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the essential role of Nbs1 (zeige NBN ELISA Kits) is via its interaction with Mre11 and that most of the Nbs1 (zeige NBN ELISA Kits) protein is dispensable for Mre11 complex functions and suggest that Mre11 and Rad50 (zeige RAD50 ELISA Kits) directly activate ATM (zeige ATM ELISA Kits).
Low MRE11 expression is associated with B-cell lymphomas.
cyclin A2 (zeige 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 (zeige 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 (zeige ATM ELISA Kits) can be activated by DNA double-strand breaks in the absence of the Mre11-Rad50 (zeige RAD50 ELISA Kits)-NBS1 (zeige NBN ELISA Kits) (MRN) sensor complex.
TRIP13 (zeige TRIP13 ELISA Kits)-deficient spermatocytes also progress to an H1t (zeige HIST1H1T ELISA Kits)-positive stage if ATM (zeige ATM ELISA Kits) activity is attenuated by hypomorphic mutations in Mre11 or Nbs1 (zeige NBN ELISA Kits) or by elimination of the ATM (zeige ATM ELISA Kits)-effector kinase CHK2 (zeige 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 (zeige 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
The critical role of the MRE11 GAR motif in DSB repair is a mechanistic link between post-translational modifications at the MRE11 GAR motif and DSB processing, as well as the ATR (zeige ATR ELISA Kits)/CHK1 (zeige CHEK1 ELISA Kits) checkpoint signaling.
Low MRE11 expression is associated with low-grade epithelial ovarian cancer.
although recruitment of the MRE11-RAD50 (zeige RAD50 ELISA Kits)-NBS1 (zeige NBN ELISA Kits) (MRN) DSB-sensing complex to viral genomes and activation of the ATM (zeige ATM ELISA Kits) kinase can promote KSHV replication, proteins involved in nonhomologous end joining (NHEJ) repair restrict amplification of viral DNA.
Mre11-Rad50 (zeige RAD50 ELISA Kits)-Nbs1 (zeige NBN ELISA Kits) complex initiates DNA double strand break repair.
we show that Plk1 (zeige 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 (zeige RAD51 ELISA Kits), the unprotected newly replicated genome is degraded by the exonuclease (zeige 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 (zeige TDP2 ELISA Kits), an enzyme that eliminates covalent Top2 (zeige TOP2A ELISA Kits) conjugates; thus, the essential role of Mre11 nuclease (zeige DCLRE1C ELISA Kits) activity is likely to remove the DNA lesions.
The results illuminate the important role of Nbs1 (zeige NBN ELISA Kits) and CtIP (zeige RBBP8 ELISA Kits) in determining the substrates and consequences of human Mre11/Rad50 (zeige RAD50 ELISA Kits) nuclease (zeige 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 (zeige 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