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Chicken Polyclonal MRE11A Primary Antibody for ChIP, FACS - ABIN151076
Wang, Cortez, Yazdi, Neff, Elledge, Qin: BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures. in Genes & development 2000
Show all 156 Pubmed References
Human Monoclonal MRE11A Primary Antibody for ELISA, Func - ABIN151920
Carney, Maser, Olivares, Davis, Le Beau, Yates, Hays, Morgan, Petrini: The hMre11/hRad50 protein complex and Nijmegen breakage syndrome: linkage of double-strand break repair to the cellular DNA damage response. in Cell 1998
Show all 24 Pubmed References
Polyclonal MRE11A Primary Antibody for IHC (fro), IF - ABIN540672
Eward, Obermann, Shreeram, Loddo, Fanshawe, Williams, Jung, Prevost, Blow, Stoeber, Williams: DNA replication licensing in somatic and germ cells. in Journal of cell science 2004
Show all 6 Pubmed References
Dog (Canine) Polyclonal MRE11A Primary Antibody for ELISA, WB - ABIN538415
Archambault, Ikui, Drapkin, Cross: Disruption of mechanisms that prevent rereplication triggers a DNA damage response. in Molecular and cellular biology 2005
Show all 3 Pubmed References
Human Polyclonal MRE11A Primary Antibody for IHC, WB - ABIN6670065
Li, Zhang, Chen, Guo, Zhang, Tang, Xu, Zhang, Tao, Wang, Jiang, Sun, Mao: Impaired DNA double-strand break repair contributes to the age-associated rise of genomic instability in humans. in Cell death and differentiation 2017
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Human Polyclonal MRE11A Primary Antibody for IHC, WB - ABIN3016250
Zhang, Tang, Jiang, Mao: The transcription factor GATA3 is required for homologous recombination repair by regulating CtIP expression. in Oncogene 2017
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Human Polyclonal MRE11A Primary Antibody for IF (p), IHC (p) - ABIN747293
Yuan, Han, Cong, Ge, Ma, Dai, Li, Bi: Docetaxel-loaded solid lipid nanoparticles suppress breast cancer cells growth with reduced myelosuppression toxicity. in International journal of nanomedicine 2014
Human Polyclonal MRE11A Primary Antibody for IHC (p), WB - ABIN4335394
Salvati, Scarsella, Porru, Rizzo, Iachettini, Tentori, Graziani, DIncalci, Stevens, Orlandi, Passeri, Gilson, Zupi, Leonetti, Biroccio: PARP1 is activated at telomeres upon G4 stabilization: possible target for telomere-based therapy. in Oncogene 2010
the essential role of Nbs1 is via its interaction with Mre11 and that most of the Nbs1 protein is dispensable for Mre11 complex functions and suggest that Mre11 and Rad50 directly activate ATM.
Low MRE11 expression is associated with B-cell lymphomas.
cyclin A2 controlled Mre11 abundance through a C-terminal RNA binding domain that selectively and directly binds Mre11 transcripts to mediate polysome loading and translation.
MRE11 complex influences the elimination of oocytes with unrepaired meiotic double-strand breaks post-natally, in addition to its previously described role in double-strand break repair and homologous synapsis during female meiosis.
Inhibiting MRE11 by mirin during meiotic maturation results in anaphase bridges and also increases the number of gammaH2AX foci in metaphase II. Compromised DNA integrity in mirin-treated oocytes indicates a role for MRE11 in chromosome integrity during meiotic maturation.
The authors demonstrate that ATM can be activated by DNA double-strand breaks in the absence of the Mre11-Rad50-NBS1 (MRN) sensor complex.
TRIP13-deficient spermatocytes also progress to an H1t-positive stage if ATM activity is attenuated by hypomorphic mutations in Mre11 or Nbs1 or by elimination of the ATM-effector kinase CHK2
Impairment of Mre11 complex functions promotes the progression of mammary hyperplasias into invasive and metastatic breast cancers
results suggest that the MRE11-RAD50 complex plays important roles in recognition of dsDNA and initiation of STING-dependent signaling, in addition to its role in DNA-damage responses
The critical role of the MRE11 GAR motif in DSB repair is a mechanistic link between post-translational modifications at the MRE11 GAR motif and DSB processing, as well as the ATR/CHK1 checkpoint signaling.
Mre11 is present in mitochondria where it binds to mtDNA and that the amount in mitochondria varies depending on cellular stress and differentiation.
Data show that CS-mediated SCC lethality was mitigated in irradiated gain-of-function Rad50(s/s) mice, and epistasis studies order Rad50 upstream of Mre11.
MRE11-RAD50-NBS1 complex dictates DNA repair independent of H2AX.
The data indicate that even subtle perturbation of Mre11 complex functions results in severe genotoxic stress, and that the complex is critically important for homeostasis of proliferative tissues.
following high NaCl, Mre11 exits from the nucleus, DNA double-strand breaks accumulate in the S and G2 phases of the cell cycle, and DNA repair is inhibited.
Results suggest that in Mre11(ATLD1/ATLD1) mice, genome instability and cell cycle checkpoint defects reduce viability in early embryos and in proliferating cells, while promoting malignancy in the context of an initiating lesion.
The Mre11 complex influences DNA repair, synapsis, and crossing over in murine meiosis.
ATM activation by the Rad50S-containing Mre11 complex enhances the proliferation of LSK cells, a population consisting of hematopoietic stem cells and multipotent progenitor cells.
The MRE11-RAD50-Nijmegen breakage syndrome 1 (NBS1 [MRN]) complex accumulates at sites of DNA double-strand breaks (DSBs) in microscopically discernible nuclear foci.
Nucleolytic processing by Mre11 is an essential function of fundamental importance in DNA repair, distinct from MRN control of ATM signaling.
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]
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.
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.
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.
GFI1 facilitates efficient DNA repair by regulating PRMT1 dependent methylation of MRE11 and 53BP1.
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.
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.
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.
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.
MRE11A gene polymorphism is associated with colorectal cancer.
Low MRE11 expression is associated with low-grade epithelial ovarian cancer.
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.
Mre11-Rad50-Nbs1 complex initiates DNA double strand break repair.
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
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.
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.
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.
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.
Ataxia-telangiectasia-like disease (A-TLD) is clinically similar to mild Ataxia-telangiectasia and caused by hypomorphic mutations in the MRE11 gene.
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.
This gene encodes a nuclear protein involved in homologous recombination, telomere length maintenance, and DNA double-strand break repair. By itself, the protein has 3' to 5' exonuclease activity and endonuclease activity. The protein forms a complex with the RAD50 homolog\; this complex is required for nonhomologous joining of DNA ends and possesses increased single-stranded DNA endonuclease and 3' to 5' exonuclease activities. In conjunction with a DNA ligase, this protein promotes the joining of noncomplementary ends in vitro using short homologies near the ends of the DNA fragments. This gene has a pseudogene on chromosome 3. Alternative splicing of this gene results in two transcript variants encoding different isoforms.
meiotic recombination 11 homolog A
, MRE11 meiotic recombination 11 homolog A (S. cerevisiae)
, MRE11 homolog 1
, MRE11 homolog A
, double-strand break repair protein MRE11A
, meiotic recombination 11 homolog 1
, AT-like disease
, DNA recombination and repair protein
, endo/exonuclease Mre11
, meiotic recombination 11-like protein