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
- BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disorder and the leading cause of dementia. Currently, no treatment method can treat AD completely successfully.ObjectiveThis work seeks to uncover new genetic signatures linking B-cell senescence to AD, elucidate the immune-related pathological mechanisms of AD.MethodsThe GSE85426 and GSE168813 for AD were obtained from public databases. Differential analysis of expression matrix in GSE85426 was conducted to screen differentially expressed genes (DEGs), WGCNA was explored to obtain B cell and cell senescence related hub genes. Then the key genes for AD were screened by intersection, Mendelian randomization (MR), receiver operating characteristic (ROC) curve, and Wilcoxon test. Additionally, enrichment analysis, immune infiltration analysis, and molecular docking were performed to investigate the molecular mechanism of key genes and drug targets related to key genes, respectively.ResultsIn this study, CCDC86 and PARP9 were identified as key genes, genetic association analysis suggested CCDC86 correlates with higher AD susceptibility while PARP9 tends to correlate with lowered AD risk. We also found that these two key genes were highly correlated with B cells, and the abundance of B cells in AD increased significantly. Finally, our calculation revealed that the binding free energy between PARP9 and bisphenol A was -7.6 kcal/mol, implying a favorable simulated binding tendency between the two molecules.ConclusionsThese findings suggest that PARP9 may serve as a promising and reliable drug target for clinical therapy, which may represent a tentative candidate worthy of further experimental validation for subsequent biomarker and therapeutic target research in AD. - Source: PubMed
Publication date: 2026/08/12
Yuan RongLiao GuihuaSu ShaohuiShan JiayanTang Shanhong - m5C modification plays a vital role in the progression of human cancers, including breast cancer (BC), but the function of NOP2/Sun RNA methyltransferase 2 (NSUN2), an RNA m5C modification enzyme, remains largely unclear. - Source: PubMed
Publication date: 2026/07/19
Li XinYan ChangjiaoYi JunYun JunCui FengqiangXu XiaolongLi YikeXu Xin - : Resistance to sunitinib represents a major clinical obstacle in the management of clear cell renal cell carcinoma (ccRCC). This investigation aims to identify genes associated with sunitinib resistance and elucidate potential molecular pathways in ccRCC. : To identify differentially expressed genes (DEGs) in sunitinib-resistant ccRCC cells and their parental cells, bioinformatic analysis was performed on the GSE216494 dataset. Protein-protein interaction (PPI) network and topological analyses pinpointed a hub gene. Sunitinib-resistant A498 and 786-O cell lines were employed for validation. Sunitinib sensitivity and cell proliferation were evaluated using functional assays, such as colony formation and Cell Counting Kit-8 (CCK-8). Protein interactions and signaling pathway activity are investigated using co-immunoprecipitation (Co-IP), dual-luciferase reporter assays, and immunofluorescence. In resistant cells and patient-derived organoids (PDOs), the therapeutic potential of olaparib, either by itself or in conjunction with sunitinib, was assessed. : Sunitinib-resistant cells and patient tissues were shown to exhibit consistent upregulation of poly (ADP-ribose) polymerase 9 (). knockdown sensitized resistant cells to sunitinib, suppressing proliferation. Conversely, its overexpression induced resistance in parental cells. Additionally, STAT1 and PARP9 interact to promote nuclear translocation and STAT1 phosphorylation. Activation of the / axis further enhanced the expression of and . Olaparib treatment can increase sunitinib-resistant ccRCC cells. Olaparib can weaken the / signaling pathway and prevent sunitinib-resistant ccRCC cells from proliferating. Importantly, combination treatment with olaparib and sunitinib showed superior antitumor efficacy in ccRCC PDOs. : This study demonstrates that promotes sunitinib resistance in ccRCC by activating the / pathway and upregulating /. - Source: PubMed
Publication date: 2026/06/16
Luo LeiGuan FengjuWang ZhankunLi BinDing XuemeiSong LeileiSun Lijiang - The dynamic synthesis and removal of poly (ADP-ribose) (pADPr) by poly (ADP-ribose) polymerase 1 and poly (ADP-ribose) glycohydrolase (PARG), respectively, is essential for the maintenance of genome integrity, particularly during DNA replication. However, the precise role of the pADPr-binding chromatin remodeler chromodomain helicase DNA binding protein 1-like (CHD1L) in resolving endogenous DNA damage remains unclear. Here, we identified CHD1L as a critical modulator of Okazaki fragment maturation. We demonstrated that CHD1L loss was synthetic lethal with severe inhibition of PARG. This synthetic lethality stemmed from the toxic accumulation of pADPr specifically in S-phase cells, originating from unprocessed Okazaki fragment intermediates. Rescue experiments confirmed that both the ATPase and pADPr-binding macrodomain of CHD1L were indispensable for preventing this toxic accumulation. Mechanistically, quantitative chromatin proteomics revealed that CHD1L deficiency caused the persistent and aberrant retention of single-strand break (SSB) repair factors and others including the E3 ubiquitin ligases RNF114 and DTX3L/PARP9, challenging the previous models that CHD1L loss would limit chromatin accessibility of DNA repair factors. These findings establish a novel housekeeping function for CHD1L in facilitating the efficient turnover of DNA repair factors at replication-associated SSBs. - Source: PubMed
Nie LitongFu JialingHuang MinZhang HuiminMa TiantianYang ChangLi SitingWang ChaoChen Junjie - Diabetic Kidney Disease (DKD) is a major complication driven by chronic inflammation and impaired tissue homeostasis. While mesenchymal stem cells (MSCs) show promise, the precise mechanisms by which human adipose-derived MSCs (hASCs) modulate macrophage-mediated resolution of inflammation remain to be fully elucidated. - Source: PubMed
Publication date: 2026/06/18
Wu ShiwenXu WanyingYao JiaqianLi RenjieYang YanfangJin JianhongPeng XueqianLiu WenhongXu ZhiweiMi AiWang Hui