BD-PN7563

CCDC111/PRIMPOL Rabbit Polyclonal Antibody

常规抗体

CCDC111

Coiled-coil domain-containing protein 111

WB

Human,Mouse

1 mg/ml

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% New type preservative N.

201973

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=201973

Q96LW4

https://www.uniprot.org/uniprot/Q96LW4

408022

http://www.ncbi.nlm.nih.gov/sites/entrez?db=gene&term=408022

Q6P1E7

https://www.uniprot.org/uniprotkb/Q6P1E7/entry

This antibody detects endogenous levels of CCDC111/PRIMPOL at Human, Mouse

WB 1:500-2000

62kD

-15°C to -25°C/1 year(Do not lower than -25°C)

Nucleus . Mitochondrion matrix . Chromosome . Present in the nucleus, but a larger fraction is localized inside mitochondria (PubMed:24207056). Associates with nuclear chromatin during the G1 and S phases of unperturbed cell cycles (PubMed:24207056). Recruited to stalled replication forks following interaction with RPA1 (PubMed:28534480). .

DNA primase and DNA polymerase required to tolerate replication-stalling lesions by bypassing them . Required to facilitate mitochondrial and nuclear replication fork progression by initiating de novo DNA synthesis using dNTPs and acting as an error-prone DNA polymerase able to bypass certain DNA lesions . Shows a high capacity to tolerate DNA damage lesions such as 8oxoG and abasic sites in DNA . Provides different translesion synthesis alternatives when DNA replication is stalled: able to synthesize DNA primers downstream of lesions, such as ultraviolet (UV) lesions, R-loops and G-quadruplexes, to allow DNA replication to continue . Can also realign primers ahead of 'unreadable lesions' such as abasic sites and 6-4 photoproduct (6-4 pyrimidine-pyrimidinone), thereby skipping the lesion . Also able to incorporate nucleotides opposite DNA lesions such as 8oxoG, like a regular translesion synthesis DNA polymerase . Also required for reinitiating stalled forks after UV damage during nuclear DNA replication . Required for mitochondrial DNA (mtDNA) synthesis and replication, by reinitiating synthesis after UV damage or in the presence of chain-terminating nucleotides . Prevents APOBEC family-mediated DNA mutagenesis by repriming downstream of abasic site to prohibit error-prone translesion synthesis (By similarity). Has non-overlapping function with POLH . In addition to its role in DNA damage response, also required to maintain efficient nuclear and mitochondrial DNA replication in unperturbed cells . ; Involved in adaptive response to cisplatin, a chemotherapeutic that causes reversal of replication forks, in cancer cells: reinitiates DNA synthesis past DNA lesions in BRCA1-deficient cancer cells treated with cisplatin via its de novo priming activity . Repriming rescues fork degradation while leading to accumulation of internal ssDNA gaps behind the forks . ATR regulates adaptive response to cisplatin .

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