isoforms of JNK/SAPK, but not p38, in vitro. Our data suggest that GABP is targeted by signaling events from both ERK and JNK/SAPK pathways. GABP therefore is a candidate for signal integration and regulation of IL-2 transcription in T lymphocytes.

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Documento generato il 22/09/20 alle ore 20:18:21