Details of Drug Off-Target (DOT)
General Information of Drug Off-Target (DOT) (ID: OT1SL9UN)
DOT Name | Protein mono-ADP-ribosyltransferase PARP3 (PARP3) | ||||
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Synonyms |
EC 2.4.2.-; ADP-ribosyltransferase diphtheria toxin-like 3; ARTD3; DNA ADP-ribosyltransferase PARP3; EC 2.4.2.-; IRT1; NAD(+) ADP-ribosyltransferase 3; ADPRT-3; Poly polymerase 3; PARP-3; hPARP-3; Poly synthase 3; pADPRT-3
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Gene Name | PARP3 | ||||
UniProt ID | |||||
3D Structure | |||||
PDB ID | |||||
EC Number | |||||
Pfam ID | |||||
Sequence |
MAPKPKPWVQTEGPEKKKGRQAGREEDPFRSTAEALKAIPAEKRIIRVDPTCPLSSNPGT
QVYEDYNCTLNQTNIENNNNKFYIIQLLQDSNRFFTCWNRWGRVGEVGQSKINHFTRLED AKKDFEKKFREKTKNNWAERDHFVSHPGKYTLIEVQAEDEAQEAVVKVDRGPVRTVTKRV QPCSLDPATQKLITNIFSKEMFKNTMALMDLDVKKMPLGKLSKQQIARGFEALEALEEAL KGPTDGGQSLEELSSHFYTVIPHNFGHSQPPPINSPELLQAKKDMLLVLADIELAQALQA VSEQEKTVEEVPHPLDRDYQLLKCQLQLLDSGAPEYKVIQTYLEQTGSNHRCPTLQHIWK VNQEGEEDRFQAHSKLGNRKLLWHGTNMAVVAAILTSGLRIMPHSGGRVGKGIYFASENS KSAGYVIGMKCGAHHVGYMFLGEVALGREHHINTDNPSLKSPPPGFDSVIARGHTEPDPT QDTELELDGQQVVVPQGQPVPCPEFSSSTFSQSEYLIYQESQCRLRYLLEVHL |
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Function |
Mono-ADP-ribosyltransferase that mediates mono-ADP-ribosylation of target proteins and plays a key role in the response to DNA damage. Mediates mono-ADP-ribosylation of glutamate, aspartate or lysine residues on target proteins. In contrast to PARP1 and PARP2, it is not able to mediate poly-ADP-ribosylation. Involved in DNA repair by mediating mono-ADP-ribosylation of a limited number of acceptor proteins involved in chromatin architecture and in DNA metabolism, such as histone H2B, XRCC5 and XRCC6. ADP-ribosylation follows DNA damage and appears as an obligatory step in a detection/signaling pathway leading to the reparation of DNA strand breaks. Involved in single-strand break repair by catalyzing mono-ADP-ribosylation of histone H2B on 'Glu-2' (H2BE2ADPr) of nucleosomes containing nicked DNA. Cooperates with the XRCC5-XRCC6 (Ku80-Ku70) heterodimer to limit end-resection thereby promoting accurate NHEJ. Suppresses G-quadruplex (G4) structures in response to DNA damage. Associates with a number of DNA repair factors and is involved in the response to exogenous and endogenous DNA strand breaks. Together with APLF, promotes the retention of the LIG4-XRCC4 complex on chromatin and accelerate DNA ligation during non-homologous end-joining (NHEJ). May link the DNA damage surveillance network to the mitotic fidelity checkpoint. Acts as a negative regulator of immunoglobulin class switch recombination, probably by controlling the level of AICDA /AID on the chromatin. In addition to proteins, also able to ADP-ribosylate DNA: mediates DNA mono-ADP-ribosylation of DNA strand break termini via covalent addition of a single ADP-ribose moiety to a 5'- or 3'-terminal phosphate residues in DNA containing multiple strand breaks.
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Tissue Specificity |
Widely expressed; the highest levels are in the kidney, skeletal muscle, liver, heart and spleen; also detected in pancreas, lung, placenta, brain, leukocytes, colon, small intestine, ovary, testis, prostate and thymus.
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KEGG Pathway | |||||
Molecular Interaction Atlas (MIA) of This DOT
Molecular Interaction Atlas (MIA) | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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7 Drug(s) Affected the Gene/Protein Processing of This DOT
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1 Drug(s) Affected the Post-Translational Modifications of This DOT
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1 Drug(s) Affected the Protein Interaction/Cellular Processes of This DOT
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References