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the essential role of Nbs1 (show NBN ELISA Kits) is via its interaction with Mre11 and that most of the Nbs1 (show NBN ELISA Kits) protein is dispensable for Mre11 complex functions and suggest that Mre11 and Rad50 (show RAD50 ELISA Kits) directly activate ATM (show ATM ELISA Kits).
Cyclin A2 (show CCNA2 ELISA Kits) binds to Mre11 mRNA to promote Mre11 translation and repair of replication errors.
Low MRE11 expression is associated with B-cell lymphomas.
cyclin A2 (show CCNA2 ELISA Kits) controlled Mre11 abundance through a C-terminal RNA binding domain that selectively and directly binds Mre11 transcripts to mediate polysome loading and translation.
MRE11 complex influences the elimination of oocytes with unrepaired meiotic double-strand breaks post-natally, in addition to its previously described role in double-strand break repair and homologous synapsis during female meiosis.
Inhibiting MRE11 by mirin during meiotic maturation results in anaphase bridges and also increases the number of gammaH2AX (show H2AFX ELISA Kits) foci in metaphase II. Compromised DNA integrity in mirin-treated oocytes indicates a role for MRE11 in chromosome integrity during meiotic maturation.
The authors demonstrate that ATM (show ATM ELISA Kits) can be activated by DNA double-strand breaks in the absence of the Mre11-Rad50 (show RAD50 ELISA Kits)-NBS1 (show NBN ELISA Kits) (MRN) sensor complex.
TRIP13 (show TRIP13 ELISA Kits)-deficient spermatocytes also progress to an H1t (show HIST1H1T ELISA Kits)-positive stage if ATM (show ATM ELISA Kits) activity is attenuated by hypomorphic mutations in Mre11 or Nbs1 (show NBN ELISA Kits) or by elimination of the ATM (show ATM ELISA Kits)-effector kinase CHK2 (show CHEK2 ELISA Kits)
Impairment of Mre11 complex functions promotes the progression of mammary hyperplasias into invasive and metastatic breast cancers
results suggest that the MRE11-RAD50 (show RAD50 ELISA Kits) complex plays important roles in recognition of dsDNA and initiation of STING-dependent signaling, in addition to its role in DNA-damage responses
Low MRE11 expression is associated with low-grade epithelial ovarian cancer.
although recruitment of the MRE11-RAD50 (show RAD50 ELISA Kits)-NBS1 (show NBN ELISA Kits) (MRN) DSB-sensing complex to viral genomes and activation of the ATM (show ATM ELISA Kits) kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Mre11-Rad50 (show RAD50 ELISA Kits)-Nbs1 (show NBN ELISA Kits) complex initiates DNA double strand break repair.
we show that Plk1 (show PLK1 ELISA Kits) phosphorylates Mre11 at S649 during G2 DNA damage recovery and Mre11 phosphorylation at S649/S689 drives premature checkpoint termination and reduced DNA repair
In the absence of RAD51 (show RAD51 ELISA Kits), the unprotected newly replicated genome is degraded by the exonuclease (show EXO1 ELISA Kits) activity of MRE11, and the fragmented nascent DNA accumulates in the cytosol, initiating an innate immune response.
Both the genome instability and cell death of MRE11-null and MRE11-mutated H129N cells are significantly reversed by overexpression of Tdp2 (show TDP2 ELISA Kits), an enzyme that eliminates covalent Top2 (show TOP2A ELISA Kits) conjugates; thus, the essential role of Mre11 nuclease (show DCLRE1C ELISA Kits) activity is likely to remove the DNA lesions.
The results illuminate the important role of Nbs1 (show NBN ELISA Kits) and CtIP (show RBBP8 ELISA Kits) in determining the substrates and consequences of human Mre11/Rad50 (show RAD50 ELISA Kits) nuclease (show DCLRE1C ELISA Kits) activities on protein-DNA lesions.
Cdk-dependent phosphorylation of TRF1 on threonine 371 promotes TRF1 to interact with APBs in S and G2 phases independently of its binding to telomeric DNA. We have demonstrated that the interaction of (pT371)TRF1 with APBs is dependent upon ATM and homologous-recombination-promoting factors such as Mre11 and BRCA1.
Ataxia-telangiectasia-like disease (A-TLD (show BMP1 ELISA Kits)) is clinically similar to mild Ataxia-telangiectasia and caused by hypomorphic mutations in the MRE11 gene.
although Mre11 is required for efficient HR-dependent repair of ionizing-radiation-induced DSBs, Mre11 is largely dispensable for DSB resection in both chicken DT40 and human TK6 B cell lines.
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.
meiotic recombination 11 homolog A
, MRE11 meiotic recombination 11 homolog A (S. cerevisiae)
, MRE11 homolog 1
, MRE11 homolog A
, double-strand break repair protein MRE11A
, meiotic recombination 11 homolog 1
, AT-like disease
, DNA recombination and repair protein
, endo/exonuclease Mre11
, meiotic recombination 11-like protein