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Poly (ADP-ribose) polymerase 10 (PARP10)
- Target
- PARP10
- Molecular classification
- Enzyme, Mono-ADP-ribosyltransferase (not “polymerase”—distinct from canonical PARPs in activity), Poly (ADP-ribose) polymerase family
01
Overview
Poly (ADP-ribose) polymerase 10 is a unique member of the PARP family distinguished by its mono-ADP-ribosyltransferase activity—it transfers single ADP-ribose units to target proteins, unlike canonical PARPs, which form polymers. PARP10 regulates gene transcription through chromatin modification, interacts directly with proliferating cell nuclear antigen (PCNA) to maintain genome stability, and alleviates replication stress[1][3][5]. It modulates key cellular pathways—especially in DNA damage repair, cell cycle control, apoptosis, and cancer biology. Despite tumor-suppressive functions (e.g., through inhibition of Aurora A kinase and regulation of epithelial-mesenchymal transition), PARP10 overexpression is linked to increased cellular proliferation and tumorigenesis, making it a candidate therapeutic target in oncology[1][4][5]. Selective inhibition is a current research focus, though most clinical PARP inhibitors are not highly specific for PARP10[6].
- Other names
- ARTD10PAR10_HUMAN (Uniprot entry)ADP-ribosyltransferase diphtheria toxin-like 10
02
Mechanism of action
Drugs such as veliparib inhibit the ADP-ribosyltransferase activity, potentially modulating DNA repair, cell cycle progression, and apoptosis[6].
03
Biological functions
DNA damage response and repairMaintenance of genome integrityCell cycle regulation (especially G1/S transition)ApoptosisRegulation of NF-κB signalingCell proliferationReplication stress relief and fork restartMitochondrial function
04
Disease associations
Cancer (promotes oncogenic transformation and proliferation when overexpressed; also has tumor-suppressive aspects)InflammationPotential roles in metabolic and neurodegenerative disorders (early evidence)
05
Safety considerations
Targeting PARP10 might affect genome stability and DNA repair; off-target inhibition could impair normal cell functions.Potential toxicity due to disruption of replication fork restart and DNA repair in normal tissues.Therapeutic challenges include achieving selectivity between PARP family members, as most drugs target multiple family enzymes.
06
Interacting drugs
Veliparib (PARP inhibitor)
2 more in the full profile.
07
Biomarkers
PARP10 expression levels (overexpression is found in various human tumors and may indicate replication stress or tumorigenic potential)Phosphorylation status during G1/S transition (potential biomarker for cell cycle regulation)
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