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has exonuclease properties that are similar to the human WRN protein
CRL4(Wdr70) regulates H2B monoubiquitination and facilitates Exo1-dependent DNA repair resection.
MSH2 (show MSH2 Proteins), MSH6 (show MSH6 Proteins), 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 (show MLH1 Proteins) c.-93G>A, MSH2 (show MSH2 Proteins) c.211 + 9C>G, MSH3 c.3133G>A, and EXO1 c.1765G>A abnormalities of DNA MMR (show MRC1 Proteins) pathway are important determinants of head and neck squamous cell carcinoma
14-3-3 (show YWHAQ Proteins) proteins restrain the Exo1 nuclease (show DCLRE1C Proteins) to prevent over-resection in end joining
These studies establish that the Mlh1 (show MLH1 Proteins)-Pms1 (show PMS1 Proteins) endonuclease is required for MMR (show MRC1 Proteins) in a previously uncharacterized Exo1-independent MMR (show MRC1 Proteins) pathway.
EXO1 Glu589Lys polymorphism is not associated with overall cancer susceptibility.
FOXM1 (show FOXM1 Proteins) is upregulated in chemoresistant ovarian cancer samples, and defends ovarian cancer cells against cytotoxicity of cisplatin. FOXM1 (show FOXM1 Proteins) facilitates DNA repair through regulating EXO1 to protect ovarian cancer cells from cisplatin-mediated apoptosis.
This study reports that, contrary to earlier reports, and unlike the catalytic site mutant D173A, the EXO1 E109K variant resembled the wild-type enzyme on all tested substrates.
The results establish a key role for EXO1 in modulating the severity of hypomorphic MRE11 (show MRE11A Proteins) complex mutations.
Exo1-mediated HR is dispensable for stem cell function in quiescent HSC (show FUT1 Proteins), whereas it is essential to HSC (show FUT1 Proteins) 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 (show DCLRE1B Proteins), POT1b, CST (show CORT Proteins), 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.
Apc (show APC Proteins)(1638N) Exo1 Fen1 (show FEN1 Proteins) 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.
Switch Junction Position Is Altered in Exo1-/- Mi
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.
, exonuclease I Exo1
, RNA exonuclease
, exonuclease 1
, rad2 nuclease family member, homolog of S. cerevisiae exonuclease 1
, exonuclease I
, exonuclease ExoI