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Last update 08 May 2025

PARP6

Last update 08 May 2025

Basic Info

Synonyms

ADP-ribosyltransferase diphtheria toxin-like 17, ARTD17, PARP-6

+ [5]

Introduction

Mono-ADP-ribosyltransferase that mediates mono-ADP-ribosylation of target proteins.

Drugs associated with PARP6

EV-400

Target

PARP6 x SIRT1

Mechanism

PARP6 stimulators [+1]

Active Org.

Evrys Bio LLC

Originator Org.

Evrys Bio LLC

Active Indication

Influenza, Human

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AZ0108

Target

PARP1 x PARP2 x PARP6

Mechanism

PARP1 inhibitors [+2]

Active Org.-

Originator Org.-

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

AZ9482

Target

PARP1 x PARP2 x PARP6

Mechanism

PARP1 inhibitors [+2]

Active Org.-

Originator Org.

AstraZeneca PLC

Active Indication-

Inactive Indication

Breast Cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with PARP6

100 Translational Medicine associated with PARP6

0 Patents (Medical) associated with PARP6

Literatures (Medical) associated with PARP6

01 May 2024·Journal of Assisted Reproduction and Genetics

The chromosomal characteristics of spontaneous abortion and its potential associated copy number variants and genes

Article

Author: Wu, Jianli ; Feng, Ling ; Sha, Menghan ; Chen, Suhua ; Sun, Yanan ; Touch, Koksear ; Qin, Yu ; Xiao, Juan ; Zhang, Shunran ; Wu, Yuanyuan

PURPOSEThis study aimed to investigate the correlation between chromosomal abnormalities in spontaneous abortion with clinical features and seek copy number variations (CNVs) and genes that might be connected to spontaneous abortion.METHODSOver 7 years, we used CNV-seq and STR analysis to study POCs, comparing chromosomal abnormalities with clinical features and identifying critical CNVs and genes associated with spontaneous abortion.RESULTSTotal chromosomal variants in the POCs were identified in 66.8% (2169/3247) of all cases, which included 45.2% (1467/3247) numerical abnormalities and 21.6% (702/3247) copy number variants (CNVs). Chromosome number abnormalities, especially aneuploidy abnormalities, were more pronounced in the group of mothers aged ≥ 35 years, the early miscarriage group, and the chorionic villi group. We further analyzed 212 pathogenic and likely pathogenic CNVs in 146 POCs as well as identified 8 statistically significant SORs through comparison with both a healthy population and a group of non-spontaneously aborted fetuses. Our analysis suggests that these CNVs may play a crucial role in spontaneous abortion. Furthermore, by utilizing the RVIS score and MGI database, we identified 86 genes associated with spontaneous abortion, with particular emphasis on PARP6, ISLR, ULK3, FGFRL1, TBC1D14, SCRIB, and PLEC.CONCLUSIONWe found variability in chromosomal abnormalities across clinical features, identifying eight crucial copy number variations (CNVs) and multiple key genes that may be linked to spontaneous abortion. This research enhances the comprehension of genetic factors contributing to spontaneous abortion.

01 Apr 2024·Biochemical Genetics

Ferroptosis and Preeclampsia: Genetic Analysis of Potential Biomarkers and Therapeutic Targets

Article

Author: Wang, Baimiao ; Wang, Qingmin ; Xiong, Zhihui ; Wang, Wei ; Zheng, Huiling

Ferroptosis is the oxidative death of cells attributed to an imbalance in intracellular lipid reactive oxygen species metabolism, a reduction in cell antioxidant capacity, and an accumulation of membrane lipid peroxides. Trophoblast cells are a group of cells susceptible to ferroptosis. The ferroptosis of trophoblast cells has a major effect on the development of preeclampsia (PE), although the impact of ferroptosis-related genes (FRGs) on PE has not been well characterized. This study obtained PE-related information from the Gene Expression Omnibus database and FRGs from the FerrDb ferroptosis database. Seventeen PE-related differentially expressed ferroptosis-related genes (DE-FRGs) that were closely associated with cellular regulation and immune response were obtained. According to the results of a subsequent functional enrichment analysis, it was found that the above marker genes may impact PE by regulating immune response, amino acid metabolism, the cell cycle, and multiple pathways correlated with PE pathogenesis. Subsequently, we used LASSO and support vector machine recursive feature elimination algorithms to help identify GOT1, CFL1, FZD7, VDR, PARP6, TMSB4X, VCP, and ENO3 as marker genes from the 17 obtained genes. According to the results of single-sample gene set enrichment analysis (ssGSEA), the immune microenvironment of PE changed, possibly due to the GOT1 and TMSB4X genes. Furthermore, 23 drugs targeting one marker gene were determined. A constructed ceRNA network revealed a complicated regulatory link based on the eight marker genes. In this study, diagnostic potency was developed, and insight into the mechanism of PE was provided. In-depth research should be conducted before clinical application to evaluate the diagnostic value of DE-FRGs in PE.

01 Oct 2022·Clinical and Translational Medicine

Comprehensive methylome sequencing reveals prognostic epigenetic biomarkers for prostate cancer mortality

Article

Author: Daly, Roger J. ; Stricker, Phillip ; Kench, James G. ; Pidsley, Ruth ; Korbie, Darren ; Stirzaker, Clare ; Horvath, Lisa G. ; Lam, Dilys ; Qu, Wenjia ; Clark, Susan J. ; Peters, Timothy J. ; Luu, Phuc‐Loi

AbstractBackgroundProstate cancer is a clinically heterogeneous disease with a subset of patients rapidly progressing to lethal‐metastatic prostate cancer. Current clinicopathological measures are imperfect predictors of disease progression. Epigenetic changes are amongst the earliest molecular changes in tumourigenesis. To find new prognostic biomarkers to enable earlier intervention and improved outcomes, we performed methylome sequencing of DNA from patients with localised prostate cancer and long‐term clinical follow‐up.MethodsWe used whole‐genome bisulphite sequencing (WGBS) to comprehensively map and compare DNA methylation of radical prostatectomy tissue between patients with lethal disease (n = 7) and non‐lethal (n = 8) disease (median follow‐up 19.5 years). Validation of differentially methylated regions (DMRs) was performed in an independent cohort (n = 185, median follow‐up 15 years) using targeted multiplex bisulphite sequencing of candidate regions. Survival was assessed via univariable and multivariable analyses including clinicopathological measures (log‐rank and Cox regression models).ResultsWGBS data analysis identified cancer‐specific methylation patterns including CpG island hypermethylation, and hypomethylation of repetitive elements, with increasing disease risk. We identified 1420 DMRs associated with prostate cancer‐specific mortality (PCSM), which showed enrichment for gene sets downregulated in prostate cancer and de novo methylated in cancer. Through comparison with public prostate cancer datasets, we refined the DMRs to develop an 18‐gene prognostic panel. Applying this panel to an independent cohort, we found significant associations between PCSM and hypermethylation at EPHB3, PARP6, TBX1, MARCH6 and a regulatory element within CACNA2D4. Strikingly in a multivariable model, inclusion of CACNA2D4 methylation was a better predictor of PCSM versus grade alone (Harrell's C‐index: 0.779 vs. 0.684).ConclusionsOur study provides detailed methylome maps of non‐lethal and lethal prostate cancer and identifies novel genic regions that distinguish these patient groups. Inclusion of our DNA methylation biomarkers with existing clinicopathological measures improves prognostic models of prostate cancer mortality, and holds promise for clinical application.

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PARP6

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