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ATR — MYLIP

Text-mined interactions from Literome

Tamminga et al., Cell cycle (Georgetown, Tex.) 2008 : Here, we for the first time show that the DNA damage induced and ATR/Rfx1 mediated increase of miR-709 expression in exposed testes may be a protective mechanism that effectively decreases a cellular level of BORIS to prevent massive aberrant erasure of DNA methylation after radiation exposure
Chang et al., RNA Biol 2012 : Overexpression of miR-3928 induced DNA damage, activated ATR , and phosphorylated Chk1 accompanied by G1 arrest
Chang et al., PloS one 2013 (Lung Neoplasms) : Using quantitative PCR, we found that MIR promoted the expression levels of ATM ( ataxia telangiectasia mutated ), ATR ( ataxia-telangiectasia and Rad3 related and Rad3 related ), TP53 ( tumor protein p53 ), p21 ( CDKN1A, cyclin dependent kinase inhibitor 1A ) and GADD45 ( growth arrest and DNA-damage inducible ), but decreased the expression levels of cyclin B coding genes, CCNB1 and CCNB2, as well as CDK1 ( Cyclin dependent kinase 1 )
Wang et al., Cell death & disease 2013 : We also demonstrated that miR-185 negatively regulates ATR expression at post-transcriptional level ... In conclusion, our findings indicate a previously unreported regulatory mechanism for ATR expression mediated by miR-185 and shed light on the potential application of miRNAs both as direct cancer therapeutics and as tools to sensitize tumor cells to radiotherapy