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Titolo:
A NOVEL JUXTAMEMBRANE DELETION IN RAT TRKA BLOCKS DIFFERENTIATIVE BUTNOT MITOGENIC CELL SIGNALING IN RESPONSE TO NERVE GROWTH-FACTOR
Autore:
MEAKIN SO; MACDONALD JIS;
Indirizzi:
JOHN P ROBARTS RES INST,NEURODEGENERAT GRP,100 PERTH DR LONDON ON N6A5K8 CANADA UNIV WESTERN ONTARIO,DEPT BIOCHEM LONDON ON CANADA UNIV WESTERN ONTARIO,GRAD PROGRAM NEUROSCI LONDON ON CANADA
Titolo Testata:
Journal of neurochemistry
fascicolo: 5, volume: 71, anno: 1998,
pagine: 1875 - 1888
SICI:
0022-3042(1998)71:5<1875:ANJDIR>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEDIATED RECEPTOR INTERNALIZATION; PC12 PHEOCHROMOCYTOMA CELLS; TYROSINE KINASE-ACTIVITY; HIGH-AFFINITY; NPXY MOTIF; CYTOPLASMIC DOMAIN; INSULIN-RECEPTOR; BINDING-SITES; PROTEIN; SHC;
Keywords:
TRKA; NERVE GROWTH FACTOR; SIGNALING; CELL CYCLE; SNT; DIFFERENTIATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
55
Recensione:
Indirizzi per estratti:
Citazione:
S.O. Meakin e J.I.S. Macdonald, "A NOVEL JUXTAMEMBRANE DELETION IN RAT TRKA BLOCKS DIFFERENTIATIVE BUTNOT MITOGENIC CELL SIGNALING IN RESPONSE TO NERVE GROWTH-FACTOR", Journal of neurochemistry, 71(5), 1998, pp. 1875-1888

Abstract

We have generated a novel rat TrkA receptor mutant (TrkAS3) by deletion of five conserved residues ((IMENP497)-I-493) in the juxtamembrane domain. TrkAS3 receptors cannot support nerve growth factor (NGF)-induced cell cycle arrest or neuronal differentiation but retain cell survival responses as well as Ras-dependent mitogenic signaling. Cells of the nnr5 line stably expressing TrkAS3 induce NGF-dependent SHC phosphorylation and phosphatidylinositol 3-kinase, phospholipase Cy-l, and prolonged mitogen-activated protein kinase activation to absolute levels comparable to those in PC12 cells. Although the stoichiometry of TrkAS3-SHC binding is reduced, cells overexpressing TrkAS3 exhibit NGF-dependent SHC-Grb-2/Sos binding, essential for Ras activation, as well as NGF-dependent SNT phosphorylation to absolute levels comparable to those in PC12 cells. Collectively, these data suggest that the TrkAS3 deletion either directly affects a novel Ras-independent TrkA binding protein or that the decrease in TrkAS3-SHC association affects a Res-independent SHC binding protein essential for cell cycle arrest and/or neurite outgrowth.

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Documento generato il 03/04/20 alle ore 04:23:36