Prolactin-induced Jak2 phosphorylation of RUSH: a key element in Jak/RUSH signaling.
Prolactin-induced Jak2 phosphorylation of RUSH: a key element in Jak/RUSH signaling.
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DOI:
10.1016/j.mce.2010.05.010
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发表时间:
2010-08-30
影响因子:
4.1
通讯作者:
Chilton, Beverly S.
中科院分区:
文献类型:
--
作者:
Helmer, Rebecca A.;Panchoo, Marlyn;Dertien, Janet S.;Bhakta, Suhani M.;Hewetson, Aveline;Chilton, Beverly S.
Jak2/Stat-mediated prolactin signaling culminates in Stat5a-DNA-binding. However, not all Jak2-dependent genes have Stat5 sites. Western analysis with inhibitors showed Jak2 is a proximal intermediate in prolactin-induced RUSH phosphorylation. Transfection assays with HRE-H9 cells showed the RUSH-binding site mediated the ability of prolactin to augment progesterone-dependent transcription of the RUSH gene. Jak2 inhibitors or targeted RUSH-site mutation blocked the prolactin effect. RUSH co-immunoprecipitated with phospho-Jak2 from nuclear extracts. Jak2 inhibitors abolished the nuclear pool of phospho-RUSH not the nuclear content of RUSH in HRE-H9 cells. Nucleolar-affiliated partners, e.g. nucleolin, were identified by μLC/MS/MS analysis of nuclear proteins that co-immunoprecipitated with RUSH/GST-RING. RUSH did not exclusively co-localize with fibrillarin to the nucleolus. MG-132 (proteasomal inhibitor) failed to block Tyrene CR4-mediated decrease in phospho-RUSH, and did not promote RUSH accumulation in the nucleolus. These studies authenticate prolactin-dependent Jak2 phosphorylation of RUSH, and provide functional implications on the RUSH network of nuclear interactions.
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影响因子:
4.8
作者:
LI, WI;CHEN, CL;CHOU, JY
通讯作者:
CHOU, JY
影响因子:
--
作者:
HaywardLester, A;Hewetson, A;Chilton, BS
通讯作者:
Chilton, BS
影响因子:
4.8
作者:
Hewetson, A;Chilton, BS
通讯作者:
Chilton, BS
DOI:
10.1111/j.1432-1033.1996.0153n.x
发表时间:
1996-04-01
期刊:
EUROPEAN JOURNAL OF BIOCHEMISTRY
影响因子:
--
作者:
Li, YP;Busch, RK;Busch, H
通讯作者:
Busch, H
影响因子:
--
作者:
Hewetson, A;Hendrix, EC;Chilton, BS
通讯作者:
Chilton, BS