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These results suggested that the expression of APE1 was an important basis for the maintenance of poly (ADP-ribose) polymerase 1 (show PARP1 ELISA Kits), and the deletion of APE1 may be related to the resistance of triple-negative breast cancer to olaparib.
Alleles in mitochondrial transcription factor A (TFAM (show TFAM ELISA Kits)) and AP endonuclease 1 (APE1) are associated with reduced cognitive performance.
Study shows that TRX1 (show MLL ELISA Kits) and APEX1 expressions are up regulated in new Multiple Sclerosis (MS) patients compared to controls and might be implicated in pathogenesis of the disease.
Ku antigen displays the AP lyase activity on a certain type of double-stranded DNA.
study demonstrates that APE1 overexpression is an independent prognostic marker, but exclusively in ERG (show ERG ELISA Kits)-negative prostate cancers
These results suggest that degradation of endogenous APE1 by Parkin (show PARK2 ELISA Kits) occur when cells are stressed to activate Parkin (show PARK2 ELISA Kits), and imply a role of Parkin (show PARK2 ELISA Kits) in maintaining the quality of APE1, and loss of Parkin (show PARK2 ELISA Kits) may contribute to elevated APE1 levels in glioblastoma.
The efficiency of AP site cleavage by APE1 was affected by the benzo[a]pyrenyl-DNA adduct (BPDE-dG) in the opposite strand.
This study supported the hypothesis that the APE1 rs1760944 T>G polymorphism may be associated with N,N-dimethylformamide -induced abnormal liver function in the Chinese Han population.
Repair of the uracil adjacent to cisplatin ICLs proceeds through the classical BER pathway, highlighting the importance of specific proteins in this redundant pathway. Removal of uracil is followed by the generation of an abasic site and subsequent cleavage by AP endonuclease 1 (APE1). Inhibition of either the repair or redox domain of APE1 gives rise to cisplatin resistance.
Overexpressed APE1 promotes ovarian cancer growth and metastasis. Downregulated APE1 could suppress cell activity via AP-1 (show FOSB ELISA Kits) pathway, suggesting that APE1 gene may be a potential therapeutic target for ovarian cancer.
Study shows the methylation of the APE1 promoter and its role in mediating the functional effects of redox reactions induced by oxidative stress.
Meiosis progression and female age affect expression profile of DNA repair APEX1 gene in bovine oocytes.
prediction of the 3D structure of bovine AP lyase (BAP1); models of mutants showed substitution of Arg176-->Ala leads to the loss of DNA binding whereas mutation of Asp282-->Ala and His308-->Asn leads to a decrease in the enzymatic activity.
findings provide evidence that endogenous APE1 protects against ischemic infarction in both gray and white matter and facilitates the functional recovery of the central nervous system after mild stroke injury
Suppression of Ape1/Ref-1 redox function leads to an increased cell surface retention of IL-12 (show IL12A ELISA Kits) and enhances Th1 (show HAND1 ELISA Kits) responses.
Is closely associated with upregulation of the Ref1 (show THOC4 ELISA Kits)/Nrf2 (show NFE2L2 ELISA Kits) signalling pathway.
Results show the stimulatory effect of PARP-1 (show PARP1 ELISA Kits) on APE1-dependent base excision repair (BER). PARP-1 (show PARP1 ELISA Kits) and APE1 appear to have a functional interaction in BER since PARP-1 (show PARP1 ELISA Kits) can stimulate the strand incision activity of APE1.
increases in APEX1 level confer protection against the murine paternal age effect, thus highlighting the role of APEX1 in preserving reproductive health with increasing age and in protection against genotoxin-induced mutagenesis in somatic cells
Endothelial cell tumor proliferation was found to be dependent on Apex-1 expression.
Expression of OGG1 (show OGG1 ELISA Kits) and APEX1 was decreased at 3h after last exposure to Aroclor 1254 and only the expression level of APEX1 was recovered at 24-h after, so inhibition of DNA repair can be a potential mode of action of Aroclor 1254 gonadal toxicity.
Data indicate that the endonuclease activity of APE1 is required for class switch recombination (CSR).
These results suggest that mitochondrial APE1/Ref-1 is contributed to the protective role to protein kinase C (show PKC ELISA Kits)-induced mitochondrial dysfunction in endothelial cells.
Spinal motor neurones down-regulate APE1 upon oxidative stress. This property renders motor neurones susceptible to continuous challenge of oxidative stress in pathological conditions.
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 the major AP endonuclease in human cells. Splice variants have been found for this gene\; all encode the same protein.
DNA-(apurinic or apyrimidinic site) lyase
, APEX nuclease 1
, APEX nuclease (multifunctional DNA repair enzyme) 1
, AP endonuclease class I
, AP lyase
, apurinic-apyrimidinic endonuclease 1
, apurinic/apyrimidinic (abasic) endonuclease
, deoxyribonuclease (apurinic or apyrimidinic)
, protein REF-1
, redox factor-1
, AP endonuclease 1
, apurinic/apyrimidinic endonuclease 1
, apurinic/apyrimidinic endonuclease
, Apurinic-apyrimidinic endonuclease 1
, Redox factor-1
, APEX nuclease