GoPubMed Proteins lists recent and important papers and reviews for
proteins. Page last changed on 14 Mar 2013.
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)
Papers on
Mre11
NBS1 directly activates ATR independently of MRE11 and TOPBP1.
New
Kanazawa, Japan. In Genes Cells, 31 Mar 2013
We found that CHK1 phosphorylation and FANCD2 ubiquitination induced by various DNA replication-stalling agents were abrogated in Nbs1 knockout DT40 cells but not in conditional Mre11 knockout cells, indicating an MRE11-independent role for NBS1 in ATR activation.
Processing of DNA double-strand breaks and intermediates of recombination and repair by Saccharomyces cerevisiae Mre11 and its stimulation by Rad50, Xrs2 and Sae2 proteins.
New
India. In J Biol Chem, 26 Mar 2013
Saccharomyces cerevisiae RAD50, MRE11, and XRS2 genes are essential for telomere length maintenance, cell cycle check-point signalling, meiotic recombination and DSB repair via non-homologous end-joining and homologous recombination.
Clinical Course of Two Italian Siblings with Ataxia-Telangiectasia-Like Disorder.
New
Siena, Italy. In Cerebellum, 23 Mar 2013
Ataxia-telangiectasia-like disorder (ATLD) due to mutations in the MRE11 gene is a very rare autosomal recessive disease, described so far in only 20 patients.
DNA damage sensor MRE11 recognizes cytosolic double-stranded DNA and induces type I interferon by regulating STING trafficking.
New
Ōsaka, Japan. In Proc Natl Acad Sci U S A, 19 Mar 2013
Here we show that the DNA damage sensor, meiotic recombination 11 homolog A (MRE11), serves as a cytosolic sensor for dsDNA.
Impairment of BRCA1-Related DNA Double-Strand Break Repair Leads to Ovarian Aging in Mice and Humans.
New
Rye, United States. In Sci Transl Med, 13 Mar 2013
In parallel, expression of key DNA DSB repair genes BRCA1, MRE11, Rad51, and ATM, but not BRCA2, declines in single mouse and human oocytes.
Dna Mismatch Repair Protein Msh2 Dictates Cellular Survival in Response to Low Dose Radiation in Endometrial Carcinoma Cells.
New
Dublin, Ireland. In Cancer Lett, 03 Mar 2013
Maintenance of the arrest was associated with persistent MRE11, γH2AX, RAD51 foci at 2 h after irradiation.
A structural basis for the assembly and functions of a viral polymer that inactivates multiple tumor suppressors.
New
Impact
Los Angeles, United States. In Cell, Nov 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
New
Livermore, United States. In Mutat Res, Oct 2012
ATM, ATR, DNA-PK, Chk1, Chk2, PARP1/2/3, 53BP1, BRCA1, BRCA2, BLM, RAD51, and the MRE11-RAD50-NBS1 complex.
Site-specific DICER and DROSHA RNA products control the DNA-damage response.
New
Impact
Milano, Italy. In Nature, Sep 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.
New
Impact
Ann Arbor, United States. In Cell, Sep 2012
Here, we identify by whole-exome resequencing, mutations of MRE11, ZNF423, and CEP164 as causing NPHP-RC.
Mechanistic links between ATM and histone methylation codes during DNA repair.
Review
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.
Functional interplay of the Mre11 nuclease and Ku in the response to replication-associated DNA damage.
GeneRIF
New York City, United States. In Mol Cell Biol, 2011
propose that Mre11 nuclease- and Sae2-dependent DNA end processing, which initiates DSB resection prevents Ku from engaging DSBs, thus promoting Exo1-dependent resection
Involvement of MRE11A and XPA gene polymorphisms in the modulation of DNA double-strand break repair activity: a genotype-phenotype correlation study.
GeneRIF
Torino, Italy. In Dna Repair (amst), 2011
these results showed a strong correlation between the MRE11A DNA repair gene (on both a SNP and a haplotype level) and gammaH2AX dephosphorylation
Human Mre11/human Rad50/Nbs1 and DNA ligase IIIalpha/XRCC1 protein complexes act together in an alternative nonhomologous end joining pathway.
GeneRIF
Baltimore, United States. In J Biol Chem, 2011
Human Mre11/human Rad50/Nbs1 and DNA ligase IIIalpha/XRCC1 protein complexes act together in an alternative nonhomologous end joining pathway.
Mre11 is expressed in mammalian mitochondria where it binds to mitochondrial DNA.
GeneRIF
Bethesda, United States. In Am J Physiol Regul Integr Comp Physiol, 2011
Mre11 is present in mitochondria where it binds to mtDNA and that the amount in mitochondria varies depending on cellular stress and differentiation.
Identification of Mre11 as a target for heat radiosensitization.
GeneRIF
Indianapolis, United States. In Radiat Res, 2011
findings implicate Mre11 as a target for heat radiosensitization and suggest that heat radiosensitization and inhibition of DSB repair may be mediated by heat-induced conformational changes in Mre11
Double-strand break repair-independent role for BRCA2 in blocking stalled replication fork degradation by MRE11.
Impact
GeneRIF
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
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
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.
Differences in the DNA replication of unicellular eukaryotes and metazoans: known unknowns.
Review
London, United Kingdom. In Embo Rep, 2010
Finally, the dependence of DNA replication on homologous recombination proteins such as RAD51 and the MRE11-RAD50-NBS1 complex is also different; they are dispensable for yeast S-phase but essential for accurate DNA replication in metazoans under unchallenged conditions.
