H2A.X becomes phosphorylated on serine 139 (to form gamma-H2AFX or H2AX139ph) in response to DNA double strand breaks (DSBs) generated by exogenous genotoxic agents and by stalled replication forks, which promotes DNA repair and maintains genomic stability. The calculated molecular weight of H2A...
(1). DNA damage, caused by ionizing radiation, UV-light, or radiomimetic agents, results in rapid phosphorylation of H2A.X at Ser139 by PI3K-like kinases, including ATM, ATR, and DNA-PK (2,3). Within minutes following DNA damage, H2A.X is phospho...
(1). DNA damage, caused by ionizing radiation, UV-light, or radiomimetic agents, results in rapid phosphorylation of H2A.X at Ser139 by PI3K-like kinases, including ATM, ATR, and DNA-PK (2,3). Within minutes following DNA damage, H2A.X is phosphorylated at Ser139 a...
Studies have shown that many tumor cells under a hypoxic microenvironment are less sensitive to chemotherapeutic agents because these agents typically require oxygen for maximum activity [12]. Regardless of oxygen concentrations required for anticancer drug activity, researches have also revealed that the ...
Viral mimicry was previously associated with the expression of dsRNA following the administration of DNA demethylating agents89. Orthogonal evidence supports this notion, including (i) increased expression of ISG genes following increased macroH2A2 levels, (ii) decreased expression of ISG genes upon ...
(F–I) The activity of STK39 increases PAAD cells’ resistance to DNA damage agents. BxPC-3 (F and G) and MIA PaCa-2 (H and I) cells were infected with lentivirus expressing FLAG-STK39 WT or D212A mutant (kinase-dead mutation, CS). STK39 WT and D212A mutant cells were treated...
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et al. DNA-demethylating agents target colorectal cancer cells by inducing viral mimicry by endogenous transcripts article DNA-demethylating agents target colorectal cancer cells by inducing viral mimicry by endogenous transcripts. Cell 162, 961–973 (2015). Chiappinelli, K. B. et al. ...
16prompted us to investigate whether sH2As may contribute to cancer. Previous work showed that expression of H2A.B causes increased sensitivity to DNA damaging agents, shortens S-phase22, and alters splicing17,19,22, each of which are associated oncogenesis. Additional evidence for a role for ...
Studies in yeast indicate that loss of H2A.Z leads to increased sensitivity to DNA-damaging agents and increased genomic instability (Morillo-Huesca et al., 2010; Papamichos-Chronakis et al., 2011). In Drosophila, H2Av (which combines the function of H2AX and H2A.Z) is acetylated by ...