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Genomic instability in mice lacking histone H2AX.
Celeste A, Petersen S, Romanienko PJ, Fernandez-Capetillo O, Chen HT, Sedelnikova OA, Reina-San-Martin B, Coppola V, Meffre E, Difilippantonio MJ, Redon C, Pilch DR, Olaru A, Eckhaus M, Camerini-Otero RD, Tessarollo L, Livak F, Manova K, Bonner WM, Nussenzweig MC, Nussenzweig A. Celeste A, et al. Science. 2002 May 3;296(5569):922-7. doi: 10.1126/science.1069398. Epub 2002 Apr 4. Science. 2002. PMID: 11934988 Free PMC article.
Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiolog …
Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histo …
Geminin ablation in vivo enhances tumorigenesis through increased genomic instability.
Champeris Tsaniras S, Villiou M, Giannou AD, Nikou S, Petropoulos M, Pateras IS, Tserou P, Karousi F, Lalioti ME, Gorgoulis VG, Patmanidi AL, Stathopoulos GT, Bravou V, Lygerou Z, Taraviras S. Champeris Tsaniras S, et al. J Pathol. 2018 Oct;246(2):134-140. doi: 10.1002/path.5128. Epub 2018 Aug 21. J Pathol. 2018. PMID: 29952003
Survival is also significantly reduced in mice lacking geminin during lung carcinogenesis. A significant increase in the total number and grade of lesions (hyperplasias, adenomas, and carcinomas) was also confirmed by hematoxylin and eosin staining. ...Taken togethe …
Survival is also significantly reduced in mice lacking geminin during lung carcinogenesis. A significant increase in the total …
PARP-2 sustains erythropoiesis in mice by limiting replicative stress in erythroid progenitors.
Farrés J, Llacuna L, Martin-Caballero J, Martínez C, Lozano JJ, Ampurdanés C, López-Contreras AJ, Florensa L, Navarro J, Ottina E, Dantzer F, Schreiber V, Villunger A, Fernández-Capetillo O, Yélamos J. Farrés J, et al. Cell Death Differ. 2015 Jul;22(7):1144-57. doi: 10.1038/cdd.2014.202. Epub 2014 Dec 12. Cell Death Differ. 2015. PMID: 25501596 Free PMC article.
Here we show that deletion of poly(ADP-ribose) polymerase-2 (PARP-2) in mice leads to chronic anemia at steady state, despite increased erythropoietin plasma levels, a phenomenon not observed in mice lacking PARP-1. ...In erythroblasts, PARP-2 deficiency trig …
Here we show that deletion of poly(ADP-ribose) polymerase-2 (PARP-2) in mice leads to chronic anemia at steady state, despite increas …
Genotoxicity of tetrahydrofolic acid to hematopoietic stem and progenitor cells.
García-Calderón CB, Bejarano-García JA, Tinoco-Gago I, Castro MJ, Moreno-Gordillo P, Piruat JI, Caballero-Velázquez T, Pérez-Simón JA, Rosado IV. García-Calderón CB, et al. Cell Death Differ. 2018 Nov;25(11):1967-1979. doi: 10.1038/s41418-018-0089-4. Epub 2018 Mar 6. Cell Death Differ. 2018. PMID: 29511342 Free PMC article.
We uncover a detrimental role of tetrahydrofolic acid (THF) in cells lacking Adh5 or the FA repair pathway. We show that Adh5- or FA-deficient cells are hypersensitive to formaldehyde and to THF, presenting DNA damage and genome instability. ...Moreover, the hematop …
We uncover a detrimental role of tetrahydrofolic acid (THF) in cells lacking Adh5 or the FA repair pathway. We show that Adh5- or FA- …
Redundant and nonredundant functions of ATM and H2AX in alphabeta T-lineage lymphocytes.
Yin B, Lee BS, Yang-Iott KS, Sleckman BP, Bassing CH. Yin B, et al. J Immunol. 2012 Aug 1;189(3):1372-9. doi: 10.4049/jimmunol.1200829. Epub 2012 Jun 22. J Immunol. 2012. PMID: 22730535 Free PMC article.
However, combined germline inactivation of Atm and H2ax in mice causes early embryonic lethality associated with substantial cellular genomic instability, indicating that ATM and H2AX exhibit nonredundant functions in embryonic cells. ...Yet, in …
However, combined germline inactivation of Atm and H2ax in mice causes early embryonic lethality associated with substantial c …
Monoubiquitination of H2AX protein regulates DNA damage response signaling.
Pan MR, Peng G, Hung WC, Lin SY. Pan MR, et al. J Biol Chem. 2011 Aug 12;286(32):28599-607. doi: 10.1074/jbc.M111.256297. Epub 2011 Jun 15. J Biol Chem. 2011. PMID: 21676867 Free PMC article.
Double strand breaks (DSBs) are the most deleterious of the DNA lesions that initiate genomic instability and promote tumorigenesis. Cells have evolved a complex protein network to detect, signal, and repair DSBs. In mammalian cells, a key component in this network …
Double strand breaks (DSBs) are the most deleterious of the DNA lesions that initiate genomic instability and promote tumorige …
The role of p53-mediated apoptosis as a crucial anti-tumor response to genomic instability: lessons from mouse models.
Attardi LD. Attardi LD. Mutat Res. 2005 Jan 6;569(1-2):145-57. doi: 10.1016/j.mrfmmm.2004.04.019. Mutat Res. 2005. PMID: 15603759 Review.
Genomic instability is a major force driving human cancer development. ...This apoptotic response can be rescued through crosses to p53-deficient mice, but has dire consequences: mice predisposed to genomic instability and lacking …
Genomic instability is a major force driving human cancer development. ...This apoptotic response can be rescued through cross …
53BP1 mediates the fusion of mammalian telomeres rendered dysfunctional by DNA-PKcs loss or inhibition.
Rybanska-Spaeder I, Ghosh R, Franco S. Rybanska-Spaeder I, et al. PLoS One. 2014 Sep 29;9(9):e108731. doi: 10.1371/journal.pone.0108731. eCollection 2014. PLoS One. 2014. PMID: 25264618 Free PMC article.
Telomere dysfunction promotes genomic instability and carcinogenesis via inappropriate end-to-end chromosomal rearrangements, or telomere fusions. Previous work indicates that the DNA Damage Response (DDR) factor 53BP1 promotes the fusion of telomeres rendered dysfu …
Telomere dysfunction promotes genomic instability and carcinogenesis via inappropriate end-to-end chromosomal rearrangements, …
Defective DNA double-strand break repair underlies enhanced tumorigenesis and chromosomal instability in p27-deficient mice with growth factor-induced oligodendrogliomas.
See WL, Miller JP, Squatrito M, Holland E, Resh MD, Koff A. See WL, et al. Oncogene. 2010 Mar 25;29(12):1720-31. doi: 10.1038/onc.2009.465. Epub 2010 Jan 11. Oncogene. 2010. PMID: 20062078 Free PMC article.
Progression of platelet-derived growth factor (PDGF)-induced oligodendrogliomas was accelerated in mice lacking the cyclin-cdk binding activities of p27(kip1). To understand how p27 deficiency contributes, cell lines were developed from RCAS-PDGF infection of nestin …
Progression of platelet-derived growth factor (PDGF)-induced oligodendrogliomas was accelerated in mice lacking the cyclin-cdk …
Ataxia telangiectasia mutated (ATM) is dispensable for endonuclease I-SceI-induced homologous recombination in mouse embryonic stem cells.
Rass E, Chandramouly G, Zha S, Alt FW, Xie A. Rass E, et al. J Biol Chem. 2013 Mar 8;288(10):7086-95. doi: 10.1074/jbc.M112.445825. Epub 2013 Jan 26. J Biol Chem. 2013. PMID: 23355489 Free PMC article.
Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, including histone H2AX on serine 139 (Ser-139) to form gamma-H2AX. Through interaction with MDC1, gamma-H2AX promot …
Ataxia telangiectasia mutated (ATM) is activated upon DNA double strand breaks (DSBs) and phosphorylates numerous DSB response proteins, inc …
11 results