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anti-Human POLB Antibodies:
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Human Polyclonal POLB Primary Antibody for IHC - ABIN966877
Patterson, Little, Cheng, Widen, Kumar, Beard, Wilson: Molecular cloning and high-level expression of human polymerase beta cDNA and comparison of the purified recombinant human and rat enzymes. in Protein expression and purification 2000
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Human Polyclonal POLB Primary Antibody for IHC - ABIN966876
Dobashi, Kubota, Shuin, Torigoe, Yao, Hosaka: Polymorphisms in the human DNA polymerase beta gene. in Human genetics 1995
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Human Polyclonal POLB Primary Antibody for IHC - ABIN966879
Chyan, Ackerman, Shepherd, McBride, Widen, Wilson, Wood: The human DNA polymerase beta gene structure. Evidence of alternative splicing in gene expression. in Nucleic acids research 1994
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Human Polyclonal POLB Primary Antibody for IHC - ABIN966878
Widen, Kedar, Wilson: Human beta-polymerase gene. Structure of the 5'-flanking region and active promoter. in The Journal of biological chemistry 1988
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Human Monoclonal POLB Primary Antibody for IHC (fro), IHC (p) - ABIN153074
Fotiadou, Henegariu, Sweasy: DNA polymerase beta interacts with TRF2 and induces telomere dysfunction in a murine mammary cell line. in Cancer research 2004
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Mouse (Murine) Polyclonal POLB Primary Antibody for IHC, WB - ABIN3022385
Xu, Zhang, Zhang, Meng, Zhang, Jiang, Xu, Van Meter, Seluanov, Gorbunova, Mao: SIRT6 rescues the age related decline in base excision repair in a PARP1-dependent manner. in Cell cycle (Georgetown, Tex.) 2015
DNA polymerase beta is sensitive to Mn2+ and Mg2+ and its optimumal pH is 9.
In brief, the major differences in BER performed by early stage embryos and adults are the absence of DNA polymerase-beta, leading to predominance of replicative polymerases, in early stage embryos.
our study therefore identified a pathway in which DNA damage-induced poly(ADP-ribosyl)ation (PARylation) promotes SUMOylation of XRCC1, which leads to more efficient recruitment of POLB to complete base excision repair
These findings strongly suggest that DNA polymerase beta is causative in senescence induction, reasonably pointing to DNA polymerase beta as a likely factor driving the premature senescence in Down syndrome.
point mutation (C-->G) in position 725 in exon 12, which shifts proline to arginine (P242R).This is a newly reported somatic mutation of pol beta in ovarian carcinoma patients from India
Presently, we describe the preparation of three Pol beta enzymes modified at position 72 with aminooxy or hydrazinyl analogues of lysine. These enzymes form transient covalent bonds with the 5'-dRP moiety of the damaged DNA, in the form of an oxime or hydrazone, respectively
MSH2-MSH3 not only stimulates pol beta to copy through the repeats but also enhances formation of the flap precursor for expansion.
Bond formation and cleavage reactions catalyzed by base excision repair DNA polymerases beta and lambda has been described.
POLB, is located in the mitochondria and plays a significant role in mitochondrial BER, mtDNA integrity and mitochondrial function. [REVIEW]
In the mitochondrial extracts from APTX-/- cells, the strong pol beta lyase and FEN1 activities appear able to repair the blocked BER intermediates with 5'-AMP-dRP groups.Neither pol gamma lyase nor FEN1 alone is able to complement APTX deficiency in the absence of pol beta.
human polymerase beta, accommodates 8-oxoG at the primer terminus opposite cytosine and adenine.
POLB functions in base excision repair to fill in single-nucleotide gaps and exhibits mutation E288K associated with colon cancer. Data suggest that E288K mutant POLB exhibits faster rate of closing of fingers domain combined with slower rate of nucleotide release compared to wild-type POLB; loss of fidelity appears due to defect in interaction of E288K mutant POLB with DNA, resulting in stable, closed enzyme structure.
Unencumbered polymerase beta lyase activity in nucleosome core particles during base excision repair has been reported.
pol beta and BRCA1 appeared to have a functional interaction, observed in both DT40 and human cell lines, in protecting cells against alkylating MMS-induced cytotoxicity; but pol beta had no protective effect in the absence of BRCA1. In vivo and in vitro assays for a base excision repair role of BRCA1 were negative.
hPolbeta discriminates against L-stereochemistry through accumulation of several active site rearrangements that lead to a decreased nucleotide binding affinity and incorporation rate. The two NRTIs escape some of the active site selection through the base and sugar modifications but are selected against through the inability of hPolbeta to complete thumb domain closure.
pol beta contains a specific NLS sequence in the N-terminal lyase domain that promotes transport of the protein independent of its interaction partners. Active nuclear uptake allows development of a nuclear/cytosolic concentration gradient against a background of passive diffusion.
Data suggest that POLB activity is not essential for HIV-1 integration into human macrophages and other cells; limited cellular dNTP pools, but not POLB expression, are primary factor for HIV-1 DNA gap repair, particularly in non-dividing cells.
High DNA polymerase beta mRNA expression is associated with Graves' thyroid tissue.
Polbeta was shown to inhibit the 3'->5' exonuclease activity of APE1 when both enzymes were added simultaneously and to insert the correct nucleotide into the gap arising after hydrolysis of AP site clustered with the benzo[a]pyrene adducts.
Remote mutations induce functional changes in active site residues of human DNA polymerase beta.
It has been concluded based on calculations and the experimental pH profile that the most likely path for the wild-type (WT) and the D256E and D256A mutants is a proton transfer (PT) to the bulk, although the WT may also use a PT to Asp 256.
The homozygous/heterozygous genotypes containing the African allele showed higher POLB expression than the homozygous white allele genotype (P < .001). A replication study using a GEO data set validated all 5 eQTLs and also showed a statistically significant difference in POLB expression based on genetic ancestry (P = .002).
To evaluate whether Polb might be causative in senescence induction, the study evaluated the impact of murine Polb nullizygosity on senescence. Unexposed DNA polymerase beta-null primary fibroblasts exhibit a robust increase in the number of senescent cells compared to wild-type (11-fold, P < 0.001), demonstrating that loss DNA polymerase betais sufficient to induce senescence.
Mitochondria from pol beta-deficient mouse fibroblasts had compromised DNA repair and showed elevated levels of superoxide radicals after hydrogen peroxide treatment. Mitochondria in pol beta-deficient fibroblasts displayed altered morphology by electron microscopy.
Analyses of DNA damage and apoptosis revealed significantly greater degeneration of olfactory bulb neurons in transgenic Alzheimer's (3xTgAD)/Polbeta(+/-) mice compared to 3xTgAD mice.
pol beta plays an important role in bypassing a 5',8-cyclo-dA during DNA replication and repair.
we show here that heterozygosity for a Y265C mutation in Polbeta, a key polymerase in the BER pathway, is enough to significantly reduce both the number of expansions seen in paternal gametes and the extent of somatic expansion in some tissues
The aberrant DNA replication mediated by the PCNA-DNA pol-b complex induces p53-dependent neuronal cell death
Y265C POLB mutation leads to several pathologies associated with SLE and short CDR3 regions during VDJ recombination in B cells.
Pol beta deficiency could enable ROS accumulation.
Results show that deficiency of either DNA polymerases beta or lambda or both results in a modest but significant decrease in V region somatic hypermutation (SHM) with no effect on mutation specificity, suggesting no direct role in SHM.
Transient OGG1, APE1, PARP1 and Polbeta expression in an Alzheimer's disease mouse model.
Data indicate an association of ovarian stimulation with a downregulation of mRNAs encoding the base excision repair proteins APEX1 and POLB as well as the 5-methyl-CpG-binding domain protein MBD3 in individual morula embryos.
Overexpression of Pol beta could reduce oxidative damage and protect cells from hydroquinone genotoxicity.
Polbeta could play a role in protecting cell lines from genotoxicity and genetic instability induced by benzo(a)pyrene.
Polbeta could protect cells from apoptosis induced by hydroquinone through decrease of ROS level and depolarization of mitochondria.
SAF-A interacts with BRG1 and both components are required for RNA Polymerase II Mediated Transcription
data clearly demonstrate that the DNA polymerase activity of pol beta is essential for survival and genome stability
Key residues for the rat DNA polymerase beta conformational transition was studied using elastic network model.
Pol beta is critical for genome stability in the germline
both pol lambda and pol beta interact with the upstream DNA glycosylases for repair of alkylated and oxidized DNA bases
The protein encoded by this gene is a DNA polymerase involved in base excision and repair, also called gap-filling DNA synthesis. The encoded protein, acting as a monomer, is normally found in the cytoplasm, but it translocates to the nucleus upon DNA damage. Several transcript variants of this gene exist, but the full-length nature of only one has been described to date.
DNA-directed DNA polymerase beta
, DNA polymerase beta
, polymerase (DNA directed), beta
, DNA polymerase beta-like
, DNA pol beta
, DNA polymerase beta subunit
, mutant DNA polymerase beta
, Pol beta