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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
NBS1 is required for macrophage homeostasis and functional activity in mice.
New
Celada et al., Barcelona, Spain. In Blood, 01 Oct 2015
UNASSIGNED: Nijmegen breakage syndrome 1 (NBS1) is a component of the MRE11 complex that is a sensor of DNA double-strand breaks and plays a crucial role in the DNA damage response.
Viral and Cellular Genomes Activate Distinct DNA Damage Responses.
New
Impact
O'Shea et al., Los Angeles, United States. In Cell, 27 Sep 2015
In response to cellular genome breaks, MRE11/RAD50/NBS1 (MRN) activates a global ATM DNA damage response (DDR) that prevents cellular replication.
When two is not enough: a CtIP tetramer is required for DNA repair by Homologous Recombination.
New
Pellegrini et al., Cambridge, United Kingdom. In Nucleus, 25 Sep 2015
The specific arrangement of protein chains in the CtIP/Ctp1 tetramer indicates that an ability to bridge DNA ends might be an important feature of CtIP/Ctp1 function, establishing an intriguing similarity with the known ability of the MRE11-RAD50-NBS1 complex to link DNA ends.
The WRN exonuclease domain protects nascent strands from pathological MRE11/EXO1-dependent degradation.
New
Pichierri et al., Roma, Italy. In Nucleic Acids Res, 14 Sep 2015
Here, we show that, in response to replication perturbation induced by low doses of the TOP1 inhibitor camptothecin, loss of the WRN exonuclease resulted in enhanced degradation and ssDNA formation at nascent strands by the combined action of MRE11 and EXO1, as opposed to the limited processing of nascent strands performed by DNA2 in wild-type cells.
ATM-dependent phosphorylation of MRE11 controls extent of resection during homology directed repair by signalling through Exonuclease 1.
New
Lavin et al., Brisbane, Australia. In Nucleic Acids Res, 03 Sep 2015
UNASSIGNED: The MRE11/RAD50/NBS1 (MRN) complex plays a central role as a sensor of DNA double strand breaks (DSB) and is responsible for the efficient activation of ataxia-telangiectasia mutated (ATM) kinase.
Functions of the MRE11 complex in the development and maintenance of oocytes.
New
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.
Recognition and repair of chemically heterogeneous structures at DNA ends.
Review
New
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.
Functional Role of NBS1 in Radiation Damage Response and Translesion DNA Synthesis.
Review
New
Komatsu et al., Kyoto, Japan. In Biomolecules, Dec 2014
The C-terminus of NBS1 is essential for interactions with MRE11, a homologous recombination repair nuclease, and ATM, a key player in signal transduction after the generation of DNA double-strand breaks (DSBs), which is induced by IR.
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, 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-fluorouracil/mitomycin C plus radiation.
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.
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.
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