Target intelligence / Profile preview

Poly(ADP-ribose) polymerase family member 10 (PARP10)

Target
PARP10
Molecular classification
Enzyme, Transferase, ADP-ribosyltransferase
01

Overview

Poly(ADP-ribose) polymerase family member 10 (PARP10) is a human enzyme encoded by the PARP10 (ARTD10) gene and is part of the poly(ADP-ribose) polymerase family, a group of enzymes involved in DNA repair, genomic stability, and the regulation of chromatin structure and gene transcription[3][7]. Specifically, PARP10 functions as a mono-ADP-ribosyltransferase, mediating the transfer of a single ADP-ribose moiety to target proteins such as histones, thereby modulating transcriptional activity and chromatin organization[9]. While clinical therapeutics have focused on other PARPs (such as PARP1/2) in cancer, PARP10 is increasingly studied for its role in gene regulation and potential oncogenic pathways[4][7]. Several PARP inhibitors (e.g., veliparib, 3-aminobenzamide) have been used in structural and functional studies of PARP10, but selective inhibition and disease-specific targeting of PARP10 remains under investigation[4].

Other names
Poly [ADP-ribose] polymerase 10Mono-ADP-ribosyltransferase PARP10ADP-ribosyltransferase diphtheria toxin-like 10ARTD10
02

Mechanism of action

Inhibition of enzyme catalytic activity (by small molecule PARP inhibitors)[4]

03

Biological functions

Regulation of gene transcriptionChromatin modificationMono-ADP-ribosylation of proteinsEpigenetic regulationCell signaling
04

Disease associations

CancerOther (potential, as broad PARP function implicated in inflammation, genomic instability, and cell death)
05

Safety considerations

As with other PARP inhibitors, potential risks include bone marrow suppression, genotoxicity, and off-target effects due to broad roles in DNA repair, but specific safety data for PARP10-targeted inhibition is not well defined[4]
06

Interacting drugs

3-aminobenzamide (research tool)[2]

2 more in the full profile.

07

Biomarkers

Currently, specific biomarkers for PARP10-directed therapies are not established; PARP1/2 biomarkers or response indicators in DNA-damage pathways may overlap, but no direct evidence for PARP10-driven biomarkers[3][6][9]

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