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MRE11 meiotic recombination 11 homolog A

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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Rad50, NBS1, Atm, CAN, Rad51
Papers on Mre11
Functions of the MRE11 complex in the development and maintenance of oocytes.
Petrini et al., New York City, United States. In Chromosoma, 01 Sep 2015
UNASSIGNED: The MRE11 complex (MRE11, RAD50, and NBS1) is a central component of the DNA damage response, governing both double-strand break repair and DNA damage response signaling.
Localized movement and morphology of UBF1-positive nucleolar regions are changed by γ-irradiation in G2 phase of the cell cycle.
Bártová et al., Brno, Czech Republic. In Nucleus, 24 Aug 2015
Moreover, many DNA repair pathway proteins, including ATM, ATR kinases, MRE11, PARP1 and Ku70/80, localize to the nucleolus (Moore et al., 2011).
Processing by MRE11 is involved in the sensitivity of subtelomeric regions to DNA double-strand breaks.
Murnane et al., San Francisco, United States. In Nucleic Acids Res, 23 Aug 2015
We now show that inhibition of MRE11 3'-5' exonuclease activity with Mirin reduces the frequency of large deletions and GCRs at both interstitial and subtelomeric DSBs, but has little effect on the frequency of small deletions.
Recognition and repair of chemically heterogeneous structures at DNA ends.
Williams et al., United States. In Environ Mol Mutagen, Jan 2015
Nucleolytic processing enzymes such as the MRE11/RAD50/NBS1/CtIP complex, Flap endonuclease (FEN1) and the apurinic endonucleases (APE1 and APE2) also act in the chemical "cleansing" of DNA breaks to prevent genomic instability and disease, and promote progression of DNA- and RNA-DNA damage response (DDR and RDDR) pathways.
Development of a multiparameter flow cytometric assay as a potential biomarker for homologous recombination deficiency in women with high-grade serous ovarian cancer.
Kohn et al., Bethesda, United States. In J Transl Med, Dec 2014
We hypothesized that measuring γH2AX as an indicator of DNA double-strand breaks (DSB), and MRE11 or RAD51 as an indicator of DSB repair, would reflect HR status and predict response to PARPi-based therapy.
MCM8-9 complex promotes resection of double-strand break ends by MRE11-RAD50-NBS1 complex.
Dutta et al., Charlottesville, United States. In Nat Commun, Dec 2014
Here we report that MCM8-9 is required for DNA resection by MRN (MRE11-RAD50-NBS1) at DSBs to generate ssDNA.
Hereditary genes and SNPs associated with breast cancer.
Nasiri et al., Mashhad, Iran. In Asian Pac J Cancer Prev, 2012
The most important loci which include mutations are; BRCA1, BRCA2, PTEN, ATM, TP53, CHEK2, PPM1D, CDH1, MLH1, MRE11, MSH2, MSH6, MUTYH, NBN, PMS1, PMS2, BRIP1, RAD50, RAD51C, STK11 and BARD1.
A structural basis for the assembly and functions of a viral polymer that inactivates multiple tumor suppressors.
O'Shea et al., Los Angeles, United States. In Cell, 2012
E4-ORF3 forms a nuclear polymer and simultaneously inactivates p53, PML, TRIM24, and MRE11/RAD50/NBS1 (MRN) tumor suppressors.
Recognition, signaling, and repair of DNA double-strand breaks produced by ionizing radiation in mammalian cells: the molecular choreography.
Thompson, Livermore, United States. In Mutat Res, 2012
ATM, ATR, DNA-PK, Chk1, Chk2, PARP1/2/3, 53BP1, BRCA1, BRCA2, BLM, RAD51, and the MRE11-RAD50-NBS1 complex.
Adenovirus regulates sumoylation of Mre11-Rad50-Nbs1 components through a paralog-specific mechanism.
Hearing et al., Stony Brook, United States. In J Virol, 2012
Mre11 and Nbs1 are sumoylated during Ad5 infection and the E4-ORF3 protein is necessary and sufficient to induce SUMO conjugation. Relocalization of Mre11 and Nbs1 into E4-ORF3 nuclear tracks is required for this modification to occur.
Site-specific DICER and DROSHA RNA products control the DNA-damage response.
d'Adda di Fagagna et al., Milano, Italy. In Nature, 2012
Through RNA deep sequencing and the study of DDR activation at a single inducible DNA double-strand break, we demonstrate that DDR foci formation requires site-specific DICER- and DROSHA-dependent small RNAs, named DDRNAs, which act in a MRE11–RAD50–NBS1-complex-dependent manner (MRE11 also known as MRE11A; NBS1 also known as NBN).
Exome capture reveals ZNF423 and CEP164 mutations, linking renal ciliopathies to DNA damage response signaling.
Hildebrandt et al., Ann Arbor, United States. In Cell, 2012
Study identifies by whole-exome resequencing, mutations of MRE11, ZNF423, and CEP164 as causing Nephronophthisis-related ciliopathies.
Mre11-dependent degradation of stalled DNA replication forks is prevented by BRCA2 and PARP1.
Helleday et al., Oxford, United Kingdom. In Cancer Res, 2012
findings not only show that Mre11 activity is required for the survival of BRCA2 mutant cells but also elucidate roles for both the BRCA2 and PARP1 proteins in protecting stalled replication forks
Human Ku70/80 protein blocks exonuclease 1-mediated DNA resection in the presence of human Mre11 or Mre11/Rad50 protein complex.
Chen et al., Dallas, United States. In J Biol Chem, 2012
Human Ku70/80 protein blocks exonuclease 1-mediated DNA resection in the presence of human Mre11 or Mre11/Rad50 protein complex.
Mre11 regulates CtIP-dependent double-strand break repair by interaction with CDK2.
Ferguson et al., Ann Arbor, United States. In Nat Struct Mol Biol, 2012
The authors show that, in human and mouse, Mre11 controls these events through a direct interaction with CDK2 that is required for CtIP phosphorylation and BRCA1 interaction in normally dividing cells.
Mechanistic links between ATM and histone methylation codes during DNA repair.
Price et al., Boston, United States. In Prog Mol Biol Transl Sci, 2011
The activation of ATM involves its recruitment to the DSB through interaction with the mre11-rad50-nbs1 complex, followed by the acetylation of ATM by the Tip60 acetyltransferase.
Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11.
Jasin et al., New York City, United States. In Cell, 2011
BRCA2 prevents chromosomal aberrations on replication stalling, which are alleviated by inhibition of MRE11, the nuclease responsible for this form of fork instability.
[DNA repair and tumour radiosensitivity: focus on ATM gene].
Favaudon et al., Paris, France. In Bull Cancer, 2011
Measure of residual double-strand breaks by immunochemistry of H2AX, but also ATM or MRE11, is another way to evaluate tumour radiosensitivity.
The MRE11 complex: starting from the ends.
Petrini et al., Barcelona, Spain. In Nat Rev Mol Cell Biol, 2011
The MRE11 complex, composed of the meiotic recombination 11 (MRE11), RAD50 and Nijmegen breakage syndrome 1 (NBS1; also known as nibrin) proteins is central to the DDR, and recent insights into its structure and function have been gained from in vitro structural analysis and studies of animal models in which the DDR response is deficient.
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