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MRE11 meiotic recombination 11 homolog A

Mre11
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
Formation of Linear Amplicons with Inverted Duplications in Leishmania Requires the MRE11 Nuclease.
New
Ouellette et al., Québec, Canada. In Plos Genet, 31 Dec 2014
We hypothesized that the Leishmania infantum DNA repair protein MRE11 is required for linear amplicons following rearrangements at the level of inverted repeats.
Regulation of DNA damage responses and cell cycle progression by hMOB2.
New
Hergovich et al., London, United Kingdom. In Cell Signal, 21 Dec 2014
Thus, to gain mechanistic insight, we screened for novel binding partners of hMOB2, revealing that hMOB2 interacts with RAD50, facilitating the recruitment of the MRE11-RAD50-NBS1 (MRN) DNA damage sensor complex and activated ATM to DNA damaged chromatin.
Novel neoadjuvant therapy paradigms for bladder cancer: Results from the National Cancer Center Institute Forum.
Review
New
Bajorin et al., New York City, United States. In Urol Oncol, 24 Nov 2014
A second clinical trial was planned that will examine the relationship between expression of the DNA repair protein MRE11 and complete response in patients treated with concurrent 5-flurouracil/mitomycin C plus radiation.
γH2AX foci on apparently intact mitotic chromosomes: Not signatures of misrejoining events but signals of unresolved DNA damage.
New
Genescà et al., Barcelona, Spain. In Cell Cycle, Nov 2014
Finally, when analyzing the presence of other DNA-damage response (DDR) factors we found that all γH2AX foci-regardless their coincidence with a visible break-always colocalized with MRE11, but not with 53BP1.
DNA end resection is needed for the repair of complex lesions in G1-phase human cells.
New
Taucher-Scholz et al., Darmstadt, Germany. In Cell Cycle, Sep 2014
Resection of complex DSBs is driven by meiotic recombination 11 homolog A (MRE11), CTBP-interacting protein (CtIP), and exonuclease 1 (EXO1) but seems not controlled by the Ku heterodimer or by phosphorylation of H2AX.
Identification of the Interactors of Human Nibrin (NBN) and of Its 26 kDa and 70 kDa Fragments Arising from the NBN 657del5 Founder Mutation.
New
di Masi et al., Roma, Italy. In Plos One, Dec 2013
UNLABELLED: Nibrin (also named NBN or NBS1) is a component of the MRE11/RAD50/NBN complex, which is involved in early steps of DNA double strand breaks sensing and repair.
Hereditary genes and SNPs associated with breast cancer.
Review
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.
Impact
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.
Review
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.
GeneRIF
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.
Impact
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.
Impact
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
Review
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.
Impact
GeneRIF
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].
Review
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.
Review
Impact
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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