scholarly journals Germ Cell Nuclear Factor (GCNF) Represses Oct4 Expression and Globally Modulates Gene Expression in Human Embryonic Stem (hES) Cells

2016 ◽  
Vol 291 (16) ◽  
pp. 8644-8652 ◽  
Author(s):  
Hongran Wang ◽  
Xiaohong Wang ◽  
Xueping Xu ◽  
Michael Kyba ◽  
Austin J. Cooney
Keyword(s):  
Gene Expression ◽  
Germ Cell ◽  
Embryonic Stem ◽  
Nuclear Factor ◽  
Oct4 Expression ◽  
Hes Cells ◽  
Germ Cell Nuclear Factor

scholarly journals Mouse Germline Restriction of Oct4 Expression by Germ Cell Nuclear Factor

2001 ◽  
Vol 1 (3) ◽  
pp. 377-387 ◽  
Author(s):  
Guy Fuhrmann ◽  
Arthur C.-K. Chung ◽  
Kathy J. Jackson ◽  
Geoffrey Hummelke ◽  
Aria Baniahmad ◽  
...  
Keyword(s):  
Germ Cell ◽  
Nuclear Factor ◽  
Oct4 Expression ◽  
Germ Cell Nuclear Factor

cDNA cloning of two closely related forms of human germ cell nuclear factor (GCNF)

1997 ◽  
Vol 1352 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Marcus Kapelle ◽  
Jörn Krätzschmar ◽  
Manfred Husemann ◽  
Wolf-Dieter Schleuning
Keyword(s):  
Germ Cell ◽  
Cdna Cloning ◽  
Nuclear Factor ◽  
Germ Cell Nuclear Factor

scholarly journals Hepatocyte nuclear factor-1 beta protects endometriotic cells against apoptotic cell death by up-regulating the expression of antiapoptotic genes†

2019 ◽  
Vol 101 (4) ◽  
pp. 686-694 ◽  
Author(s):  
Umma Hafsa Preya ◽  
Jeong-Hwa Woo ◽  
Youn Seok Choi ◽  
Jung-Hye Choi
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Antiapoptotic Gene ◽  
Nuclear Factor 1 ◽  
Hes Cells

Abstract The overexpression of hepatocyte nuclear factor-1 beta (HNF1β) in endometriotic lesion has been demonstrated. However, the role of HNF1β in endometriosis remains largely unknown. Human endometriotic 12Z cells showed higher level of HNF1β when compared with normal endometrial HES cells. In human endometriotic 12Z cells, HNF1β knockdown increased susceptibility to apoptotic cell death by oxidative stress, while HNF1β overexpression suppressed apoptosis. In addition, HNF1β knockdown and overexpression significantly decreased and increased, respectively, the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-dependent antiapoptotic genes. Knockdown of the antiapoptotic genes significantly reduced the HNF1β-induced resistance against oxidative stress in 12Z cells. Furthermore, HNF1β regulated the transcriptional activity of NF-κB, and an NF-κB inhibitor suppressed the HNF1β-enhanced NF-κB-dependent antiapoptotic gene expression and the resistance of the 12Z cells against cell death. Taken together, these data suggest that HNF1β overexpression may protect endometriotic cells against oxidative damage by augmenting antiapoptotic gene expression.

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