scholarly journals XIAP Gene Expression Protects β-Cells and Human Islets from Apoptotic Cell Death

2010 ◽  
Vol 7 (5) ◽  
pp. 1655-1666 ◽  
Author(s):  
Hao Wu ◽  
Ravikiran Panakanti ◽  
Feng Li ◽  
Ram I. Mahato
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Human Islets ◽  
Apoptotic Cell Death ◽  
Β Cells

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.

scholarly journals Overexpression of PU.1 Induces Growth and Differentiation Inhibition and Apoptotic Cell Death in Murine Erythroleukemia Cells

Blood ◽  
1997 ◽  
Vol 89 (4) ◽  
pp. 1383-1393 ◽  
Author(s):  
Toshiyuki Yamada ◽  
Nobuo Kondoh ◽  
Mana Matsumoto ◽  
Midori Yoshida ◽  
Akihiko Maekawa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Growth Inhibition ◽  
Apoptotic Cell ◽  
Globin Gene ◽  
Apoptotic Cell Death ◽  
Activation Domain ◽  
Ets Domain ◽  
Murine Erythroleukemia ◽  
Globin Gene Expression

Abstract PU.1 is a member of the ets family of transcription factors and is expressed in Friend virus-induced murine erythroleukemia (MEL) cells as a consequence of proviral integration into the PU.1/Spi-1 locus. After induction of MEL cell differentiation by treatment with dimethylsulfoxide (DMSO), expression of the PU.1/Spi-1 gene decreased before induction of β-globin gene expression. Overexpression of PU.1 by using a zinc-inducible expression plasmid in MEL cells resulted in unexpected growth inhibition of the transfectants. When PU.1-overexpressing transfectants were treated with DMSO, growth inhibition became much pronounced and apoptosis was induced. Expression of the β-globin gene was not induced under this condition. Neither growth inhibition nor apoptosis was induced in MEL cells after expression of mutant PU.1 proteins with a deletion of the activation domain or the DNA-binding Ets domain irrespective of the presence of DMSO. Interestingly, β-globin gene expression was not induced in the transfectants expressing the former mutant, whereas it was induced in those expressing the latter one in the presence of DMSO. These results indicate that overexpression of PU.1 in MEL cells results in growth and differentiation inhibition and, in conjunction with DMSO treatment, apoptotic cell death. These results also suggest that the activation domain and the Ets domain of PU.1 contribute differently to induction of these effects.

scholarly journals Inhibition of Autophagic Turnover in β-Cells by Fatty Acids and Glucose Leads to Apoptotic Cell Death

2014 ◽  
Vol 290 (10) ◽  
pp. 6071-6085 ◽  
Author(s):  
Shakeel U. R. Mir ◽  
Nicholas M. George ◽  
Lubna Zahoor ◽  
Robert Harms ◽  
Zachary Guinn ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Β Cells

Induction of cyclooxygenase (COX)-2 but not COX-1 gene expression in apoptotic cell death

1998 ◽  
Vol 89 (1-2) ◽  
pp. 142-149 ◽  
Author(s):  
Lap Ho ◽  
Hiroshi Osaka ◽  
Paul S Aisen ◽  
Giulio Maria Pasinetti
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Cox 2 ◽  
Cox 1

Casticin induced apoptotic cell death and altered associated gene expression in human colon cancer colo 205 cells

2016 ◽  
Vol 32 (8) ◽  
pp. 2041-2052 ◽  
Author(s):  
Hung-Sheng Shang ◽  
Jia-You Liu ◽  
Hsu-Feng Lu ◽  
Han-Sun Chiang ◽  
Chia-Hain Lin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Human Colon ◽  
Apoptotic Cell Death ◽  
Human Colon Cancer

scholarly journals Nip21 Gene Expression Reduces Coxsackievirus B3 Replication by Promoting Apoptotic Cell Death via a Mitochondria-Dependent Pathway

2002 ◽  
Vol 90 (12) ◽  
pp. 1251-1258 ◽  
Author(s):  
Huifang M. Zhang ◽  
Bobby Yanagawa ◽  
Paul Cheung ◽  
Honglin Luo ◽  
Ji Yuan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Coxsackievirus B3 ◽  
Apoptotic Cell Death ◽  
Dependent Pathway
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