scholarly journals JDP2 (Jun Dimerization Protein 2)-deficient Mouse Embryonic Fibroblasts Are Resistant to Replicative Senescence

2009 ◽  
Vol 284 (16) ◽  
pp. 10808-10817 ◽  
Author(s):  
Koji Nakade ◽  
Jianzhi Pan ◽  
Takahito Yamasaki ◽  
Takehide Murata ◽  
Bohdan Wasylyk ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals JDP2 (Jun dimerization protein 2)-deficient mouse embryonic fibroblasts are resistant to replicative senescence.

2009 ◽  
Vol 284 (23) ◽  
pp. 16060.6-16060
Author(s):  
Koji Nakade ◽  
Jianzhi Pan ◽  
Takahito Yamasaki ◽  
Takehide Murata ◽  
Bohdan Wasylyk ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

MicroRNA-33 promotes the replicative senescence of mouse embryonic fibroblasts by suppressing CDK6

2016 ◽  
Vol 473 (4) ◽  
pp. 1064-1070 ◽  
Author(s):  
Shun Xu ◽  
Haijiao Huang ◽  
Nanhong Li ◽  
Bing Zhang ◽  
Yubin Jia ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Phosphatidylinositol 3,4,5-trisphosphate modulation in SHIP2-deficient mouse embryonic fibroblasts

FEBS Journal ◽  
2005 ◽  
Vol 272 (10) ◽  
pp. 2512-2522 ◽  
Author(s):  
Daniel Blero ◽  
Jing Zhang ◽  
Xavier Pesesse ◽  
Bernard Payrastre ◽  
Jacques E. Dumont ◽  
...  
Keyword(s):  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Mammalian Target of Rapamycin Complex I (mTORC1) Activity in Ras Homologue Enriched in Brain (Rheb)-Deficient Mouse Embryonic Fibroblasts

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81649 ◽  
Author(s):  
Marlous J. Groenewoud ◽  
Susan M. I. Goorden ◽  
Jorien Kassies ◽  
Wendy Pellis-van Berkel ◽  
Richard F. Lamb ◽  
...  
Keyword(s):  
Complex I ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Caspase3-deficient cells require fibronectin for protection against autophagy-dependent death

2021 ◽  
Author(s):  
David B. Weir ◽  
Lawrence H. Boise
Keyword(s):  
Cell Death ◽  
Survival Advantage ◽  
Deficient Mouse ◽  
Wild Type ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Serum Withdrawal ◽  
Presence And Absence ◽  
Induced Apoptosis

ABSTRACTCaspases are required for execution of apoptosis. However, in their absence, signals that typically induce apoptosis can still result in cell death. Our laboratory previously demonstrated that Casp3-deficient mouse embryonic fibroblasts (MEFs) have increased fibronectin (FN) secretion, and an adhesion-dependent survival advantage compared to wild type (WT) MEFs. Here, we show that FN is required for survival of Casp3-deficient MEFs following serum withdrawal. Furthermore, when FN is silenced, serum withdrawal-induced death is caspase-independent. However, procaspase-7 is cleaved, suggesting that MOMP is taking place. Indeed, in the absence of FN, cytochrome c release is increased following serum withdrawal in Casp3-deficient MEFs. Yet death does not correspond to cytochrome c release in Casp3-deficient MEFs. This is true both in the presence and absence of FN. Additionally, caspase-independent death is inhibited by Bcl-XL overexpression. These findings suggest that Bcl-XL is not inhibiting death through regulation of Bax/Bak insertion into the mitochondria, but through a different mechanism. One such possibility is autophagy and induction of autophagy is associated with caspase-independent death in Casp3-deficient cells. Importantly, when ATG5 is ablated in Casp3-deficient cells, autophagy is blocked and death is largely inhibited. Taken together, our data indicate that Casp3-deficient cells incapable of undergoing canonical serum withdrawal-induced apoptosis, are protected from autophagy-dependent death by FN-mediated adhesion.

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