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Titolo:
ABNORMAL SPLICING OF THE LEPTIN RECEPTOR IN DIABETIC MICE
Autore:
LEE GH; PROENCA R; MONTEZ JM; CARROLL KM; DARVISHZADEH JG; LEE JI; FRIEDMAN JM;
Indirizzi:
ROCKEFELLER UNIV,HOWARD HUGHES MED INST,1230 YORK AVE NEW YORK NY 10021 ROCKEFELLER UNIV,DEPT MOLEC GENET NEW YORK NY 10021
Titolo Testata:
Nature
fascicolo: 6566, volume: 379, anno: 1996,
pagine: 632 - 635
SICI:
0028-0836(1996)379:6566<632:ASOTLR>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
YEAST; FRAGMENTS; MUTATION; CLONING; GENES; DNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
G.H. Lee et al., "ABNORMAL SPLICING OF THE LEPTIN RECEPTOR IN DIABETIC MICE", Nature, 379(6566), 1996, pp. 632-635

Abstract

MUTATIONS in the mouse diabetes (db) gene result in obesity and diabetes in a syndrome resembling morbid human obesity(1), Previous data suggest that the db gene encodes the receptor for the obese (ob) gene product, leptin(2-7). A leptin receptor was recently cloned from choroidplexus and shown to map to the same 6-cM interval on mouse chromosome4 as db(8). This receptor maps to the same 300-kilobase interval as db, and has at least six alternatively spliced forms. One of these splice variants is expressed at a high level in the hypothalamus, and is abnormally spliced in C57BL/Ks db/db mice, The mutant protein is missing the cytoplasmic region, and is likely to be defective in signal transduction. This suggests that the weight-reducing effects of leptin maybe mediated by signal transduction through a leptin receptor in the hypothalamus.

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Documento generato il 06/04/20 alle ore 01:38:13