Ask about this productRelated genes to: PARP10 antibody
- Gene:
- PARP10 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 10
- Previous symbol:
- -
- Synonyms:
- FLJ14464
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-08-25
- Date modifiied:
- 2018-07-03
Related products to: PARP10 antibody
Related articles to: PARP10 antibody
- ADP-ribosylation is a conserved modification that uses NAD+ as a co-substrate to regulate essential cellular processes, such as genome stability and transcription, with Poly(ADP-ribose) Polymerases (PARPs) serving as the major catalyzing enzymes in humans. Historically defined as a protein post-translational modification, ADP-ribosylation on nucleic acids has been increasingly recognized in recent years, particularly in bacterial systems, but remains poorly understood in higher organisms. Here, we identify human PARP10 as a candidate enzyme that ADP-ribosylates nucleic acid bases, showing apparent activity on uracil bases in RNA, and a relatively weaker activity toward thymine bases in DNA. Furthermore, we show that human TARG1, a neurodegenerative disorder-linked protein previously reported to hydrolyse thymine base ADP-ribosylation, also efficiently reverses uracil base ADP-ribosylation (U-ADPr). To improve the efficient characterization of the enzymes for U-ADPr reversal, we developed chemical probes. Using these probes, we demonstrated that human TARG1 and TARG1-like macrodomain proteins are the efficient hydrolases for U-ADPr reversal in humans, Drosophila melanogaster, and bacterial homologues. The widespread distribution of U-ADPr hydrolases among different organisms suggests the potential evolutionary conservation of U-ADPr as a biological signal. - Source: PubMed
Lu YangTang LiStrømland ØyvindChatrin ChatrinZhu KangMunnur DeekshaGroslambert JoséphineMikolčević PetraSchüler HerwigTiminszky GyulaGabant GuillaumeSuskiewicz Marcin JMikoč AndrejaAucagne VincentAhel DraganaLiu QiangAhel Ivan - Zika virus (ZIKV) infection is a major health concern, particularly during pregnancy, as it can lead to neurodevelopmental delays and congenital brain abnormalities, including microcephaly. Here, we investigated the mechanisms of NAD depletion in the brains of ZIKV-infected neonatal mice, a model that developmentally corresponds to third-trimester infection in humans. We observed a progressive decline in NAD levels, which became significant at later stages of infection (18-30 dpi). This decrease did not correlate with viral replication and early or induction, which increased alongside expression, possibly as a compensatory response to NAD consumption. Instead, NAD depletion coincided with increased CD38 expression and activity, while CD38 inhibition prevented NAD loss. Late-stage NAD depletion was preceded by an induction of inflammatory markers (, , and ) and coincided with the infiltration of CD38 immune cells - especially lymphocytes - into the brain, suggesting a link between neuroinflammation and NAD metabolism dysregulation. - Source: PubMed
Publication date: 2025/11/12
Saraiva Georgia NSousa Bruna GSouza Nicole M SVitorino Louise Cda Silva Raquel CBacelar Thiago SAtella Matheus OFernandes-Siqueira Lorena OSouza Isis Nem de OliveiraChini Eduardo NunesCamacho-Pereira JulianaPassos Giselle FDa Poian Andrea TZeidler Julianna D - The role of epigenetic regulation of RNAs in the tumorigenesis remains incompletely understood. This study uncovers a critical function of the 5-methylcytosine (mC) RNA modification reader protein ALYREF (also termed, ALY; BEF) in ovarian cancer. ALYREF is elevated in ovarian cancer patient samples, and its depletion reduces ovarian tumorigenesis and metastasis in mice in a mC-dependent manner. Mechanistically, ALYREF binds to the mC-modified mRNA of ADP-ribosyltransferase PARP10, competing with exosome complex component MTR4, and enhancing the stability and nuclear export of PARP10 mRNA. Further, ALYREF forms condensates in the nucleus of ovarian cancer cells, and depletion or mutation of ALYREF's intrinsically disordered regions rescues its control on PARP10 mRNA nucleoplasmic distribution and stability, reduces tumor growth and is required for promotion of ovarian cancer aggressiveness and proliferation. Finally, ALYREF and PARP10 expression correlate with poor prognosis in ovarian cancer patients. Together, these findings suggest that ALYREF phase separation facilitates the malignant progression of ovarian cancer by promoting PARP10 expression and thereby enhancing PARP10-dependent proliferative pathways in a mC-dependent manner. - Source: PubMed
Publication date: 2025/12/01
Zhao HongyanWei QinglvLuo ZhiLiu XiaoyiYang ChenyueChen NingxuanWang YuanLuo XinZuo XinzhaoLuo QingyaYang YuZhou YangLiu JiaqiZhang TeYang DanLong YingfeiMobet YouchaouXu JingWang WeiLiu TaoYi Ping - Stress granules (SGs) are cytoplasmic biomolecular condensates enriched with RNA and translation factors. They form in response to stress, in part through phosphorylation of the translation initiation factor eIF2α, and are implicated in viral infection, tumorigenesis, and neurodegeneration. Although ADP-ribosylation plays a key role in SG assembly, the enzyme responsible for this ADP-ribosylation during SG assembly remains unidentified. Here, we systematically knock down the human ADP-ribosyltransferase family and identify PARP10 as pivotal for SG assembly. Live-cell imaging reveals PARP10's crucial role in regulating initial SG assembly kinetics. Further, we pinpoint the core SG component, G3BP1, as a PARP10 substrate and find that PARP10 regulates SG assembly via G3BP1 or a synthetic mimic that recapitulates its domain architecture. PARP10 knockdown reduces eIF2α phosphorylation and alters the SG core composition, notably decreasing translation factor presence. Based on our findings, we propose a model in which ADP-ribosylation acts as a rate-limiting step, initiating the formation of SGs. - Source: PubMed
Publication date: 2025/10/09
Jayabalan Aravinth KumarBhambhani KrishnaLeung Anthony Kl - The identification of novel functional biomarkers is crucial in recognizing high-risk colorectal cancer (CRC) patients. Despite this need, no prognostic biomarker has been implemented in clinical practice for CRC. To address this gap, we utilized integrated transcriptomic data from public databases alongside our original multi-omics data, including proteome and chromatin accessibility datasets. Bioinformatics studies on transcriptomic datasets from 487 CRC patients led us to identify three Golgi apparatus prognostic genes: NIPAL1, ZYG11B, and PARP10. We found that decreased expression of NIPAL1 and ZYG11B, as well as increased expression of PARP10, elevated the risk of CRC. These genes are potentially involved in cellular processes such as nucleotide excision repair and DNA replication. Additionally, our original multi-omics datasets, encompassing proteomic data and chromatin accessibility profiling from assay for transposase-accessible chromatin with sequencing (ATAC-Seq), identified alterations in protein levels of potential upstream transcription factors CDX2 and YY1 for three genes. Furthermore, chromatin accessibility at DNA binding regions corresponding to transcription factors such as SPI1 and JUND changed, potentially explaining the observed variations in mRNA levels for these genes. Our findings highlight the biological activities of these genes, including NIPAL1, PARP10, and ZYG11B, and their upstream regulators, offering a functional context for future in-depth mechanistic studies. - Source: PubMed
Publication date: 2025/09/26
Zhu PengShen ShisiWang XiLi JieTang DongeDai YongTang MinZhang WeiSun Guoping