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Apurinic/apyrimidinic (AP) sites occur frequently in DNA molecules by spontaneous hydrolysis, by DNA damaging agents or by DNA glycosylases that remove specific abnormal bases. De plus, nous expédions APEX2 Protéines (3) et APEX2 Kits (2) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal APEX2 Primary Antibody pour WB - ABIN4281061
Karkhanis, Wang, Tae, Hu, Imbalzano, Sif: Protein arginine methyltransferase 7 regulates cellular response to DNA damage by methylating promoter histones H2A and H4 of the polymerase δ catalytic subunit gene, POLD1. dans The Journal of biological chemistry 2012
Determinants in nuclease (Montrer DCLRE1C Anticorps) specificity of Ape1 (Montrer APEX1 Anticorps) and Ape2, human homologues of Escherichia coli exonuclease (Montrer EXO1 Anticorps) III
Ape2 exhibits strong 3'-5' exonuclease and 3'-phosphodiesterase activities and has only a very weak AP-endonuclease activity.
Ape2 may be involved in repair of oxidative DNA damage and PCNA (Montrer PCNA Anticorps)-dependent repair synthesis.
APE2 associates with Chk1 (Montrer CHEK1 Anticorps); a serine residue (S86) in the Chk1 (Montrer CHEK1 Anticorps)-binding motif of APE2 is essential for Chk1 (Montrer CHEK1 Anticorps) phosphorylation, indicating a Claspin (Montrer CLSPN Anticorps)-like but distinct role for APE2 in ATR (Montrer ATR Anticorps)-Chk1 (Montrer CHEK1 Anticorps) signaling.
expression of Apex 2 in chondrocytes appears to be associated with the degeneration of articular cartilage in osteoarthritis.
Results indicate a role for apurinic/apyrimidinic endonuclease (APE (Montrer RPLP0 Anticorps)) 2 (Apex2) in the protection of germinal center (GC) cells from activation-induced cytidine deaminase (Montrer AICDA Anticorps) (AID)-independent damage.
data provide new insight into error-prone repair of AID-induced lesions, which we propose is facilitated by down-regulation of APE1 (Montrer APEX1 Anticorps) and up-regulation of APE2 expression in germinal center B cells.
Extensive analysis of bone marrow hematopoiesis in APE2-deficient mice finds inhibition of the pro-B to pre-B lymphocyte (Montrer AKAP17A Anticorps) transition, due to a p53 (Montrer TP53 Anticorps)-dependent DNA damage response, independent from its ubiquitous and essential homolog APE1 (Montrer APEX1 Anticorps).
APEX2 is required for proper cell cycle progression of proliferating lymphocytes.
Both APE1 (Montrer APEX1 Anticorps) and APE2 function in antibody switch recomibination, resulting in double stranded breaks necesary for this recombination.
The present study clearly demonstrates that APEX2-null lymphocytes have a higher frequency of DNA breaks, indicating that APEX2 may play an important role(s) during their generation and/or repair.
Apex2 is required for efficient somatic hypermutation of immunoglobulin genes.
Apurinic/apyrimidinic (AP) sites occur frequently in DNA molecules by spontaneous hydrolysis, by DNA damaging agents or by DNA glycosylases that remove specific abnormal bases. AP sites are pre-mutagenic lesions that can prevent normal DNA replication so the cell contains systems to identify and repair such sites. Class II AP endonucleases cleave the phosphodiester backbone 5' to the AP site. This gene encodes a protein shown to have a weak class II AP endonuclease activity. Most of the encoded protein is located in the nucleus but some is also present in mitochondria. This protein may play an important role in both nuclear and mitochondrial base excision repair. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene.
AP endonuclease 2
, AP endonuclease XTH2
, DNA-(apurinic or apyrimidinic site) lyase 2
, apurinic/apyrimidinic endonuclease-like 2
, APEX nuclease 2
, apurinic-apyrimidinic endonuclease 2
, APEX nuclease (apurinic/apyrimidinic endonuclease) 2
, DNA-(apurinic or apyrimidinic site) lyase 2-like