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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
FANCD2-Controlled Chromatin Access of the Fanconi-Associated Nuclease FAN1 Is Crucial for the Recovery of Stalled Replication Forks.
Sobeck et al., Minneapolis, United States. In Mol Cell Biol, 01 Dec 2014
Importantly, FANCD2 has additional independent functions: it binds chromatin and coordinates the restart of aphidicolin (APH)-stalled replication forks in concert with the BLM helicase, while protecting forks from nucleolytic degradation by MRE11.
Identification of TRIM27 as a Novel Degradation Target of Herpes Simplex Virus 1 ICP0.
Knipe et al., Boston, United States. In J Virol, 15 Nov 2014
Cellular candidates resulting from our analysis included the ubiquitin-specific protease USP7, the transcriptional repressor TRIM27, DNA repair proteins NBS1 and MRE11, regulators of apoptosis including BIRC6, and the proteasome.
Nucleotide Excision Repair-dependent DNA Double-strand Break Formation and ATM Signaling Activation in Mammalian Quiescent Cells.
Matsunaga et al., Suita, Japan. In J Biol Chem, 10 Nov 2014
The NER-dependent DSB formation activates ATM kinase and triggers the accumulation of its downstream factors, MRE11, NBS1, and MDC1, at UV-damaged sites.
The Human SRCAP Chromatin Remodeling Complex Promotes DNA-End Resection.
Huang et al., Hangzhou, China. In Curr Biol, 22 Oct 2014
In vertebrates, DSB resection is initiated by the collaborative action of CtIP and the MRE11-RAD50-NBS1 (MRN) complex.
Deletion of BRCA2 exon 27 causes defects in response to both stalled and collapsed replication forks.
Hasty et al., San Antonio, United States. In Mutat Res Fundam Mol Mech Mutagen, Aug 2014
The BRC-RAD51 associations enable DSB repair while the Ex27-RAD51 association protects the nascent replication strand from MRE11-mediated degradation.
MRE11-Deficiency Associated with Improved Long-Term Disease Free Survival and Overall Survival in a Subset of Stage III Colon Cancer Patients in Randomized CALGB 89803 Trial.
Maizels et al., Seattle, United States. In Plos One, Dec 2013
PURPOSE: Colon cancers deficient in mismatch repair (MMR) may exhibit diminished expression of the DNA repair gene, MRE11, as a consequence of contraction of a T11 mononucleotide tract.
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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