PARP9 antibody - N-terminal region (ARP33776_P050)
- Known as:
- PARP9 (anti-) - N-terminal region (ARP33776_P050)
- Catalog number:
- arp33776_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PARP9 antibody - N-terminal region (ARP33776_P050)
Related genes to: PARP9 antibody - N-terminal region (ARP33776_P050)
- Gene:
- PARP9 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 9
- Previous symbol:
- -
- Synonyms:
- BAL, BAL1
- Chromosome:
- 3q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-09-30
- Date modifiied:
- 2015-11-06
Related products to: PARP9 antibody - N-terminal region (ARP33776_P050)
Related articles to: PARP9 antibody - N-terminal region (ARP33776_P050)
- Androgen receptor (AR) signalling is central to both normal prostate physiology and prostate cancer (PCa) progression. Its activity is tightly regulated by localization, transcriptional control, and post-translational modifications. Among these, poly (ADP-ribose) polymerase (PARP) mediated ADP-ribosylation has emerged as a key regulator. Multisite cysteine mono-ADP-ribosylation of AR by PARP7 modulates its function. Molecular recognition of ADP-ribosyl-cysteine by PARP9/DTX3L influences AR-driven gene expression. Importantly, defects in homologous recombination repair (HRR) genes have made PARP inhibitors (PARPi) an effective treatment for BRCA (Breast cancer susceptibility genes 1 and 2)-mutated metastatic castration-resistant prostate cancer (mCRPC). Clinical trials such as TALAPRO-2 show that combining PARPi with AR signalling inhibitors can be effective; however, their benefit in tumours without HRR mutations remains unclear. PARP enzymes regulate AR via MARylation and PARylation, with inhibitors such as Olaparib, which disrupts AR-PARP crosstalk. In this review, we present current knowledge on the interplay between ADP-ribosylation and AR signalling in prostate cancer, emphasizing the roles of distinct PARP enzymes in shaping AR activity and therapeutic response. Herein, we focus on the combined contributions of MARylation and PARylation to prostate tumorigenesis. We also discuss how this complex regulatory network may contribute to the development of advanced prostate cancer therapies in the future. This could improve PARP inhibitor and AR signalling inhibitor combinations and allow more patients to benefit from them. - Source: PubMed
Publication date: 2026/04/14
Reddy Gali Sri Venkata Sai RishmaSamanta KrishnaKar Pulak - Although pancreatic ductal adenocarcinoma (PDAC) is generally considered an immunologically "cold" tumor, approximately 20% of cases can be classified as immune-hot. However, this immune-enriched (IE) phenotype does not confer a significant survival advantage, highlighting the need to investigate its underlying mechanisms and identify effective therapies. By integrating in vitro drug screening and in silico sensitivity prediction, we identified the HDAC inhibitor vorinostat (SAHA) as a potent sensitizer to chemoimmunotherapy specifically in the IE-PDAC. This effect was validated using T cell-organoid co-cultures and patient-derived xenografts with humanized immune systems. Mechanistically, abundant cytokines (TNF-α, FGF) in the IE tumor microenvironment promote FASN and PARP9 expression. This leads to free fatty acid accumulation and enhanced oxidative phosphorylation, supporting tumor cell survival. SAHA disrupts this "metabolic trap" by concurrently suppressing FASN and PARP9. Single-cell RNA sequencing revealed that the Gemcitabine-SAHA combination remodels the tumor microenvironment by enhancing CD8 T cell function and depleting cancer-associated fibroblasts. Clinically, we defined a CD8/FASN/PARP9 signature that identifies an IE patient subgroup with poor survival, representing those most likely to benefit from the "Gemcitabine-Nivolumab-SAHA" triple-combination therapy. - Source: PubMed
Publication date: 2026/04/13
Chen ChenLi DingruLiao YingnaWang ZehuaZhu ChunbinZhang ZifengJin LiquanChen YueyueChen JiaoshunXu JunyiWei MiaoyanTang RongYu XianjunShi Si - Poly(ADP-ribose) polymerase 9 (PARP9) is an interferon-inducible PARP family member implicated in tumor cell survival, immune signalling, and poor prognosis, suggesting potential value as a biomarker and therapeutic target in cancer. Its expression pattern and clinical relevance in acute myeloid leukaemia (AML) is unclear. We investigated the expression of in AML patient samples. We analysed transcriptomic data from TCGA-LAML, GTEx, Human Protein Atlas, DepMap, and BloodSpot to characterise PARP9 expression across cancers, hematopoietic hierarchies, and AML subgroups. Cross-cancer analysis showed significantly higher expression in AML compared with most non-hematologic malignancies ( < 0.001). Within hematopoietic lineages, expression was significantly high in megakaryocyte-erythroid progenitors ( < 0.05), B cells < 0.001), polymorphonuclear cells ( < 0.001), and monocytes ( < 0.001), with the highest expression in polymorphonuclear cells. AML samples exhibited ~ 2.4-fold higher expression of when compared to normal tissues ( < 0.001). high expression was found to be associated with specific FAB subtypes M0, M1, M2, M4 and M5 and in patients exhibiting intermediate and adverse cytogenetic risk profiles ( < 0.05). Additionally, patients with high expression showed significantly poor overall survival outcomes (log-rank = 0.035; HR 1.49, 95% CI 1.03-2.16), although PARP9 was not independently prognostic after adjustment for age and cytogenetic risk in multivariable Cox regression. Furthermore, the differential expression analysis identified 457 upregulated and 1141 downregulated genes associated with high expression, which in silico analysis linked to immune and cancer-related pathways, including PD‑1/PD‑L1 signalling, NOD-like receptor signalling, cytokine-cytokine receptor interaction, and hematopoietic lineage. Overall, was consistently highly expressed in AML and associated with adverse-risk categories, distinct transcriptional pathways, and poor survival outcomes, highlighting its potential as a biomarker warranting further study to validate its role in AML. - Source: PubMed
Publication date: 2026/03/31
Alshammari AbdullahAlgarni AbdulrahmanGuru PriyankaAlruwaili Mohammed M - To investigate the variances in inhibitory effects and potential immunological mechanisms of transfer factors (TFs) from different origins against avian reticuloendotheliosis virus (REV) infection in chickens, this study firstly compared the protein expression profiles of spleens from REV-infected chickens, Newcastle disease (ND) vaccine-immunized chickens, and specific pathogen-free (SPF) chickens. TFs were subsequently extracted from the spleens of these groups, and the alterations in splenic proteomics were monitored post-administration of these TFs to chickens. Furthermore, the CD4⁺/CD8⁺ T cell subsets and the levels of cytokines such as IFN-γ and IL-2 were determined, followed by REV challenge experiments. The results demonstrated that TFs sourced from REV-infected spleens, which enriched virus-specific immune-related proteins such as STAT1 and OASL, significantly boosted cellular immune responses by activating the NOD-like receptor signaling pathway and establishing an efficient STAT1-OASL-PARP9-IRF7 protein-protein interaction network, consequently inhibiting REV replication efficiently. TFs obtained from vaccine-immunized spleens only amplified humoral immunity with restricted anti-REV effects, while TFs derived from SPF spleens had no substantial immunomodulatory activity. Notably, TFs extracted from REV-infected spleens exhibited superior anti-REV efficacy. This study furnishes crucial evidence for the selection of sources and molecular mechanism analysis of high-efficiency TF preparations. - Source: PubMed
Publication date: 2026/03/18
Wang XinliSong MengyuWu QingyueRen ZhihaoCui WenpingChang ShuangWang YixinZhao Peng - Sjögren's disease (SjD) is a group of chronic autoimmune diseases primarily targeting exocrine glands, including the lacrimal glands (LG). Involvement of the lacrimal glands leads to severe dry eye, also known as Sjögren's disease-associated dry eye (SjD-DE). Current, available animal models of SjD are achieved by using autoantigens from salivary gland. This study establishes a novel lacrimal gland-specific autoimmune model that recapitulates key features of SjD-DE, providing a tool for investigating LG-focused mechanisms in SjD. - Source: PubMed
Publication date: 2026/02/13
Li SiyuanLiu ShanLi YaqiongZhang PengLei FengyangTian LeiJie Ying