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In each of these domains, key molecules and pathways have now been identified, including the glycolytic enzymes PFKFB3 and G6PD; the DNA repair molecules ATM, DNA-PKcs and MRE11A; and the podosome marker protein TKS5. Some of these molecules may help in defining targetable pathways to slow the T cell aging process. [review]
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it is discovered that MRE11 and NBS1 should start diffusion from significantly different starting positions which suggests that diffusion might not be the only transport mechanism of repair protein recruitment to the DNA break.
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The effects of chronic smoking on oral mucosa led to the methylation of genes MRE11A PMS2, XRCC1 and MLH3, but resulted in a reduction of gene expression of MRE11A and PMS2, which showed >/=50% methylation. These results provide evidence that smoking cause methylation and reduced expression of repair genes.
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This study confirms that H2AFX variants are associated with an increased risk of BC. The above-reported sequence variants of MRE11 genes may not constitute a risk factor of breast cancer in the Polish population.
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GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.
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Expression levels of MRN complex proteins(MRE11/RAD50/NBS1) significantly predict disease-free survival in rectal cancer patients, including those treated with neoadjuvant radiotherapy, and may have value in the management of these patients.
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Study proposes a new mechanism by which loss of PTEN and consequent activation of the PI3K-AKT-mTORC1-S6K1 signalling pathway impairs DNA repair by downregulation of MRE11.
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ATM-dependent phosphorylation of CtIP and the epistatic and coordinated actions of MRE11 and CtIP nuclease activities are required to limit the stable loading of Ku on single-ended DNA double-strand breaks.
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These evidences suggest that NBS1 is regulated by two kind of mechanisms: complex formation dependent on ATM, and protein degradation mediated by an unknown MG132-resistant pathway.
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MRE11A gene polymorphism is associated with colorectal cancer.
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Low MRE11 expression is associated with low-grade epithelial ovarian cancer.
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although recruitment of the MRE11-RAD50-NBS1 (MRN) DSB-sensing complex to viral genomes and activation of the ATM kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
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Mre11-Rad50-Nbs1 complex initiates DNA double strand break repair.
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we show that Plk1 phosphorylates Mre11 at S649 during G2 DNA damage recovery and Mre11 phosphorylation at S649/S689 drives premature checkpoint termination and reduced DNA repair
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In the absence of RAD51, the unprotected newly replicated genome is degraded by the exonuclease activity of MRE11, and the fragmented nascent DNA accumulates in the cytosol, initiating an innate immune response.
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Both the genome instability and cell death of MRE11-null and MRE11-mutated H129N cells are significantly reversed by overexpression of Tdp2, an enzyme that eliminates covalent Top2 conjugates; thus, the essential role of Mre11 nuclease activity is likely to remove the DNA lesions.
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The results illuminate the important role of Nbs1 and CtIP in determining the substrates and consequences of human Mre11/Rad50 nuclease activities on protein-DNA lesions.
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Cdk-dependent phosphorylation of TRF1 on threonine 371 promotes TRF1 to interact with APBs in S and G2 phases independently of its binding to telomeric DNA. We have demonstrated that the interaction of (pT371)TRF1 with APBs is dependent upon ATM and homologous-recombination-promoting factors such as Mre11 and BRCA1.
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Ataxia-telangiectasia-like disease (A-TLD) is clinically similar to mild Ataxia-telangiectasia and caused by hypomorphic mutations in the MRE11 gene.
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although Mre11 is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
