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Titolo:
beta 3-integrin-deficient mice are a model for Glanzmann thrombasthenia showing placental defects and reduced survival
Autore:
Hodivala-Dilke, KM; McHugh, KP; Tsakiris, DA; Rayburn, H; Crowley, D; Ullman-Cullere, M; Ross, FP; Coller, BS; Teitelbaum, S; Hynes, RO;
Indirizzi:
MIT, Howard Hughes Med Inst, Ctr Canc Res, Cambridge, MA 02139 USA MIT Cambridge MA USA 02139 ed Inst, Ctr Canc Res, Cambridge, MA 02139 USA MIT, Dept Biol, Cambridge, MA 02139 USA MIT Cambridge MA USA 02139MIT, Dept Biol, Cambridge, MA 02139 USA Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pathol, St Louis, MO 63110 USA CUNY Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA CUNY Mt Sinai Sch Med New York NY USA 10029 t Med, New York, NY 10029 USA
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 2, volume: 103, anno: 1999,
pagine: 229 - 238
SICI:
0021-9738(199901)103:2<229:B3MAAM>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARG-GLY-ASP; PLATELET GLYCOPROTEIN-IIIA; INTEGRIN ALPHA(V)BETA(3); CELL-ADHESION; HUMAN CYTOTROPHOBLASTS; ENDOVASCULAR INVASION; BONE-RESORPTION; MATRIX PROTEINS; IRAQI-JEWISH; P-SELECTIN;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Hynes, RO MIT,mbridge,Hughes Med Inst, Ctr Canc Res, 77 Massachusetts Ave,E17-227, Ca MIT 77 Massachusetts Ave,E17-227 Cambridge MA USA 02139 -227, Ca
Citazione:
K.M. Hodivala-Dilke et al., "beta 3-integrin-deficient mice are a model for Glanzmann thrombasthenia showing placental defects and reduced survival", J CLIN INV, 103(2), 1999, pp. 229-238

Abstract

beta 3 integrins have been implicated in a wide variety of functions, including platelet aggregation and thrombosis (alpha IIb beta 3) and implantation, placentation, angiogenesis, bone remodeling, and tumor progression (alpha v beta 3). The human bleeding disorder Glanzmann thrombasthenia (GT) canresult from defects in the genes for either the alpha IIb or the beta 3 subunit. In order to develop a mouse model of this disease and to further studies of hemostasis, thrombosis, and other suggested roles of beta 3 integrins, we have generated a strain of beta 3-null mice. The mice are viable andfertile, and show all the cardinal features of GT (defects in platelet aggregation and clot retraction, prolonged bleeding times, and cutaneous and gastrointestinal bleeding). Implantation appears to be unaffected, but placental defects do occur and lead to fetal mortality. Postnatal hemorrhage leads to anemia and reduced survival. These mice will allow analyses of the other suggested functions of beta 3 integrins and we report that postnatal neovascularization of the retina appears to be beta 3-integrin-independent, contrary to expectations from inhibition experiments.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 19:48:57