B7_H4 Antibody
- Known as:
- B7_H4 Antibody
- Catalog number:
- AF1134a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- B7_H4 Antibody
Related genes to: B7_H4 Antibody
- Gene:
- VTCN1 NIH gene
- Name:
- V-set domain containing T cell activation inhibitor 1
- Previous symbol:
- -
- Synonyms:
- B7-H4, FLJ22418, B7S1, B7x, B7H4
- Chromosome:
- 1p13.1-p12
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-25
- Date modifiied:
- 2019-03-06
Related products to: B7_H4 Antibody
Related articles to: B7_H4 Antibody
- A combination of gemcitabine (GEM)-based chemotherapy and an immune checkpoint inhibitor is the standard treatment for patients with advanced intrahepatic cholangiocarcinoma (iCCA). However, 70% of patients develop progressive disease following GEM treatment, highlighting the urgent need for therapeutic strategies targeting GEM-resistant (GR) disease. - Source: PubMed
Publication date: 2026/08/24
Pan Yi-RuLin Sheng-HsuanChang Yu-ChanJung Shih-MingWu Chiao-EnHuang Wen-KuanYeh Chun-Nan - Immune checkpoint inhibitors (ICIs) have improved outcomes for patients with melanoma and are now the standard of care for high-risk and advanced disease. However, long-term benefits are observed in only around 25% of patients, with significant risk for immune-related adverse events, highlighting the need for predictive biomarkers. To develop a minimally invasive, pre-treatment biomarker strategy, we profiled functional and subset-specific transcripts in peripheral blood T lymphocytes (PBTLs) and applied machine learning to identify predictive signatures. Patients were enrolled prior to receiving ICI monotherapy in the adjuvant (Exploratory n=61, Validation=78) or metastatic (Exploratory n=48, Validation=46) settings. Following feature selection, random forest models were trained and benchmarked against empirical null models. In the adjuvant setting, CD160 and GZMB predicted recurrence (95th percentile), while treatment-limiting toxicity was predicted by a signature comprising TNFRSF18, VTCN1, TIGIT, CCR4, and AHR (97th percentile). In the metastatic setting, baseline CD45RB, a marker of T-cell differentiation, most strongly predicted progression within one year (93.9th percentile). Distinct signatures in the adjuvant and metastatic settings suggest differences in T-cell programs associated with patient outcomes. These findings support further evaluation of pre-treatment circulating T-cell transcriptional profiles as predictors of ICI response and toxicity in melanoma. - Source: PubMed
Publication date: 2026/08/25
Lepola NoahDravillas CarolineGray ShannonBodnar Michael SArya NamrataWu RichardVerschraegen ClaireCarson William EKendra Kari LSpakowicz Daniel JBurd Christin E - Autoimmune diseases affect 5-10% of the global population, with a prevalence of 13% in women and 7% in men. Despite advances in immunology, the molecular basis of immune dysregulation remains limited. Nardilysin (NRD convertase, NRDc), a zinc-dependent metalloendopeptidase, has been identified as an enzyme involved in this dysregulation. Recent studies have identified NRDc dysregulation as a shared feature across type 1 diabetes (T1D), rheumatoid Arthritis (RA), and vitiligo, though the specific mechanism implicated differs by the disease involved. Reported roles for NRDc include modulating the release of the immune checkpoint protein VTCN1 (B7-H4), modulation of pro-inflammatory cytokines, and activation of ADAM17-mediated release of TNF-α and its receptors. While NRDc is recognized for its role in immune signaling, gene transcription, cell differentiation, proliferation, homeostasis, thermogenesis, and metabolism, a unified framework connecting NRDc's multifaceted enzymatic activity to autoimmunity is currently lacking. We review current literature to construct such a framework, positioning it as hypothesis-generating by outlining specific, testable predictions to guide future investigation. Based on the literature, we propose that NRDc functions as a crucial molecular indicator and a therapeutic interface, rather than just a bystander enzyme. - Source: PubMed
Publication date: 2026/08/07
Choudhary YashikaMoutughimou Ben AliUpadhye Vijay JagdishJadeja Shahnawaz DVaishnav Jayvadan - Experimental validation and functional optimization remain bottlenecks in AI-based protein design. We present a scalable workflow for developing AI-designed minibinders against cancer-associated surface proteins. Screening thousands of designs using mammalian cell-surface display identifies several high-affinity PD-L1 minibinders but far fewer for CD276 (B7-H3) and VTCN1 (B7-H4), highlighting substantial target dependence. Interface predicted template modeling (ipTM) scores generated by Chai-1 with ESM embeddings correlate with binding success and capture deleterious effects of interface mutations. Fluorophore-labeled AI-minibinders enable flow-cytometric staining comparable to conventional antibodies. However, when incorporated into chimeric antigen receptors (CAR), some show poor cell-surface trafficking and limited functionality. Redesign through a genetic algorithm-based diversification strategy that preserves the binding interface while changing non-binding surfaces experimentally reveals an isoelectric point (pI) window that improves CAR expression and enhances target-selective tumor cell killing. Our findings identify biochemical optimization beyond the binding interface as a critical requirement for translating AI-minibinders into functional applications. - Source: PubMed
Publication date: 2026/08/20
Broske BiancaMcEnroe Benjamin AFrechen Sophie CKempchen Tim NFandrey Caroline ITan ElisabethFerber DominicYong Michelle C RKleinert MarieMessmer Julia MKonopka PeterHoch AlexanderBlumenstock KatjaTödtmann Jan M POldenburg JohannesRühl HeikoSemaan AlexanderToma Marieta IMarkova KristinaKobold SebastianRollenske TimGeyer MatthiasMenzel StephanBald TobiasSchmid-Burgk Jonathan LHagelueken GregorHölzel Michael - Small bowel gastrointestinal stromal tumors (GISTs) are more aggressive than gastric GISTs, yet the biologic basis for this difference remains poorly understood. We hypothesized that differential expression of immune checkpoints contributes to this site-specific behavior. Bulk RNA sequencing of 42 primary GISTs (36 gastric, 6 small bowel) revealed marked upregulation of , which encodes the inhibitory checkpoint B7-H4, in small bowel tumors (logFC = 7.95, adjusted < 0.001). In contrast, expression of the therapeutically targeted checkpoints PD-L1, PD-1, and CTLA-4 was comparable between sites. Concordantly, B7-H4 enrichment was accompanied by an immunosuppressive tumor microenvironment, characterized by reduced antigen-presenting cells, fewer effector-memory CD8 T cells, lower granzyme B expression, and suppression of interferon and inflammatory signaling pathways. Notably, the differences in B7-H4 expression were independent of imatinib-treatment status. These findings were corroborated in an external cohort of 77 untreated GISTs, in which was similarly enriched in small bowel tumors. Independent immunohistochemical analysis of a tissue microarray comprising 68 untreated primary GISTs confirmed the pattern, showing median B7-H4 positivity of 78.6% in duodenal, 20.5% in jejunal/ileal, and 0% in gastric tumors, with staining localized to tumor cells rather than stroma. Collectively, these data identify B7-H4 as a site-specific feature of small bowel GISTs and a potential therapeutic target for tumors that have not responded to conventional checkpoint blockade. - Source: PubMed
Publication date: 2026/08/08
Singer HenryMorris MontanaMaestro RobertaTos Angelo Paolo DeiDeMatteo Ronald PVitiello Gerardo A