Faculty Opinions recommendation of Promoter hypermethylation of progesterone receptor isoform B (PR-B) in endometriosis.

2006 ◽  
Author(s):  
Kevin Osteen
Keyword(s):  
Progesterone Receptor ◽  
Promoter Hypermethylation ◽  
Isoform B

scholarly journals Promoter Hypermethylation of Progesterone Receptor Isoform B (PR-B) in Endometriosis

Epigenetics ◽  
2006 ◽  
Vol 1 (2) ◽  
pp. 106-111 ◽  
Author(s):  
Yan Wu ◽  
Estil Strawn ◽  
Zainab Basir ◽  
Gloria Halverson ◽  
Sun-Wei Guo
Keyword(s):  
Progesterone Receptor ◽  
Promoter Hypermethylation ◽  
Isoform B

Progesterone receptor isoform B expression in pulmonary neuroendocrine cells decreases cell proliferation

2019 ◽  
Vol 190 ◽  
pp. 212-223 ◽  
Author(s):  
Teeranut Asavasupreechar ◽  
Ryoko Saito ◽  
Dean P. Edwards ◽  
Hironobu Sasano ◽  
Viroj Boonyaratanakornkit
Keyword(s):  
Cell Proliferation ◽  
Progesterone Receptor ◽  
Neuroendocrine Cells ◽  
Pulmonary Neuroendocrine Cells ◽  
Isoform B

scholarly journals Two Domains of the Progesterone Receptor Interact with the Estrogen Receptor and Are Required for Progesterone Activation of the c-Src/Erk Pathway in Mammalian Cells

2003 ◽  
Vol 23 (6) ◽  
pp. 1994-2008 ◽  
Author(s):  
Cecilia Ballaré ◽  
Markus Uhrig ◽  
Thomas Bechtold ◽  
Elena Sancho ◽  
Marina Di Domenico ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptor ◽  
Mammalian Cells ◽  
Estrogen Receptor Alpha ◽  
Gene Mutations ◽  
Direct Interaction ◽  
Sh2 Domain ◽  
Erk Pathway ◽  
Isoform B ◽  
Necessary And Sufficient

ABSTRACT In breast cancer cells, estrogens activate the Src/Erk pathway through an interaction of the estrogen receptor alpha (ERα) with the SH2 domain of c-Src. Progestins have been reported to activate also this pathway either via an interaction of the progesterone receptor isoform B (PRB) with ERα, which itself activates c-Src, or by direct interaction of PRB with the SH3 domain of c-Src. Here we identify two domains of PRB, ERID-I and -II, mediating a direct interaction with the ligand-binding domain of ERα. ERID-I and ERID-II flank a proline cluster responsible for binding of PRB to c-Src. In mammalian cells, the interaction of PRB with ERα and the progestin activation of the Src/Erk cascade are abolished by deletion of either ERID-I or ERID-II. These regions are not required for transactivation of a progesterone-responsive reporter gene. Mutations in the proline cluster of PRB that prevent a direct interaction with c-Src do not affect the strong activation of c-Src by progestins in the presence of ERα. Thus, in cells with ERα, ERID-I and ERID-II are necessary and sufficient for progestin activation of the endogenous Src/Erk pathway.

Anti-estrogenic mechanism of unliganded progesterone receptor isoform B in breast cancer cells

2007 ◽  
Vol 110 (1) ◽  
pp. 111-125 ◽  
Author(s):  
Ze-Yi Zheng ◽  
Si-Min Zheng ◽  
Boon-Huat Bay ◽  
Swee-Eng Aw ◽  
Valerie C-L Lin
Keyword(s):  
Breast Cancer ◽  
Progesterone Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Isoform B

Progesterone Receptor B Promoter Hypermethylation in Human Placenta After Labor Onset

2014 ◽  
Vol 22 (3) ◽  
pp. 335-342 ◽  
Author(s):  
Yanyan Zhuang ◽  
Hong Cui ◽  
Sishi Liu ◽  
Dongming Zheng ◽  
Caixia Liu
Keyword(s):  
Progesterone Receptor ◽  
Human Placenta ◽  
Promoter Hypermethylation ◽  
Progesterone Receptor B ◽  
Labor Onset
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