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Human Polyclonal POLH Primary Antibody for WB - ABIN1882183
Glick, Vigna, Loeb: Mutations in human DNA polymerase eta motif II alter bypass of DNA lesions. in The EMBO journal 2001
Show all 5 Pubmed References
Human Polyclonal POLH Primary Antibody for IP, WB - ABIN253042
Day, Palle, Barkley, Kakusho, Zou, Tateishi, Verreault, Masai, Vaziri: Phosphorylated Rad18 directs DNA polymerase η to sites of stalled replication. in The Journal of cell biology 2010
Show all 2 Pubmed References
Error-free insertion in cyclobutane pyrimidine bypass is due mainly to pol eta (translesion synthesis TLS3) in oocyte extracts during DNA replication.
POLH & POLK (show PAPD7 Antibodies) are both able to exchange with PolD1 (show POLD1 Antibodies) stalled at repetitive CFS (common fragile sites) sequences. POLD1 (show POLD1 Antibodies) synthesis was inhibited by replication stress caused by aphidicolin, preventing any replication past CFS. Importantly, POLH & POLK (show PAPD7 Antibodies) were still proficient in rescuing this stalled POLD1 (show POLD1 Antibodies) synthesis. POLD1 (show POLD1 Antibodies) stalling at CFSs allows for free exchange with specialized polymerase that is not driven by PCNA (show PCNA Antibodies).
Two novel mutations in the POLH gene, which encodes the translesion DNA polymerase eta, with loss of function due to two independent exon skippings, are reported to be associated as a compound heterozygous state in the patient.
Data suggest that DNA polymerase eta (POLH/RAD30) is able to bind DNA/DNA, RNA/DNA, and DNA/RNA duplexes with similar affinities; DNA polymerase eta (as well as DNA polymerase kappa (show PAPD7 Antibodies)) accommodates RNA as one of the two strands during primer extension; both polymerases elongate RNA/DNA and DNA/RNA hybrids; additionally, DNA polymerase eta catalyzes reverse transcription.
POLH is phosphorylated by CDK2 (show CDK2 Antibodies).POLH serine 687 is a CDK (show CDK4 Antibodies) target and is regulated during the cell cycle.POLH phosphorylation controls protein stability.
The current work explores both the fidelity of DNA polymerase eta and the role of the 3rd metal ion (magnesium), by using empirical valence bond simulations.
The results suggest that translesion synthesis by Pol eta can contribute to the accumulation of rCMP in the genome, particularly opposite modified guanines.
the targeting of Poleta to damage sites after UV exposure is regulated by SPARTAN, and this function contributes highly to its DNA-damage tolerance function.
Study shows that the posttranslational modifications of nuclear localization signal of pol eta played a dual role in polymerase switching, where Lys682 deubiquitination promotes the recruitment of pol eta to PCNA (show PCNA Antibodies) immediately prior to lesion bypass and Ser687 phosphorylation stimulates its departure from the replication fork immediately after lesion bypass.
The data directly show that, in the human genome, DNA Pol-eta and Rev1 bypass cyclobutane pyrimidine dimers and 6-4PP at replication forks, while only 6-4PP are also tolerated by a Rev3L-dependent gap-filling mechanism, independent of S phase.
p53 (show TP53 Antibodies) controls the induction of DNA polymerase eta in DNA damaged human cells. The role of DNA polymerase eta in p53 (show TP53 Antibodies)-dependent translesion synthesis.
the functions of REV3L in maintaining cell viability, embryonic viability and genomic stability are directly dependent on its polymerase activity, and cannot be ameliorated by an additional deletion of pol eta.
XP-V has a role in adipose tissue senescence and metabolic syndrome
Increase in UV-induced mutations at both G:C and A:T pairs associated with PolH deficiency suggests that PolH contributes to accurate translesion synthesis (TLS (show FUS Antibodies)) past both T- & C-containing dimers.
POLH deficiency did not affect the frequency and patterns of C:G mutations and UNG (show UNG Antibodies) POLH double deficiency showed an additive effect of single deficiency.
REV1 and Polkappa are involved in DNA damage tolerance via Poleta-REV1 interaction when Poleta fails to bypass its cognate substrates.
These results reveal genetic interactions between REV1 catalytic activity and POLH and identify an alternative pathway in the generation of C to G and G to C transversions.
these data support the existence of PCNA (show PCNA Antibodies) ubiquitination-dependent and -independent activation pathways of Poleta during somatic hypermutation and DNA damage tolerance.
inaccurate DNA synthesis by mammalian DNA polymerase eta (pol eta) contributes to somatic hypermutation (SHM (show CNTNAP1 Antibodies)) of Ig genes
suggest the involvement of the Pol eta and Pol iota (show POLI Antibodies) proteins in UV-induced skin carcinogenesis
Results reveal genetic and biochemical interactions between DNA polymerases eta (POLH) and theta (POLQ (show POLQ Antibodies)) and suggest that POLQ (show POLQ Antibodies) might cooperate with POLH to generate some of the A/T mutations during the somatic hypermutation of Ig genes.
This gene encodes a member of the Y family of specialized DNA polymerases. It copies undamaged DNA with a lower fidelity than other DNA-directed polymerases. However, it accurately replicates UV-damaged DNA\; when thymine dimers are present, this polymerase inserts the complementary nucleotides in the newly synthesized DNA, thereby bypassing the lesion and suppressing the mutagenic effect of UV-induced DNA damage. This polymerase is thought to be involved in hypermutation during immunoglobulin class switch recombination. Mutations in this gene result in XPV, a variant type of xeroderma pigmentosum.
DNA-directed DNA polymerase eta
, DNA polymerase eta
, polymerase (DNA directed), eta
, DNA polymerase eta-like
, polymerase eta
, RAD30 homolog A
, xeroderma pigmentosum variant type protein
, polymerase (DNA directed), eta (RAD 30 related)
, xeroderma pigmentosum variant type protein homolog