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Titolo:
Lack of Socs2 expression causes the high-growth phenotype in mice
Autore:
Horvat, S; Medrano, JF;
Indirizzi:
Roslin Inst, Roslin EH25 9PS, Midlothian, Scotland Roslin Inst Roslin Midlothian Scotland EH25 9PS 9PS, Midlothian, Scotland Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA Univ Calif Davis Davis CA USA 95616 s, Dept Anim Sci, Davis, CA 95616 USA
Titolo Testata:
GENOMICS
fascicolo: 2, volume: 72, anno: 2001,
pagine: 209 - 212
SICI:
0888-7543(20010301)72:2<209:LOSECT>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAPID POSTWEANING GROWTH; FACTOR-I; WEIGHT-GAIN; MAJOR GENE; SUPPRESSOR; HORMONE; RECEPTOR; MOUSE; HG;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
18
Recensione:
Indirizzi per estratti:
Indirizzo: Horvat, S Univ Ljubljana, Zootech Dept, Fac Biotech, Groblje 3, Domzale 1230, Slovenia Univ Ljubljana Groblje 3 Domzale Slovenia 1230 e 1230, Slovenia
Citazione:
S. Horvat e J.F. Medrano, "Lack of Socs2 expression causes the high-growth phenotype in mice", GENOMICS, 72(2), 2001, pp. 209-212

Abstract

Characterizing causal molecular defects in mouse models of overgrowth or dwarfism helps to identify the key genes and pathways that regulate the growth process. We report here the molecular basis for high growth (hg), a spontaneous mutation that causes a 30-50% increase in postnatal growth. We conclude that hg is an allele of the suppressor of cytokine signaling 2 (Socs2), a member of a family of regulators of cytokine signal transduction. We demonstrate mapping of Socs2 to the hg region, lack of Socs2 mRNA expression,a disruption of the Socs2 locus in high-growth (HG) mice, and a similarityof phenotypes of HG; mice and Socs2(-/-) mice generated by gene targeting,Characteristics of the HG phenotype suggest that Socs2 deficiency affects growth prenatally and postnatally most likely through deregulating the growth hormone (GH)/insulin-like growth factor I (IGF1), These results demonstrate a critical role for Socs2 in controlling growth, (C) 2001 Academic Press.

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Documento generato il 23/01/20 alle ore 18:23:23