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Titolo:
Genetic evidence that Sil is required for the sonic hedgehog response pathway
Autore:
Izraeli, S; Lowe, LA; Bertness, VL; Campaner, S; Hahn, H; Kirsch, IR; Kuehn, MR;
Indirizzi:
NCI, Expt Immunol Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA NCI Bethesda MD USA 20892 anch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA NCI, Genet Branch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA NCI BethesdaMD USA 20892 anch, Canc Res Ctr, NIH, Bethesda, MD 20892 USA GSF, Res Ctr Environm & Hlth, Inst Pathol, Neuherberg, Germany GSF Neuherberg Germany nvironm & Hlth, Inst Pathol, Neuherberg, Germany Chaim Sheba Med Ctr, Dept Pediat Hematol Oncol, IL-52621 Tel Hashomer, Israel Chaim Sheba Med Ctr Tel Hashomer Israel IL-52621 21 Tel Hashomer, Israel
Titolo Testata:
GENESIS
fascicolo: 2, volume: 31, anno: 2001,
pagine: 72 - 77
SICI:
1526-954X(200110)31:2<72:GETSIR>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-DEATH; PROLIFERATION; INHIBITION; ACTIVATION; INDUCTION; SURVIVAL; TARGET;
Keywords:
Sil; sonic hedgehog; patched; signaling; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Kuehn, MR NCI, Expt Immunol Branch, Canc Res Ctr, NIH, Bldg 10,Room 4B-36,10 Ctr Dr,Bethesda, MD 20892 USA NCI Bldg 10,Room 4B-36,10 Ctr Dr Bethesda MD USA 20892 20892 USA
Citazione:
S. Izraeli et al., "Genetic evidence that Sil is required for the sonic hedgehog response pathway", GENESIS, 31(2), 2001, pp. 72-77

Abstract

The Sil gene encodes a cytosolic protein required for mouse embryonic midline and left/right axial development. Based on the phenotype of Sil mutant embryos, we hypothesized that Sil may be required for the activity of SonicHedgehog (Shh), a secreted signaling molecule also critically important for the development of the embryonic axes and found mutated in multiple typesof cancer. Here we tested the genetic interaction between Sil and the Shh pathway by generating and analyzing embryos carrying mutations in both Sil and Patched (Ptch), a Shh receptor that normally inhibits the signaling pathway in the absence of ligand and when mutated leads to constitutive activation of the pathway. We find that Sil(-/-) Ptch(-/-) embryos do not activate the Shh pathway and instead have a phenotype indistinguishable from Sil(-/-) embryos, in which there is a loss of activity of Shh. These results provide genetic evidence that Sil is an essential component of the Shh response, acting downstream to Ptch. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/02/20 alle ore 19:28:41