scholarly journals Transcription through 8-oxoguanine in DNA repair-proficient and Csb /Ogg1 DNA repair-deficient mouse embryonic fibroblasts is dependent upon promoter strength and sequence context

Mutagenesis ◽  
2007 ◽  
Vol 22 (5) ◽  
pp. 343-351 ◽  
Author(s):  
M. Pastoriza-Gallego ◽  
J. Armier ◽  
A. Sarasin
Keyword(s):  
Dna Repair ◽  
Promoter Strength ◽  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Sequence Context ◽  
Embryonic Fibroblasts

scholarly journals DNA repair kinetics in SCID mice Sertoli cells and DNA-PKcs-deficient mouse embryonic fibroblasts

Chromosoma ◽  
2016 ◽  
Vol 126 (2) ◽  
pp. 287-298 ◽  
Author(s):  
Emad A. Ahmed ◽  
Eukene Vélaz ◽  
Michael Rosemann ◽  
Klaus-P. Gilbertz ◽  
Harry Scherthan
Keyword(s):  
Dna Repair ◽  
Sertoli Cells ◽  
Scid Mice ◽  
Deficient Mouse ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

Tuberin regulates the DNA repair enzyme OGG1

2008 ◽  
Vol 294 (1) ◽  
pp. F281-F290 ◽  
Author(s):  
Samy L. Habib ◽  
Daniel J. Riley ◽  
Lenin Mahimainathan ◽  
Basant Bhandari ◽  
Goutam Ghosh Choudhury ◽  
...  
Keyword(s):  
Dna Repair ◽  
Tumor Suppressor Genes ◽  
Transcriptional Activity ◽  
Potential Role ◽  
Marked Decrease ◽  
Mouse Embryonic Fibroblasts ◽  
Kidney Tumors ◽  
Repair Enzyme ◽  
Embryonic Fibroblasts ◽  
Mrna And Protein Expression

The tuberous sclerosis complex (TSC) is caused by defects in one of two tumor suppressor genes, TSC-1 or TSC-2. The TSC-2 gene encodes tuberin, a protein involved in the pathogenesis of kidney tumors, both angiomyolipomas and renal cell carcinomas. We investigated a potential role for tuberin in regulating a key DNA repair pathway. Downregulation of tuberin in human renal epithelial cells using siRNA resulted in a marked decrease in the abundance of the 8-oxoG-DNA glycosylase (OGG1). Mouse embryonic fibroblasts deficient in tuberin ( TSC2−/− and TSC2+/−) also had markedly decreased OGG1 mRNA and protein expression, as well as undetectable OGG1 activity accompanied by accumulation of 8-oxodG. Gel shift analyses and chromatin immunoprecipatation identified the transcription factor NF-YA as a regulator of OGG1 activity. The binding of NF-YA to the OGG1 promoter was significantly reduced in TSC2−/− compared with TSC2+/+ cells. Introduction of TSC2 cDNA into the tuberin-deficient cells restored NF-YA and OGG1 expression. Transcriptional activity of the OGG1 promoter was also decreased in tuberin-null cells. In addition, mutation of both CAAT boxes, the sites to which NF-YA binds, completely inhibits OGG1 promoter activity. These data provide the first evidence that tuberin regulates a specific DNA repair enzyme, OGG1. This regulation may be important in the pathogenesis of kidney tumors in patients with TSC.

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 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 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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