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Titolo:
High specificity of Mullerian-inhibiting substance signaling in vivo
Autore:
Mishina, Y; Whitworth, DJ; Racine, C; Behringer, RR;
Indirizzi:
Univ Texas, MD Anderson Cancer Ctr, Dept Mol Genet, Houston, TX 77030 USA Univ Texas Houston TX USA 77030 tr, Dept Mol Genet, Houston, TX 77030 USA Ecoleuge,male Super, INSERM U493, Unite Rech Endocrinol Dev, F-92120 Montro Ecole Normale Super Montrouge France F-92120 ocrinol Dev, F-92120 Montro
Titolo Testata:
ENDOCRINOLOGY
fascicolo: 5, volume: 140, anno: 1999,
pagine: 2084 - 2088
SICI:
0013-7227(199905)140:5<2084:HSOMSS>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
RIBONUCLEIC-ACID EXPRESSION; DUCT-SYNDROME; SEXUAL-DIFFERENTIATION; TESTICULAR DESCENT; TRANSGENIC MICE; GRANULOSA-CELLS; HORMONE GENE; SERUM LEVELS; RECEPTOR; ONTOGENY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Behringer, RR Univston,s, MD Anderson Cancer Ctr, Dept Mol Genet, 1515 Holcombe Blvd, Hou Univ Texas 1515 Holcombe Blvd Houston TX USA 77030 Blvd, Hou
Citazione:
Y. Mishina et al., "High specificity of Mullerian-inhibiting substance signaling in vivo", ENDOCRINOL, 140(5), 1999, pp. 2084-2088

Abstract

Female transgenic mice that ectopically express high levels of human Mullerian-inhibiting substance (hMIS) under the control of the mouse metallothionein (MT) promoter lack st uterus, oviducts, and ovaries. The loss of the uterus and oviducts is consistent with the known activities for MIS. However, it is not clear if the loss of the ovaries in these transgenic females iscaused by interactions of MIS with its normal receptor signaling pathway or by abnormal interactions with other transforming growth factor-p (TGF-B) super family receptor signaling pathways. To address this question. female mice carrying the MT-hMIS transgene that were also homozygous for a targeted deletion of the MIS type II receptor gene were generated. Although these females had high levels of circulating MIS, they had normal reproductive tracts and ovaries with germ cells. In addition, these females were able to become pregnant and gave birth to pups. These findings demonstrate that all of the abnormalities of the reproductive system that are found in female transgenic mice that ectopically express high levels of hMIS are caused by signaling through the MIS type II receptor. These in vivo data demonstrate a high specificity for MIS and its receptor.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 11:12:35