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Validated All-in-One™ qPCR Primer for POLB(NM_002690.2) Search again
Product ID:
HQP013422
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
-
Gene Description:
DNA polymerase beta
Target Gene Accession:
NM_002690.2(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
In eukaryotic cells, DNA polymerase beta (POLB) performs base excision repair (BER) required for DNA maintenance, replication, recombination, and drug resistance. Also see POLA (MIM 312040).[supplied by OMIM].
Gene References into function
- To determine the role of Lys-280, site-directed mutants were constructed at this position, and the proteins were expressed and purified, and their catalytic efficiency and fidelity were assessed
- dL residues may not be readily repaired by "short-patch" base excision repair but instead function as suicide substrates in the formation of protein-DNA cross-links that may require alternative modes of repair.
- lowers replication fidelity and results in a modified error-specificity; occurs during synthesis of the lagging strand
- dynamics of gapped DNA recognition
- Repair of clustered DNA lesions
- polymerase beta simulations suggest that Arg258 rotation is a slow step rather than large subdomain motions per se
- Deregulated DNA polymerase beta induces chromosome instability and tumorigenesis.
- To elucidate the molecular basis of microsatellite mutation, the in vitro error frequencies for DNA polymerase beta have been determined at template sequences representative of those found in the human genome: [GT/CA]10, [TC/AG]11, and [TTCC/AAGG]9.
- readily expands triplet repeats at strand breaks under physiological dNTP and salt concentrations
- analysis of the efficiency of dNTP (correct and incorrect) insertion for a low fidelity mutant of DNA polymerase beta shows that a strong correlation exists between the ability to synthesize DNA and the probability that the polymerase will make a mistake
- Acetylation of Polbeta acts as an intranuclear regulatory mechanism and implies that p300 plays a critical regulatory role in base excision repair
- Data report the first structure of a polymerase, DNA polymerase beta, with a promutagenic lesion in its active site.
- The Werner syndrome protein stimulates this enzyme's strand didsplacement DNA synthesis via its helicase activity
- human RNA polymerase II (RNAP II) pausing and transcript cleavage is controlled by transcription factor IIF, hepatitis delta antigen, and stimulatory factor II
- majority of single-strand DNA interruptions produced during the repair of alkylated DNA bases are repaired by the pathway mediated by Pol beta and either Lig I or Lig III
- To probe molecular interactions in the dNTP-binding pocket, we analyzed the kinetic behavior of wild-type pol beta on modified DNA substrates that alter the structure of the DNA terminus and represent mutagenic intermediates.
- identified a sequence in APC that binds DNA polymerase beta and blocks DNA polymerase beta-mediated strand-displacement synthesis in long patch BER without affecting short patch BER
- pol beta cooperates with FEN1 to remove DNA damage via a "Hit and Run" mechanism, involving alternating short gap production by FEN1 and gap filling by pol beta
- Splice variations of DNA polymerase beta may be caused by aberrant splicing.
- Interplay between APE1, DNA polymerase beta and poly(ADP-ribose) polymerase-1 during base excision repair.
- blockade of pol II-mediated transcription induces p53 accumulation in mitochondria and is the critical factor for eliciting p53-dependent but transcription-independent apoptosis
- DNA polymerase beta variant (pol betadelta208-236) is ubiquitous and not breast cancer specific.
- ectopic expression of TEIF in HeLa cells could upregulate both levels of endogenous beta-pol mRNA and protein, and consequently increases resistance to the oxidative stress of H2O2
- Following incision by AP endonuclease, DNA pol beta recognizes and binds to the incised abasic site and promotes recruitment of the DNA ligase III alpha-X-ray cross-complementing protein 1 (XRCC1) through its interaction with XRCC1.
- cell-free extracts incubated with Ape1-incised 2-deoxyribonolactone substrates under non-repair conditions give rise to DNA-protein cross-links, with a major species dependent on the presence of polbeta
- DNA pol-beta is an essential component of the DNA replication machinery in neuronal cell death in Alzheimer's disease.
- down-regulation of the normal base excision repair gap-filling DNA polymerase, pol beta, accompanies induced somatic hypermutation
- Both pol-beta and Fen-1 interact with a 138-amino-acid peptide from adenomatosis polyposis coli protein at the DNA repair inhibitory domain.
- use dGTP analogues replacing the beta,gamma-bridging O with CH2, CHF, CF2, or CCl2 to explore leaving-group effects on the nucleotidyl transfer mechanism and fidelity of DNA polymerase (pol) beta
- The correlation coefficients show that the strength of the H-bond between dCTP and Asn279 is a strong predictor of the mutation-induced changes in the catalytic efficiency of pol beta.
- The erroneous nucleotide incorporations catalyzed by DNA polymerases lambda and beta as well as the subsequent ligation catalyzed by a DNA ligase during base excision repair are a threat to genomic integrity.
- 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
- The E295K gastric carcinoma pol beta variant acts in a dominant-negative manner by interfering with base excision repair.
- The Leu22Pro DNA polymerase beta variant has very little dRP lyase activity but retains its polymerase activity.
- The fidelity of DNA polymerase beta was studied by analysing the chemical transition state of its catalytic site using analogues of dGTP.
- Data show that CHIP-mediated degradation and DNA damage-dependent stabilization regulate base excision repair proteins XRCC1, DNA polymerase beta, and DNA ligase III.
- Data report the crystallographic structures of DNA polymerase beta with dG-dAMPCPP and dC-dAMPCPP mismatches in the active site.
- the mispaired primer terminus affects the geometry of the dNTP binding pocket such that the I260Q variant has a higher affinity for the incoming dNTP than wild-type polymerase beta.
- replication protein A and proliferating cell nuclear antigen act as molecular switches to activate the DNA pol lambda- dependent highly efficient and faithful repair of A:8-oxo-G mismatches in human cells and to repress DNA pol beta activity.
- dATP was a preferential substrate for DNA polymerase beta and dGMP was the only substrate for DNA polymerase lambda.