Ask about this productRelated genes to: PARP9 antibody
- 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
Related articles to: PARP9 antibody
- Targeted radionuclide therapy with Lu-PSMA-617 prolongs radiographical progression-free survival in prostate-specific membrane antigen (PSMA)-positive metastatic castration-resistant prostate cancer (mCRPC), yet 13% of patients develop symptomatic skeletal events. The authors hypothesized that hemoglobin-based oxygen carriers (HBOCs) could potentiate Lu-PSMA-617 by reprogramming bone marrow (BM) immunity.Using PSMA-expressing xenografts, they demonstrated that concomitant HBOC administration significantly reduced tumor volume without increasing systemic toxicity. To dissect the underlying mechanism, the authors performed high-resolution single-cell RNA sequencing of murine BM.HBOC treatment markedly expanded mature neutrophils, plasmacytoid dendritic cells, classical monocytes, natural killer T cells, and mature B cells, while concomitantly upregulating DNA damage repair genes such as , , and within these subsets. Gene set enrichment analysis confirmed significant activation of DNA damage response pathways, implying enhanced cellular radioresistance and improved tolerance to β-particle irradiation. Thus, HBOCs improve Lu-PSMA-617 antitumor efficacy indirectly via immune-subset expansion and DNA-repair reinforcement, offering a clinically feasible and safe strategy to optimize combination protocols for patients with mCRPC. - Source: PubMed
Publication date: 2026/05/22
Qu DanyueShao ChenyiJi XinyuanHuang YichiTian ChenLi JiazeZhou HuShi YileiWang HongLiu JiaxinZhao Yu - Ageing is accompanied by progressive microvascular dysfunction, a key determinant of organ performance and longevity. The molecular drivers of this process remain incompletely defined, and the mechanisms by which exercise counters vascular ageing are unclear. This study investigated whether exercise-regulated long noncoding RNAs (lncRNAs) contribute to microvascular ageing and age-related cardiac dysfunction. - Source: PubMed
Publication date: 2026/05/19
Li HaoboXiao XiaoZhou YirongZhang YajingKang JiayiYuan ZixunHe JiaqiGuerra JustinLerchenmüller CarolinMargulies Kenneth BAguirre Aaron DRoh Jason DRosenzweig Anthony - 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