Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
WILD-TYPE P53 TRANSGENIC MICE EXHIBIT ALTERED DIFFERENTIATION OF THE URETERAL BUD AND POSSESS SMALL KIDNEYS
Autore:
GODLEY LA; KOPP JB; ECKHAUS M; PAGLINO JJ; OWENS J; VARMUS HE;
Indirizzi:
NCI,VARMUS LAB,NIH BETHESDA MD 20892 NCI,VARMUS LAB,NIH BETHESDA MD 20892 UNIV CALIF SAN FRANCISCO,DEPT BIOCHEM & BIOPHYS SAN FRANCISCO CA 94143 NIDDKD,METAB DIS BRANCH,KIDNEY DIS SECT,NIH BETHESDA MD 20892 UNIV CALIF SAN FRANCISCO,DEPT MICROBIOL & IMMUNOL SAN FRANCISCO CA 94143 NIH,NATL CTR RES RESOURCES,VET RESOURCES PROGRAM BETHESDA MD 20892 NIH,OFF DIRECTOR BETHESDA MD 20892
Titolo Testata:
Genes & development
fascicolo: 7, volume: 10, anno: 1996,
pagine: 836 - 850
SICI:
0890-9369(1996)10:7<836:WPTMEA>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
BINDING-PROTEIN; APOPTOSIS; GLOMERULOSCLEROSIS; TRANSFORMATION; TRANSCRIPTION; EXPRESSION; MUTANT; GENE;
Keywords:
P53; TRANSGENIC MICE; KIDNEY DEVELOPMENT; URETERAL BUD;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
54
Recensione:
Indirizzi per estratti:
Citazione:
L.A. Godley et al., "WILD-TYPE P53 TRANSGENIC MICE EXHIBIT ALTERED DIFFERENTIATION OF THE URETERAL BUD AND POSSESS SMALL KIDNEYS", Genes & development, 10(7), 1996, pp. 836-850

Abstract

Transgenic mice expressing wild-type murine p53 under the control of the mouse mammary tumor virus long terminal repeat (MMTV LTR) undergo progressive renal failure due to abnormal kidney development. Similar phenotypes are observed in two transgenic lines that express wild-typep53 within the ureteric bud but not in transgenic animals expressing a dominant-negative p53 mutant allele. Defective differentiation of the ureteric bud, as evidenced by altered marker expression during development, accompanies expression of the p53 transgene. At E17.5-18.5, metanephric mesenchymal cells undergo high rates of apoptosis, and fewercells than normal are converted to tubular epithelium. As a result, p53 transgenic kidneys grow to only half of their expected size and contain about half of the normal number of nephrons, with compensatory hypertrophy of the glomeruli. In this setting, rather than arrest the cell cycle or induce apoptosis directly, abnormally high levels of wild-type p53 appear to alter cellular differentiation in embryonic ureteric buds and cause secondary effects (apoptosis and inefficient conversion to epithelium) in the adjacent undifferentiated mesenchyme.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 05:47:14