PARP-3 human recombinant
- Known as:
- PARP-3 H. sapiens Rec.
- Catalog number:
- bc-320
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- PARP-3 human recombinant
Related genes to: PARP-3 human recombinant
- Gene:
- PARP3 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 3
- Previous symbol:
- ADPRTL3
- Synonyms:
- ADPRT3, IRT1, hPARP-3, pADPRT-3
- Chromosome:
- 3p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-24
- Date modifiied:
- 2015-11-06
Related products to: PARP-3 human recombinant
Related articles to: PARP-3 human recombinant
- - Source: PubMed
Publication date: 2026/05/29
Yildirim ZuleyhaDantzer Françoise - This integrated multi-omics study delineates molecular alterations in the substantia nigra pars compacta (SNpC) across different stages of Parkinson's disease (PD) in a Korean cohort. By combining transcriptomic and proteomic analyses of postmortem tissues, we identified stage-specific molecular signatures associated with Braak Lewy body pathology. Enrichment analyses revealed upregulation of extracellular matrix-related and immune response pathways, along with downregulation of genes involved in microtubule organization and neuronal function in the SNpC of PD patients. In addition, fifteen genes and fourteen proteins showing significant fold changes (>2.0 or <0.5), high normalized expression levels (log2 >3.0) and statistical significance (p<0.05) were profiled. Hierarchical clustering and principal component analysis of transcriptomic and proteomic data from SNpC tissues of PD patients (selected based on correlation coefficients >0.8 or <-0.8) revealed distinct stage-dependent groupings aligned with Braak Lewy body pathology. Molecular profiles correlated strongly with disease progression; advanced Braak stages exhibited disrupted mitochondrial processes and elevated phospholipid binding pathways, potentially linked to α-synuclein aggregation and neurodegeneration. Notably, upregulation of genes such as and was associated with α-synuclein aggregation, cell death, and autophagy inhibition, while downregulation of , and co-occurred with neuronal loss and mitochondrial dysfunction. Proteomic analyses further highlighted increased levels of neuroinflammation and mitochondrial impairment markers, including SNCA, GPNMB, and LGALS3, some of which may serve as biomarkers of disease severity. These findings offer critical insights into PD's molecular pathogenesis and identify potential candidates for further functional validation and therapeutic intervention. - Source: PubMed
Publication date: 2026/05/14
Kim SinyeonChoi Jin GyuKim Se WoongSon MiwonKim DaehwanNam Soo JeongKim Sang JinKim Seongheon - The evolution of robust DNA repair mechanisms was a prerequisite for the conquest of land by plants, a transition that exposed them to harsh new environmental stressors. The poly (ADP-ribose) polymerase (PARP) family is central to this adaptation, as it orchestrates DNA repair and stress signaling pathways essential for coping with the elevated UV radiation and desiccation of terrestrial environments. Yet its early evolutionary origins are unknown. Here, we present a comprehensive reconstruction of the PARP family's history across the plant kingdom. Our phylogenomic analysis reveals that evolution ignited during the bryophyte radiation, expanding from a single ancestral algal gene into three distinct subfamilies (, , and ). This diversification was driven by structural innovations in DNA-binding domains and a rewiring of transcriptional networks to respond to terrestrial challenges. We provide direct experimental support for this hypothesis through functional analysis of PARPs from the extremotolerant moss . We show that its PARP proteins provide multifaceted protection against UV radiation, heat, and genotoxic agents, and that recently duplicated genes are already diverging in function. Our work pinpoints the molecular adaptations in a key DNA repair family that enabled the greening of Earth and uncovers novel genetic targets for enhancing crop resilience. - Source: PubMed
Publication date: 2025/12/22
Yi KunYang QilinDing ZhenZhang DaoyuanWang YanGao Bei - Poly (ADP-ribose) polymerases (PARPs) are a diverse family of enzymes that regulate genome stability, cell death, and stress responses through ADP-ribosylation. Among them, PARP1, PARP2, and PARP3 are central to cellular DNA repair, while tankyrases, and their isoforms, contribute to telomere maintenance, transcriptional regulation, immune signaling, and metabolism. Dysregulated PARP activity drives genomic instability, apoptosis, parthanatos, and tumor microenvironment remodeling, thereby linking PARPs to oncogenesis, immune escape, and therapy resistance. Clinically, PARP inhibitors (PARPi), such as olaparib, niraparib, rucaparib, and talazoparib, exploit synthetic lethality in homologous recombination-deficient tumors and are increasingly applied in ovarian, breast, prostate, and pancreatic cancers. Beyond oncology, preclinical studies demonstrate antiviral efficacy of PARPi against hepatitis B virus, human immunodeficiency virus, and coronaviruses, and also therapeutic potential in neurodegeneration, cardiovascular disease, fibrosis, and metabolic disorders. However, PARPi resistance arises through restoration of DNA repair, replication fork protection, epigenetic changes, and drug-target dynamics, while adverse events-including hematologic toxicity, gastrointestinal disturbance, and organ-specific effects-limit a broader use. Next-generation PARPi with improved isoform selectivity, PROteolysis-TArgeting Chimera (PROTAC) degraders, and rational combinations with ATR/CHK1 inhibitors, immune checkpoint blockade, or epigenetic modulators offer strategies to enhance efficacy and overcome resistance. Emerging biomarker-driven approaches, including liquid biopsies and functional assays, may further personalize therapy. By integrating canonical DNA repair roles with non-canonical signaling and host-virus interactions, PARPs represent pivotal regulators. Similarly, the versatile therapeutics of PARPi have implications that extend beyond oncology into a broader and diverse range of other human diseases. - Source: PubMed
Publication date: 2025/12/29
Wang FeiGuo ZhuyiCarr Michael JShi Weifeng - : Acute myeloid leukemia (AML) remains a hematopoietic clonal malignancy that is characterized by a poor prognosis, largely attributable to chemotherapy resistance and a high incidence of post-chemotherapy relapse. Therefore, the identification of novel molecular markers is crucial for optimizing treatment regimens and improving outcomes for this disease. : We first investigated the expression levels of poly(ADP-ribose)polymerase 3() mRNA in data from our center and the Gene Expression Omnibus (GEO), then explored the role of in AML through cell experiments. : Our results demonstrated that the expression levels of were significantly elevated in AML samples compared to controls ( < 0.05). Based on the median expression of , 151 cases of AML from TCGA data were divided into two groups. The results showed that -high group had markedly shorter overall survival (OS) than the -low group (OS: median: 1.18 vs. 3.88 years; < 0.001). The overexpression of was correlated with older age and high-risk stratification in the AML from TCGA data ( < 0.05). Finally, we confirmed that specifically down-regulating expression impaired AML cell proliferation, disrupted cell cycle process, inhibited migration, accelerated apoptosis, and impaired the PI3K/AKT/mTOR signaling pathway in vitro. : -mediated activation of the PI3K/AKT/mTOR signaling pathway enhances AML cell proliferation and migration, identifying it as a potential therapeutic target for poor-prognosis AML. - Source: PubMed
Publication date: 2025/09/20
Cao TingyongZhang YurongLiu HuanZhang HongbinLi LiangliangLi XiaoliZhao Li