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Validated All-in-One™ qPCR Primer for APEX1(NM_001641.3) Search again
Product ID:
HQP009061
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
APE, APE1, APEN, APEX, APX, HAP1, REF1
Gene Description:
apurinic/apyrimidinic endodeoxyribonuclease 1
Target Gene Accession:
NM_001641.3(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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.
Gene References into function
- Physical interaction of APE1 with flap endonuclease 1 (FEN1) by addition of APE1 to the excision reaction mixture slightly stimulates the removal of the displaced flap by FEN1, thus coordinating long-patch base excision repair.
- In the 58 cases analyzed, mean Ap endo activity was 7.3-fold higher in gliomas than in adjacent histologically normal brain.
- AP-endonuclease 1 and hnRNP-L interact with a nCaRE-like repressor element in the AP-endonuclease 1 promoter
- high levels of nuclear expression in pediatric embryonal rhabdomyosarcoma and low levels in alveolar rhabdomyosarcoma (ARMS; since APE activates daunomycin, ARMS is daunomycin-resistant but embryonal rhabdomyosarcoma is not.
- Determinants in nuclease specificity of Ape1 and Ape2, human homologues of Escherichia coli exonuclease III
- redox factor-1 in the regulation of endothelial oxidative stress and apoptosis
- altered posttranslational modification of Ref-1 is involved in uterine smooth muscle tumorigenesis.
- stimulates both FEN1 and DNA ligase I for progression through the base excision repair pathway
- APE/REF1 is increased &competent in the brain & spinal cord of individuals with amyotrophic lateral sclerosis. It is upredulated in spinal cord astrocytes& white matter pathways in familial ALS.
- The apurinic/apyrimidinic endonuclease activity of Ape1/Ref-1 contributes to human glioma cell resistance to alkylating agents and is elevated by oxidative stress.
- These results demonstrated that oxidoreductive modification of Cys-45 and Cys-57 via Ref-1 plays a role in redox regulation of Pax-8 in living cells.
- findings suggest a two-stage model of APE/Ref-1 behaviour during malignant thyrocyte transformation: 1) simple hyperplasia and upregulation of APE/Ref-1 in the nucleus and 2)nuclear levels drop as the cell becomes progressively undifferentiated
- H(2)O(2) induces translocation of APE/REF-1 to mitochondria in the Raji B-cell line.
- The 3(')-->5(')-exonucleolytic activity of human apurinic/apyrimidinic endonuclease 1 (APE1) on mispaired DNA at the 3(')-termini of recessed, nicked or gapped DNA molecules was analyzed.
- substrate selectivity of mammalian NTH1 and the concomitant selective stimulation of activity by APE1 are indicative of selective repair of oxidative damage in different regions of the genome
- The amino terminal portion of HSP70 stimulates the activity of HAP1.
- Repression of renin expression by intracellular calcium may be mediated by the calcium-induced translocation of Ref-1 to the nucleus, where it binds to the renin promoter nCaRE, to repress the transcription of the renin gene.
- APE1 may exist in two different conformations, and each conformation has a preference for a substrate
- AN34 and Ape1 participate in the process of chromatin fragmentation during apoptosis.
- Ape1 exonuclease has a role during BER after both DNA repair synthesis and excision of the abasic deoxyribose-5-phosphate by polymerase beta
- substrate determinants for the exonuclease activity of human apurinic endonuclease Ape1
- data presented support a model by which X-ray repair cross complementing protein 1 (XRCC1) will pass on the DNA intermediate from DNA glycosylase hOGG1 to the endonuclease APE1
- mutational analysis of the alpha8 loop supports and extends the conclusion of crystallographic studies that the loop is important for binding of AP.DNA and AP site incision
- Ape1 possesses activity as a major 3(')-5(') exonuclease in leukemia U937 cells.
- APE/ref-1 expression is not different in platinum-sensitive and platinum-refractory ovarian cancers
- APE/Ref-1 mediated CD40 activation of PAX5 and EBF.
- APE/Ref-1 expression level and intracellular localization is variable in different types of tumors compared to the corresponding non-malignant human tissue, the protein is thought to be a diagnostic and prognostic tumor marker--REVIEW
- role for APE/Ref-1 protein in the transcriptional regulation of NIS gene expression by itself and in cooperation with PAX8.
- Ape1, the major apurinic/apyrimidinic endonuclease in human cells, is the damage- specific endonuclease involved in nucleotide incision repair
- Hydrogen bonds to phosphate groups downstream of the AP cleavage site are essential for APE1's binding to the product DNA, which may be necessary for efficient functioning of the base excision repair pathway.
- Presented evidence that APE1 also acts on AP sites in single-stranded (ss) DNA.
- While nuclear base excision repair protein levels and activities were generally not altered in rho(0) cells, AP endonuclease activity was substantially reduced in nuclear and in whole cell extracts
- significant correlation between high APE1 expression levels and reduced survival times in osteosarcoma
- APE1 is the main enzyme responsible for removal of 3'-phosphoglycolate in human cell extracts.
- APE/ref-1 plays a significant role in gemcitabine resistance in some pancreatic cancer cells.
- The data show that H. pylori or reactive oxygen species enhance APE-1/Ref-1 protein synthesis and nuclear accumulation in human gastric epithelial cells and implicate APE-1/Ref-1 in the modulation of the pathogenesis of H. pylori infection.
- roles of three conserved tyrosine residues in close proximity to the active site
- Analysis of structural determinants of substrate specificity of human APE1.
- A novel physiological role for APE1/ref-1 in regulating vascular tone by governance of eNOS activity and bioavailable NO.
- Ape1 ssAP and dsAP endonuclease activities are regulated by sequence context and the relative concentrations of certain chemical elements in vivo
- Ref-1 promotes association of dimers into tetramers, and de-stacking of higher oligomeric forms into the tetrameric form in vitro, thereby enhancing p53 binding to target DNA.
- Strong downregulation of Ape1 stopped cell proliferation and activated apoptosis, which was correlated with accumulation of abasic DNA damage.
- Review of APE1/Ref-1's different functions.
- Interplay between APE1, DNA polymerase beta and poly(ADP-ribose) polymerase-1 during base excision repair.
- genetic variants in APEX1 and XRCC1 may alter the risk of lung cancer in a special population in China
- Results indicate that the DNA repair and gene regulation functions of APE1 are essential and provide evidence that mammalian cells require APE for survival, presumably to protect against spontaneous oxidative DNA damage.
- TRR-Trx and APE/Ref-1 cooperate in the control of basal p53 activity, but not in its induction by DNA-damage.
- APE1 is the major activity involved in the repair of 3'-8-oxoguanine lesions in human cells.
- A previously unidentified nuclear export signal may regulate APE1 trafficking.
- APE generates microsatellite instability by inhibiting MSH6 protein expression and DNA mismatch repair activity.
- Meta-analyses found no association between cancer risk and the APE1/APEX1 Asp148Glu and XRCC1 Arg280His polymorphisms.
- Replication protein A selectively suppresses the nontemplated ss cleavage activity of Ape1 in vivo, particularly at sites of ongoing replication/recombination, by coating the ssDNA.
- APE1 removes mismatched nucleotides from 3' terminus of DNA more efficiently than matched pairs. Both efficiency of 3'-5' exonuclease activity of APE1 & thermal stability of DNA duplexes varied depending on nature of flanking group at 5' margin of nick.
- APE-1 plays a critical role in the actions of L-configuration but not D-configuration nucleoside analogs in tumor cells.
- These results suggest that hemin activates the transcription of the ferritin H gene during K562 erythroid differentiation by Ref-1-mediated activation of these b-zip transcription factors to the Antioxidant-responsive Elements.
- Bcl2, in addition to its survival function, may also suppress DNA repair in a novel mechanism involving c-Myc and APE1, which may lead to an accumulation of DNA damage in living cells, genetic instability, and tumorigenesis
- the APE1 Glu variant, but not an ADPRT variant, may have an effect or interact with XRCC1 in the etiology of cutaneous melanoma or in linkage disequilibrium
- ERp57 appears to cooperate with Ref-1 in the regulation of gene expression mediated by redox-sensitive transcription factors and in the adaptive response of the cell to oxidative insul
- protective effects of hepatocyte growth factor against cerebral ischemia-induced cell death in the hippocampal CA1 region are related to the improvement of neuronal apex1
- No significant effect on the risk for lung cancer was seen with the APEX1 polymorphism.
- APE1 specifically recognizes an 8-oxoguanine-DNA glycosylase (OGG1)/DNA complex, distorts a stretch of DNA 5' to the OGG1 molecule, and actively displaces the glycosylase from the lesion.
- AP endo requires a tyrosine at the active site for the properties that enable it to behave as an efficient, processive endonuclease.
- the degradation of APOBEC3G-edited viral DNA mediated by virion-associated UNG2 and APE during or after reverse transcription could be partially responsible for the potent anti-HIV-1 effect by APOBEC3G in the absence of vif
- The positive rate of APE1 protein expression was 65.6% in the bone marrow specimens of patients with multiple myeloma with known clinical outcome.
- APEX1 downregulation correlates with cancer radiosensitization.
- results indicate step-by-step coordination in single-nucleotide base excision repair can rely on DNA binding specificity inherent in APE and Pol beta; coordination also may be facilitated by APE.Pol beta.DNA ternary complex formation
- Nitric oxide induces nuclear export of APE1/Ref-1 in a S-nitrosylation-dependent, and CRM1-independent manner.
- findings show that unconjugated bilirubin modulates a signaling pathway involving APE1/Ref-1, Egr-1, and PTEN
- The subcellular localization of APEX1 in hepatocellular carcinoma was studied for its possible prognostic significance.
- Human APEX transcripts were detected in oocytes, spermatozoa and preimplantation blocked embryos.
- Purified recombinant Cockayne syndrome B protein and the major human apurinic/apyrimidinic endonuclease, APE1, physically and functionally interact.
- These data together uncovers a new signaling pathway regulating APE/Ref-1 nuclear translocation involving CD40-crosslinking, TRAF2 and p38.
- Polymorphisms in DNA repair gene APE/ref-1 may be important in the aetiology of stroke.
- In addition to its AP-endonucleolytic function, APE1 possesses 3' phosphodiesterase, 3'-5' exonuclease and 3' phosphatase activities.[review]
- SNPs associated with prognosis of lung cancer was mapped to APEX1.
- Thai women with a certain XRCC1 diplotype or homozygous for two or three variant alleles of XRCC1, OGG1, and APEX1 are likely to have an increased susceptibility to breast cancer.
- The ATF4-mediated up-regulation of Ape1 and other genes plays a key role against arsenite-mediated toxicity and mutagenesis.
- Expression of VEGF and Ref-1 is associated with Trx-1 overexpression and poor prognosis in patients with liver metastases from colorectal cancer.
- Knockdown of the DNA repair and redox signaling protein Ape1/Ref-1 blocks ovarian cancer cell and tumor growth.
- Low activation energy and the enthalpy of activation, which are perhaps a result of dipole-dipole interactions, play critical roles in abasic site site binding of APE.
- Potent inhibition of apurinic/apyrimidinic endonuclease 1 by arylstibonic acids is reported.
- These results suggest the APE1 variant genotype decreases repair of 8-OHdG and that arsenic exposure is associated with oxidative stress in women who lack a functional GSTM1 detoxification enzyme.
- APE1/ref-1 is up-regulated in the tumor regions of non-small cell lung cancer
- Ape1 cleavage by granzyme K facilitates intracellular reactive oxygen species accumulation and enhances granzyme K-induced cell death.
- Tat-APE1/ref-1 might be useful to reduce vascular endothelial activation or vascular inflammatory disorders
- Wild type p53 is a negative regulator of APE1 expression.
- Bcl2 inhibition of AP site repair may occur in a novel mechanism by down-regulating APE1 endonuclease activity, which may promote genetic instability and tumorigenesis.
- APE1 regulated PTEN expression is mediated by Egr-1.
- Investigation of the properties of multilesion abasic clusters that affect Ape1 cleavage.
- APE1 148 Glu was less frequent in sporadic breast cancer.
- APE1 stimulates DNA synthesis catalyzed by DNA polymerase beta, and a human X-ray repair cross-complementing group 1 protein (XRCC1) stimulates APE1 3 -5 exonuclease activity on 3 -recessed DNA duplex.
- The unexpected involvement of Cys99 in APE1's substrate binding and catalysis provides an example of involvement of a residue far from the active site.
- The results suggest that Ape1 has the ability to incise at apurinic/apyrimidinic sites in DNA conformations formed during DNA replication, transcription, and class switch recombination, and that Ape1 can endonucleolytically destroy damaged RNA.
- APE-1 mRNA and protein expression were determined in H. pylori (CagA+) water-extract protein (HPWEP)-stimulated MKN-28 cells, gastric adenocarcinoma cell-line (AGS) cells, and human peripheral macrophages
- significant association with reduced risk of cervix cancer in APE-1 with different genotypes
- overexpression of the truncated APE1 in mitochondria appears to be a viable approach to protecting healthy cells from some deleterious effects of oxidative stress
- Significant effects of APEX1 148Asp polymorphisms was seen on the initial repair of MMS-induced DNA damage in human lymphocytes.
- Inhibition of the redox function of APE1 blocks murine endothelial cell growth and angiogenesis, and blocks the growth of human tumor cell lines. These effects are independent of the APE1 DNA-repair function.
- polymorphism rs1130409 might be involved in contributing towards breast cancer susceptibility in women of Northern India
- polymorphic variants of the APE1 gene are not independent risk factors for Alzheimer's disease
- the XRCC3 gene TT genotype and the APE1 gene AG genotype might increase the risk of myocardial infarcts
- the nuclear translocation of GAPDH during oxidative stress constitutes a protective mechanism to safeguard the genome by preventing structural inactivation of APE1.
- Association between polymorphisms in DNA base excision repair genes XRCC1, APE1, and ADPRT and differentiated thyroid carcinoma.
- Apurinic/apyrimidinic endonuclease 1 actively stimulates thymine DNA glycosylase by disrupting the product complex
- APE1 downregulation sensitizes MDR1-overexpressing tumor cells to cisplatin or doxorubicin, showing APE1's critical role in YB-1-mediated gene expression and drug resistance in tumor cells.
- the APEX1 Asp148Glu genotype constitutes an increased risk of colorectal cancer when accompanied by smoking exposure.
- inhibitory effect of angiotensin II on BK(Ca) channel function is NADPH oxidase-dependent and may be promoted by APE1/Ref-1
- MiTF regulates cellular response to reactive oxygen species by regulation of APE-1, and this may provide a mechanism of how MiTF is involved in melanoma carcinogenesis
- Gene transfer of redox factor-1 inhibits neointimal formation: involvement of platelet-derived growth factor-beta receptor signaling via the inhibition of the reactive oxygen species-mediated Syk pathway.
- interactions between DNA repair genes hMLH1, APEX1, MGMT, XRCC1 and XPD and electric transformers and power line distances from the houses of childhood acute leukemia patients revealed gene-environment interaction existed with XRCC1 Ex9+16 A allele
- Nitric oxide initiates progression of human melanoma via a feedback loop mediated by apurinic/apyrimidinic endonuclease-1/redox factor-1, which is inhibited by resveratrol
- Data show that E3330, an inhibitor of the Ape-1/Ref-1 redox domain, blocks the in vitro growth of pancreatic cancer-associated endothelial cells (PCECs) and EPCs, which is recapitulated by stable expression of a dominant-negative redox domain mutant.
- The APEX1 E148D SNP showed a significant association with glioma risk.
- The APE1 -656T>G polymorphism has an influence on the APE1 promoter activity and is significantly associated with a reduced risk for lung cancer.
- A novel interaction between nucleophosmin (NPM1) and APE1 was characterized.