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Patched1 regulates Hedgehog signaling at the primary cilium
被引:1111
作者:

Rohatgi, Rajat
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机构: Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA

Milenkovic, Ljiljana
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h-index: 0
机构: Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA

Scott, Matthew P.
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机构:
Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA
机构:
[1] Stanford Univ, Sch Med, Dept Dev Biol, Stanford, CA 94305 USA
[2] Stanford Univ, Sch Med, Dept Genet, Stanford, CA 94305 USA
[3] Stanford Univ, Sch Med, Dept Bioengn, Stanford, CA 94305 USA
[4] Stanford Univ, Sch Med, Howard Hughes Med Inst, Stanford, CA 94305 USA
[5] Stanford Univ, Sch Med, Dept Oncol, Stanford, CA 94305 USA
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D O I:
10.1126/science.1139740
中图分类号:
O [数理科学和化学];
P [天文学、地球科学];
Q [生物科学];
N [自然科学总论];
学科分类号:
07 ;
0710 ;
09 ;
摘要:
Primary cilia are essential for transduction of the Hedgehog (Hh) signal in mammals. We investigated the role of primary cilia in regulation of Patched1 (Ptc1), the receptor for Sonic Hedgehog (Shh). Ptc1 localized to cilia and inhibited Smoothened (Smo) by preventing its accumulation within cilia. When Shh bound to Ptc1, Ptc1 left the cilia, leading to accumulation of Smo and activation of signaling. Thus, primary cilia sense Shh and transduce signals that play critical roles in development, carcinogenesis, and stem cell function.
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页码:372 / 376
页数:5
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