PARP11 antibody - middle region (ARP33767_P050)
- Known as:
- PARP11 (anti-) - middle region (ARP33767_P050)
- Catalog number:
- arp33767_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- PARP11 antibody - middle region (ARP33767_P050)
Related genes to: PARP11 antibody - middle region (ARP33767_P050)
- 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 - middle region (ARP33767_P050)
Related articles to: PARP11 antibody - middle region (ARP33767_P050)
- Mono-ADP-ribosylation (MARylation) is emerging as an important regulator of anti-cancer immunity and immunosuppressive tumor microenvironment (TME). Our previous studies showed that PARP11, one of several enzymes that facilitate MARylation, regulates the activities of intratumoral cytotoxic T lymphocytes (CTLs) and regulatory T cells (Tregs). Here, we demonstrate that stimuli such as adenosine, epinephrine, or glucagon-like peptide-1 (GLP1) induced PARP11 in cancer cells. Upregulation of PARP11 in cancer cells led to PARP11-mediated MARylation, ubiquitination, and accelerated degradation of MHC-I through the autophagy-lysosomal pathway. Induction of PARP11 protected cancer cells from killing by specific CTLs and stimulated tumor growth and progression. Genetic ablation of PARP11 attenuated MHC-I MARylation, ubiquitination, and interaction with autophagy receptors. Pharmacologic inhibition of PARP11 in pancreatic ductal adenocarcinoma (PDAC) cells restored their MHC-I levels, sensitized them to killing by CTLs, inhibited tumor growth, and impeded their initial resistance to chemotherapy and their acquired resistance to targeted therapy with RAS inhibitors. Moreover, inhibition of PARP11 prevented hyperprogressive disease in a mouse melanoma model treated with immune checkpoint inhibitors (ICBs), suggesting that PARP11 is a major therapeutically actionable driver of immunosuppression in tumors. - Source: PubMed
Publication date: 2026/06/03
Sun YuchenTang YingyingSingh Vivek THolczbauer ÁgnesBasavaraja RaghavendraBui Quoc ThangLee Jeong-HwaGao RunnanEdwards A ColeGuo WeiDiehl J AlanFan YiKoumenis ConstantinosBaslan TimourStanger Ben ZCohen Michael SSpiegelman Vladimir SFuchs Serge Y - 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 an MIRO1-binding compound and bulk RNA sequencing of human glioma resections treated with the same compound ex vivo. Cross-species transcriptomic integration reveals an MIRO1-responsive program in the TME. Among shared targets, we identify as a consistently up-regulated gene in glioma, which is down-regulated after 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 E signals from another cluster of macrophages (MAC4). Targeting MIRO1 eliminates this cell circuitry and reduces the tumor cell population. Our study provides a transcriptomic framework for understanding mitochondria-immune crosstalk and nominates MIRO1-PARP11 as a potential effector axis of brain immune dysfunction. - Source: PubMed
Publication date: 2026/05/13
Du ZehuiLi MenghanBergsneider Brandon HTsai Andy PCho Kwang BogKim Lily HChoi JohnLi GordonWyss-Coray TonyLim MichaelWang Xinnan - 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