PRIMPOL report

I. Expression across cell types

II. Expression across tissues

III. Associated gene sets

GO_0009411Biological processresponse to UV
GO_0031297Biological processreplication fork processing
GO_0019985Biological processtranslesion synthesis
GO_0042276Biological processerror-prone translesion synthesis
GO_0043504Biological processmitochondrial DNA repair
GO_0062176Biological processR-loop processing
GO_0006264Biological processmitochondrial DNA replication
GO_0006269Biological processDNA replication, synthesis of primer
GO_0000428Cellular componentDNA-directed RNA polymerase complex
GO_0005657Cellular componentreplication fork
GO_0005759Cellular componentmitochondrial matrix
GO_0005634Cellular componentnucleus
GO_0030145Molecular functionmanganese ion binding
GO_0003887Molecular functionDNA-directed DNA polymerase activity
GO_0003896Molecular functionDNA primase activity
GO_0005515Molecular functionprotein binding
GO_0008270Molecular functionzinc ion binding
GO_0003682Molecular functionchromatin binding

IV. Literature review

[source]
Gene namePRIMPOL
Protein nameDNA-directed primase/polymerase protein
DNA-directed primase/polymerase protein (hPrimpol1) (EC 2.7.7.-) (Coiled-coil domain-containing protein 111)
SynonymsFLJ33167
hCG_1786938
CCDC111
DescriptionFUNCTION: 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 . .; FUNCTION: 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 . .

AccessionsENST00000503752.5 [Q96LW4-1]
D6R908
ENST00000508001.1
ENST00000515152.1
ENST00000509002.5
ENST00000506278.5
Q96LW4
ENST00000515774.5
ENST00000314970.11 [Q96LW4-1]
H0Y9N8
A0A5S6SZ32
D6R971
ENST00000512834.5 [Q96LW4-2]