PARP3 antibody
- Known as:
- PARP3 (anti-)
- Catalog number:
- orb101580
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- PARP3 antibody
Related genes to: PARP3 antibody
- 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: PARP3 antibody
Related articles to: PARP3 antibody
- Cancer cells exploit DNA repair to overcome damage and errors induced by rapid proliferation and repressed checkpoints. Thus, the loss of one DNA repair protein can make tumors more susceptible to inhibition of other repair pathways. Here, using in silico methodologies and high-content genetic and cell survival screens, we found that the antimalarial drug quinacrine impaired the DNA damage response (DDR) in multiple cancer cell lines. Quinacrine disrupted the interaction of the stress-response protein NDRG1 with the major segregase VCP, which in turn promoted the degradation of the E3 ubiquitin ligase RNF8 and other proteins that mediate the recruitment of the critical DDR protein 53BP1 to sites of DNA damage. This impaired recruitment of 53BP1 caused increases in the DNA damage marker γH2AX. High expression in tumors correlated with poor survival in patients, and high expression in various cancer cell lines correlated with quinacrine sensitivity. Colorectal carcinoma cells were particularly vulnerable to pharmacological or genetic inhibition of NDRG1, and high expression and mutations in and resulted in synthetic lethality. Our findings identify combination genetic markers that might be therapeutically exploited in colon cancer, as well as provide a platform for such discovery in distinct cancer types. - Source: PubMed
Publication date: 2026/07/21
Mkrtchyan Garik VVeviorskiy AlexanderMeisen Zarah GPetr Michael AMercurio Tobias ClausenBakula DanielaSykora PeterKuo Li-WeiRosenthal Dean SSimbulan-Rosenthal Cynthia MZhang PeiranTang QiuqiongOsipov Andreyan NOzerov Ivan VAliper AlexZhavoronkov AlexScheibye-Knudsen Morten - Epileptogenesis transforms a healthy brain into an epileptic network, yet the temporal and cell-type-specific molecular events driving this transition remain poorly defined. Neuron-glia interactions are essential in this process, but no study has systematically charted their transcriptional dynamics from the acute insult to chronic epilepsy. - Source: PubMed
Publication date: 2026/06/21
Berger Toni ChristophVigeland Magnus DehliHjorthaug Hanne SagsveenNome Cecilie GjessingBeier Christoph PatrickTaubøll ErikSelmer Kaja KristineHeuser Kjell - - 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