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Titolo:
RET ALTERNATE SPLICING INFLUENCES THE INTERACTION OF ACTIVATED RET WITH THE SH2 AND PTB DOMAINS OF SHC, AND THE SH2 DOMAIN OF GRB2
Autore:
LORENZO MJ; GISH GD; HOUGHTON C; STONEHOUSE TJ; PAWSON T; PONDER BAJ; SMITH DP;
Indirizzi:
UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT PATHOL,CRC,HUMAN CANC GENET RESGRP,BOX 238,LEVEL 3 CAMBRIDGE CB2 1TN ENGLAND UNIV CAMBRIDGE,ADDENBROOKES HOSP,DEPT PATHOL,CRC,HUMAN CANC GENET RESGRP CAMBRIDGE CB2 1TN ENGLAND MT SINAI HOSP,SAMUEL LUNENFELD RES INST,PROGRAM MOL BIOL & CANC TORONTO ON M5G 1X5 CANADA
Titolo Testata:
Oncogene
fascicolo: 7, volume: 14, anno: 1997,
pagine: 763 - 771
SICI:
0950-9232(1997)14:7<763:RASITI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
MEDULLARY-THYROID CARCINOMA; TYROSINE KINASE DOMAIN; NEOPLASIA TYPE 2B; SIGNAL-TRANSDUCTION; HIRSCHSPRUNG DISEASE; NUCLEOTIDE EXCHANGE; POINT MUTATION; PROTOONCOGENE; RECEPTOR; PROTEIN;
Keywords:
RET; MULTIPLE ENDOCRINE NEOPLASIA TYPE 2; HIRSCHSPRUNG DISEASE; SHC; GRB2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
57
Recensione:
Indirizzi per estratti:
Citazione:
M.J. Lorenzo et al., "RET ALTERNATE SPLICING INFLUENCES THE INTERACTION OF ACTIVATED RET WITH THE SH2 AND PTB DOMAINS OF SHC, AND THE SH2 DOMAIN OF GRB2", Oncogene, 14(7), 1997, pp. 763-771

Abstract

Activating germline mutations of the RET receptor tyrosine kinase arefound in the majority of cases of inherited cancer syndrome MEN 2, and inactivating mutations in some cases of dominantly inherited Hirschsprung disease. Using RET activated by a MEN 2 mutation, we show that both the SH2 and PTB domains of the adaptor protein Shc interact with RET, and we identify the PTB domain interaction site. Interaction with both the SH2 and PTB domains of She contributes to the transcriptionalactivation of a serum response element. RET alternate splicing affects the strength of interaction with both the She SH2 and PTB domains. In addition, a splice isoform-specific HSCR missense mutation, which does not inactivate the RET kinase activity, decreases the strength of the PTB domain interaction and the level of RET-dependent She phosphorylation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 03:49:42