Ask about this productRelated genes to: PARP11 antibody
- Gene:
- PARP11 NIH gene
- Name:
- poly(ADP-ribose) polymerase family member 11
- Previous symbol:
- C12orf6
- Synonyms:
- -
- Chromosome:
- 12p13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-24
- Date modifiied:
- 2016-10-05
Related products to: PARP11 antibody
Related articles to: PARP11 antibody
- PurposeThis study investigated causal relationships and underlying mechanisms between serum DNA repair proteins and liver cancer to identify biomarkers for clinical management.MethodsA two-sample bidirectional Mendelian randomization (MR) design was employed. We performed inverse variance weighted (IVW) analysis, followed by protein quantitative trait loci (pQTL), colocalization, and pathway enrichment analyses to explore biological mechanisms.ResultsMR analysis revealed significant associations: NBR1 (IVW: OR = 2.28, 95%CI: 1.17-4.45, P = 0.015) and RAD51 (IVW: OR = 2.16, 95%CI: 1.12-4.15, P = 0.021) were risk factors. PARP11 was protective for hepatocellular carcinoma (OR = 0.48, 95%CI: 0.25-0.93, P = 0.030) but a risk for intrahepatic cholangiocarcinoma (OR = 1.86, 95%CI: 1.04-3.33, P = 0.038). Mechanistically, pQTL and colocalization identified rs2793568 as a key regulator of PARP1, which was enriched in base excision repair pathways. Sensitivity analyses confirmed the robustness of these findings.ConclusionSerum NBR1, RAD51, and PARP11 are potentially causal in liver cancer pathogenesis. Specifically, the genetic regulation of PARP1 highlights a critical DNA repair mechanism, supporting their utility as predictive biomarkers. - Source: PubMed
Publication date: 2026/04/22
Lin SihaoFang KunpengGeng Li - Lung cancer remains a leading cause of cancer-related mortality, largely due to its complex immune microenvironment and molecular heterogeneity. To address gaps in understanding tumor heterogeneity and the role of long non-coding RNA (lncRNA) macromolecules, we conducted an integrative single-cell RNA sequencing (scRNA-seq) analysis of non-small cell lung cancer (NSCLC). Unsupervised clustering identified distinct immune and malignant cell populations. Differential expression analysis identified robust cell-type markers, including novel lncRNA macromolecules, AC005842.1, AC009041.2, and AC007240.1 enriched in specific tumor and immune subsets. Functional enrichment linked these lncRNAs to key cancer pathways, including epithelial-mesenchymal transition (EMT), hypoxia, and immune modulation. Targeted experimental validation using quantitative real-time PCR (qRT-PCR) in NSCLC cell lines confirmed significant upregulation of the identified lncRNAs and supported activation of EMT-associated molecular programs. Pseudotime trajectory modeling uncovered dynamic activation of hallmark programs, notably TNFA-NFκB and IL2-STAT5 signaling, suggesting progressive immune suppression and metabolic reprogramming during tumor evolution. We further identified novel transcription factor-pathway associations, including NR5A1-OXPHOS (oxidative phosphorylation) and FOXA2-mTORC1, pointing to uncharacterized axes of macromolecular regulation. To ensure reproducibility and accessibility, we developed lncScape, a modular, open-source Shiny application for integrative lncRNA analysis in single-cell datasets. lncScape implements a pipeline for clustering, lncRNA detection, pseudotime modeling, and GSVA-based pathway enrichment. It also introduces two novel scoring strategies the lncRNA Dynamics Score (LDS) and TF-lncRNA Dynamics (TLD) to prioritize dynamic regulatory lncRNAs based on expression patterns and transcription factor associations. Our findings expand understanding of lncRNA macromolecules in lung cancer and provide a practical platform for lncRNA-centric research. - Source: PubMed
Publication date: 2026/04/15
Haider AliDin Rahman UdHabib BushraLi Chunhua - Mitochondrial regulators are increasingly recognized for their influence on immune signaling within the tumor microenvironment (TME). In glioma, where immunosuppression limits therapeutic efficacy, we investigate how targeting the mitochondrial protein MIRO1 alters the TME. We combine single-nucleus RNA sequencing of murine gliomas treated in vivo with a MIRO1-binding compound and bulk RNA sequencing of human glioma resections treated with the same compound ex vivo. Cross-species transcriptomic integration reveals a conserved MIRO1-responsive program in the TME. Among shared targets, we identify as a consistently upregulated gene in glioma that is downregulated following MIRO1-binding compound treatment in both human and mouse gliomas. Cell-cell communication analysis shows that a specific cluster of macrophages (MAC1), which exhibits robust and (encoding PD-L1) expression, sends immunosuppressive signals to CD8+ cytotoxic T cells, and may receive prostaglandin E₂ signals from another cluster of macrophages (MAC4). Targeting MIRO1 eliminates this cell circuitry and reduces the tumor cell population. Our data suggest MAC4 as the originating MIRO1-driven cell cluster, which relays a macrophage-to-T cell signaling axis that may contribute to immune suppression in glioma through PARP11 regulation. Our study provides a transcriptomic framework for understanding mitochondria-immune crosstalk in the brain TME and nominates MIRO1 PARP11 as a potential effector axis of immune dysfunction. - Source: PubMed
Publication date: 2025/11/12
Du ZehuiLi MenghanBergsneider Brandon HTsai Andy PCho Kwang BogKim Lily HChoi JohnLi GordonWyss-Coray TonyLim MichaelWang Xinnan - Cryptorchidism is a notorious innate malformation in children that always leads to oligospermatism or azoospermatism. Moreover, there is a relationship between oxidative stress and spermatogenesis dysfunction caused by cryptorchidism. Ferroptosis is associated with iron metabolism and oxidative stress as a novel form of cell death regulation, which is involved in the pathogenesis of many diseases. Hence, ferroptosis may play an important role in spermatogenesis dysfunction in case of cryptorchidism. Therefore, the purpose of this study was to identify the key ferroptosis-related genes that influence spermatogenesis in patients with cryptorchidism and provided new strategies for the prevention and treatment of spermatogenesis dysfunction in cryptorchidism patients in clinical practice. Gene expression information was downloaded from the Gene Expression Omnibus (GEO) and ArrayExpress databases. The differentially expressed genes (DEGs) were selected using the limma R package. Next, one crucial module, Maroon, was identified via Weighted Gene Coexpression Network Analysis (WGCNA). Ferroptosis-related genes were downloaded from FerrDb v2 database. GO and KEGG analyses were subsequently conducted. Moreover, these differentially expressed ferroptosis-related genes (DE-FRGs) were intersected with the DEGs of AdPlus/AdMinus. Two key genes most closely associated with spermatogenesis dysfunction in cases of cryptorchidism were subsequently identified. Furthermore, immunohistochemistry (IHC) and Receiver Operating Characteristic (ROC) analyses were conducted to validate our conclusions. Finally, miRWalk3.0 and TargetScan were used to predict the pivotal target microRNAs. One critical module and two hub genes that are strongly related to the pathogenesis of spermatogenesis dysfunction in patients with cryptorchidism were identified. Gene Set Enrichment Analysis, ROC and IHC analyses were conducted and the results revealed that BRDT and PARP11 might play critical roles in spermatogenesis dysfunction in patients with cryptorchidism. Our study identified two ferroptosis-related genes, BRDT and PARP11 might play a role in the pathogenesis of spermatogenesis dysfunction in patients with cryptorchidism, which provided a novel perspective for the prevention and treatment of spermatogenesis dysfunction in patients with cryptorchidism in clinical practice. - Source: PubMed
Publication date: 2025/05/23
Du TianGe YifengZhou ZhengJing JunFeng YumingDing HualongMa JinzhaoYao Bing - Immunotherapy in clinical application faces numerous challenges pertaining to both effectiveness and safety. Poly(ADP-ribose) polymerases (PARPs) exhibit multifunctional characteristics by transferring ADP-ribose units to target proteins or nucleic acids. In recent years, more and more attention has been paid to the biological function of PARPs in immune response. This article reviews the relationship between PARP family members and immune response. PARP1 and PARP2 inhibit anti-tumor immune activity by regulating immune checkpoint expression and the cGAS/STING signaling pathway. PARP7 and PARP11 play an important role in promoting immunosuppressive tumor microenvironment. PARP9 promotes the production of Type I interferon and the infiltration of macrophages. PARP13 is a key tumor suppressor that promotes anti-tumor immune response. PARP14 plays a crucial role in promoting the differentiation of macrophages towards the M2 pro-tumor phenotype. Summarizing the molecular mechanisms of PARP7, PARP9, PARP11, PARP13 and PARP14 in regulating immune response is helpful to deepen our comprehension of the role of PARPs in immune function regulation. This provides a reference and basis for targeted PARP-based cancer treatment strategies and drug development. PARP1, PARP7 inhibitors or other PARP inhibitors in combination with immune checkpoint inhibitors or other immunotherapy strategies may be a more effective cancer therapy. - Source: PubMed
Publication date: 2025/02/16
Wang ShupingHuang JinglingZeng TingyuChen YaliXu YungenZhang Bangzhi