CCDC111/PRIMPOL Mouse mAb

Human,Mouse,Rat

WB

单克隆抗体

CCDC111

Coiled-coil domain-containing protein 111

62kD

Synthesized peptide derived from human CCDC111/PRIMPOL. AA range:264-334

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

Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.

Monoclonal,Mouse,IgG

WB 1:500-2000

The antibody was affinity-purified from mouse antiserum by affinity-chromatography using epitope-specific immunogen.

1 mg/ml

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

CCDC111;Coiled-coil domain-containing protein 111

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 .