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CDH1 -160C/A and Exo1 K589E polymorphisms are associated with increased susceptibility to prostate cancer in Bangladeshi population.
The coordinated action of EXO1 and Y family TLS polymerases promotes checkpoint activation, leads to lesion repair, and is crucial to prevent cytotoxic double-strand break formation.
These findings provide the evidence that the rs1047840, rs9350, rs10802996, rs1635498, rs1776148, rs1776177, rs3754093 and rs851797 polymorphisms may act as risk factors for cancer.
The results from gene-environment interaction assay indicated all hEXO1 SNPs interacted with smoking, alcohol consumption, HBV infection in pathogenesis of hepatocellular carcinoma.
The finding that a threading mechanism like that used by hFEN1 is also used by hEXO1 unifies the mode of operation for members of the 5'-nuclease superfamily that act on discontinuous substrates. As with hFEN1, intrinsic disorder of the arch region of the protein may explain how flaps can be threaded without a need for a coupled energy source.
These findings indicate that the coupling of EXO1 activation with its eventual degradation is a timing mechanism that limits the extent of DNA end resection for accurate DNA repair.
Mutations in the human EXO1 gene correlate with increased susceptibility to some cancers. This review summarizes recent studies on the enzymatic functions and biological roles of EXO1, its possible protective role against cancer and aging, and regulation of EXO1 by posttranslational modification. [review]
These results suggest that Metnase enhances Exo1-mediated exonuclease activity on the lagging strand DNA by facilitating Exo1 loading onto a single strand gap at the stalled replication fork.
we present evidence that the inherited EXO1 polymorphism rs9350 may have a substantial influence on prostate cancer risk in Chinese people. We believe that the rs9350 could be a useful biomarker for assessing predisposition for and early diagnosis of prostate cancer.
study concludes that Exo1 gene polymorphism Lys589Glu may be associated with an increased risk of colorectal cancer in the Polish population
Mutations within the EXO1 gene are not associated with premature ovarian failure in Han Chinese women.
EXO1 is more active on DNA at temperatures below 37 degrees C and this manifests as an increase in nuclease activity.EXO1 preferentially cleaves one nucleotide inwards in a double stranded region of forked and nicked DNA flap substrates.
CRL4(Wdr70) regulates H2B monoubiquitination and facilitates Exo1-dependent DNA repair resection.
MSH2, MSH6, and EXO1 genes were overexpressed in gastroesophageal cancers.
EXO1 and FEN1 cleaved the substrate at the boundary between the single-stranded 5' flap and the duplex, whereas FAN1 incised it three to four nucleotides in the double-stranded region.
In summary, phosphorylation of EXO1 by CDKs is a novel mechanism regulating repair pathway choice.
Our data present, for the first time, evidence that inherited MLH1 c.-93G>A, MSH2 c.211 + 9C>G, MSH3 c.3133G>A, and EXO1 c.1765G>A abnormalities of DNA MMR pathway are important determinants of head and neck squamous cell carcinoma
14-3-3 proteins restrain the Exo1 nuclease to prevent over-resection in end joining
These studies establish that the Mlh1-Pms1 endonuclease is required for MMR in a previously uncharacterized Exo1-independent MMR pathway.
EXO1 Glu589Lys polymorphism is not associated with overall cancer susceptibility.
mice homozygous for a point mutation (D173A) in Exo1 that eliminates its nuclease activity but retains its native conformation, shows a level of trinucleotide expansion that is intermediate between Exo1+/+ and Exo1-/- animals.
like canonical DNA mismatch-repair proteins, EXO1 can restrain aberrant homologous recombination events between diverged sequence elements in the genome.
The results establish a key role for EXO1 in modulating the severity of hypomorphic MRE11 complex mutations.
Exo1-mediated HR is dispensable for stem cell function in quiescent HSC, whereas it is essential to HSC response to DNA damage processing after cell cycle entry, and its loss is not compensated by intact NHEJ
In contrast to Exo1(null/null) mice, Exo1(E109K/E109K) knockin mice retain mismatch repair activity and display normal class switch recombination and meiosis.
RNAi-mediated EXO1 knockdown in mouse fibroblasts directly results in an alkylation-tolerant phenotype.
Exo1 contributes to the metabolism of DNA ends during DNA double-strand breaks repair in B lymphocytes.
Study documents the combinatorial action of Apollo, POT1b, CST, and the 5' exonuclease Exo1 in postreplicative telomere end processing in mouse cells, clarifying the mechanism by which the telomeric 3' overhang is generated and modulated.
EXO1 can convert DNA nicks and point mutations into double-stranded DNA breaks for both core nonhomologous end-joining factors and alternative end-joining pathways of class-switch recombination.
Functions in mutation avoidance and is essential for male and female meiosis.
Apc(1638N) Exo1 Fen1 mice survive longer (18 months)
EXO1 contributes to DNA damage signal induction in mammalian cells, and deletion of Exo1 can prolong survival in the context of telomere dysfunction.
Meiotic progression in female mice bearing mutations in genes of the DNA mismatch repair pathway.
Switch Junction Position Is Altered in Exo1-/- Mi
ablation of either Msh6 or Exo1 function in the Mgmt-null mouse renders these rapidly proliferating tissues alkylation-resistant. The Exo1 defect leads to a variable tissue-specific alkylation resistance phenotype
Mlh1 or Exo1 deficiencies also eliminate class switch recombination in the absence of the SmuTR
This gene encodes a protein with 5' to 3' exonuclease activity as well as an RNase H activity. It is similar to the Saccharomyces cerevisiae protein Exo1 which interacts with Msh2 and which is involved in mismatch repair and recombination. Alternative splicing of this gene results in three transcript variants encoding two different isoforms.
, rad2 nuclease family member, homolog of S. cerevisiae exonuclease 1
, hypothetical protein
, exonuclease I Exo1
, RNA exonuclease
, exonuclease I
, exonuclease 1
, exonuclease ExoI