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Titolo:
Opposing roles of Elk-1 and its brain-specific isoform, short Elk-1, in nerve growth factor-induced PC12 differentiation
Autore:
Vanhoutte, P; Nissen, JL; Brugg, B; Della Gaspera, B; Besson, MJ; Hipskind, RA; Caboche, J;
Indirizzi:
Univ Paris 06, Inst Neurosci, Lab Neurochim Anat, CNRS,UMR 7624, F-75005 Paris, France Univ Paris 06 Paris France F-75005 CNRS,UMR 7624, F-75005 Paris, France Univ Paris 06, Inst Neurosci, Lab Dev & Vieillissement SNC, CNRS,UMR 7624,F-75005 Paris, France Univ Paris 06 Paris France F-75005 , CNRS,UMR 7624,F-75005 Paris, France Univ Paris 06, Inst Neurosci, Mol Neurogenet Lab, CNRS,UMR 7624, F-75005 Paris, France Univ Paris 06 Paris France F-75005 CNRS,UMR 7624, F-75005 Paris, France CNRS, IFR 24, UMR 5535, Inst Genet Mol, F-34293 Montpellier 5, France CNRS Montpellier France 5 Inst Genet Mol, F-34293 Montpellier 5, France
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 7, volume: 276, anno: 2001,
pagine: 5189 - 5196
SICI:
0021-9258(20010216)276:7<5189:OROEAI>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASES; TERNARY COMPLEX FACTORS; SERUM RESPONSE ELEMENT; TRANSCRIPTION FACTOR ELK-1; C-FOS PROMOTER; MESSENGER-RNA; SIGNALING PATHWAYS; NEURITE OUTGROWTH; GENE-EXPRESSION; FACTOR P62TCF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
57
Recensione:
Indirizzi per estratti:
Indirizzo: Caboche, J Univ Paris 06, Inst Neurosci, Lab Neurochim Anat, CNRS,UMR 7624, F-75005 Paris, France Univ Paris 06 Paris France F-75005 624, F-75005 Paris, France
Citazione:
P. Vanhoutte et al., "Opposing roles of Elk-1 and its brain-specific isoform, short Elk-1, in nerve growth factor-induced PC12 differentiation", J BIOL CHEM, 276(7), 2001, pp. 5189-5196

Abstract

The ternary complex factor Elk-1, a major nuclear target of extracellular signal-regulated kinases, is a strong transactivator of serum-responsive element (SRE) driven gene expression. We report here that mature brain neurons and nerve growth factor (NGF)-differentiated PC12 cells also express a second, smaller isoform of Elk-1, short Elk-1 (sElk-1). sElk-1 arises from aninternal translation start site in the Elk-1 sequence, which generates a protein lacking the first 54 amino acids of the DNA-binding domain. This deletion severely compromises the ability of sElk-1 to form complexes with serum response factor on the SRE in vitro and to activate SRE reporter genes in the presence of activated Ras. Instead, sElk, but not a mutant that cannot be phosphorylated, inhibits transactivation driven by Elk-1. More pertinent to the neuronal-specific expression of sElk-1, we show it plays an opposite role to Elk-1 in potentiating NGF-driven PC12 neuronal differentiation. Overexpression of sElk-1 but not Elk-1 increases neurite extension, an effect critically linked to its phosphorylation. interestingly, in the presence of sElk-1, Elk-1 loses its strictly nuclear localization to resemble the nuclear/cytoplasm pattern observed in the mature brain. This is blocked by mutating a normally cryptic nuclear export signal in Elk-1. These data provide new insights into molecular events underlying neuronal differentiation of PC12 cells mediated by the NGF-ERK signaling cascade.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 10:02:46