sel-11 and cdc-42, two negative modulators of LIN-12/Notch activity in C. elegans.
sel-11 and cdc-42, two negative modulators of LIN-12/Notch activity in C. elegans.
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DOI：
10.1371/journal.pone.0011885
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发表时间：
2010-07-29
期刊：
影响因子：
3.7
通讯作者：
Greenwald I
中科院分区：
文献类型：
--
作者：
Choi MS;Yoo AS;Greenwald I
LIN-12/Notch信号传导对于发育期间的细胞-细胞相互作用是重要的，并且导致组成型LIN-12/Notch信号传导的突变可导致癌症。lin-12/Notch活性的负调节因子的丧失有可能影响癌症发展和发生或侵袭过程中的细胞命运决定。我们描述了两种lin-12活性的负调节剂。优雅一个基因，sel-11，最初被定义为一个lin-12亚型等位基因的抑制基因;另一个基因，cdc-42，是一个经过充分研究的Rho GT3。在这里，我们表明SEL-11对应于酵母Hrd 1 p和哺乳动物Synoviolin。我们还发现cdc-42具有与在外阴前体细胞命运特化过程中lin-12活性负调控一致的遗传特性。我们的研究结果强调了影响lin-12/Notch活性的负调控机制的多样性，并提出了组成型lin-12/Notch活性可能在癌症中加剧的新机制。
LIN-12/Notch signaling is important for cell-cell interactions during development, and mutations resulting in constitutive LIN-12/Notch signaling can cause cancer. Loss of negative regulators of lin-12/Notch activity has the potential for influencing cell fate decisions during development and the genesis or aggressiveness of cancer. We describe two negative modulators of lin-12 activity in C. elegans. One gene, sel-11, was initially defined as a suppressor of a lin-12 hypomorphic allele; the other gene, cdc-42, is a well-studied Rho GTPase. Here, we show that SEL-11 corresponds to yeast Hrd1p and mammalian Synoviolin. We also show that cdc-42 has the genetic properties consistent with negative regulation of lin-12 activity during vulval precursor cell fate specification. Our results underscore the multiplicity of negative regulatory mechanisms that impact on lin-12/Notch activity and suggest novel mechanisms by which constitutive lin-12/Notch activity might be exacerbated in cancer.
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影响因子：
14.9
作者：
Griffiths-Jones, S
通讯作者：
Griffiths-Jones, S
影响因子：
64.8
作者：
GREENWALD, I;SEYDOUX, G
通讯作者：
SEYDOUX, G
DOI：
10.1083/jcb.200807020
发表时间：
2008-12-15
期刊：
The Journal of cell biology
影响因子：
--
作者：
Harris KP;Tepass U
通讯作者：
Tepass U
影响因子：
21.3
作者：
Balklava, Zita;Pant, Saumya;Grant, Barth D.
通讯作者：
Grant, Barth D.
影响因子：
4.6
作者：
de Souza, Natalie;Vallier, Laura G.;Greenwald, Iva
通讯作者：
Greenwald, Iva