GZMA
- Known as:
- GZMA
- Catalog number:
- Y214411
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GZMA
Related genes to: GZMA
- Gene:
- GZMA NIH gene
- Name:
- granzyme A
- Previous symbol:
- HFSP, CTLA3
- Synonyms:
- -
- Chromosome:
- 5q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-31
- Date modifiied:
- 2016-10-05
Related products to: GZMA
anti-GZMA (4C6)anti-GZMA(4C6)Antibody to Granzyme A (GZMA) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitAntibody to Granzyme A (GZMA) Organism: Mus musculus (Mouse) Type: Polyclonal Source: RabbitBiotin-linked Antibody to Granzyme A (GZMA); Reactivity: Mus musculus (Mouse) Clonality: Polyclonal Source: RabbitBovine granzyme A (granzyme 1, cytotoxic T-lymphocyte-associated serine esterase 3) (GZMA) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Granzyme A(GZMA) ELISA kitBovine Granzyme A(GZMA) ELISA kit SpeciesBovineChicken GzmA (Granzyme A) ELISA KitChicken GzmA (Granzyme A) ELISA KitCLIA Autocrine thymic lymphoma granzyme-like serine protease,Ctla3,CTLA-3,Ctla-3,Fragmentin-1,Granzyme A,Gzma,Mouse,Mtsp-1,Mus musculus,T cell-specific serine protease 1,TSP-1CLIA Bos taurus,Bovine,Granzyme A,GZMACLIA CTL tryptase,CTLA3,Cytotoxic T-lymphocyte proteinase 1,Fragmentin-1,Granzyme A,Granzyme-1,GZMA,H factor,Hanukkah factor,HF,HFSP,Homo sapiens,HumanELISA Autocrine thymic lymphoma granzyme-like serine protease,Ctla3,CTLA-3,Ctla-3,Fragmentin-1,Granzyme A,Gzma,Mouse,Mtsp-1,Mus musculus,T cell-specific serine protease 1,TSP-1ELISA Bos taurus,Bovine,Granzyme A,GZMA Related articles to: GZMA
- Immune checkpoint inhibitors (ICIs) enhance antitumor responses by blocking inhibitory receptors, including PD-1 and CTLA-4. Overactivation can trigger systemic toxicity akin to autoimmune diseases, including kidney manifestations. We sought to 1) profile immune signaling and 2) interrogate potential mechanisms of ICI-related kidney injury in a Human Immune System (HIS) tumor-bearing mouse model treated with nivolumab and ipilimumab. - Source: PubMed
Publication date: 2026/05/12
Asby SarahWen XiaGoedken MichaelAmes BriannaShams ShamsThompson Lauren ELanis JordiKostka-Newman ZanderLarsen KristinaTilden ScottLang JulieAleksunes Lauren MJoy Melanie S - Feline chronic gingivostomatitis (FCGS) is a debilitating oral disease characterized by immune dysregulation and chronic inflammation. We hypothesized that CD8 + T cells from FCGS cats exhibit exhaustion features with suppressed mitochondrial pathways, and that mesenchymal stromal cell (MSC) therapy post-extractions might restore these programs. RNA sequencing was performed on peripheral CD8 + T cells from cats with active FCGS before (disease group, D) and after (treated group, M) clinical remission following full-mouth extractions and MSC therapy, with specific-pathogen-free cats as controls (control group, C). CD8 + T cells from active disease displayed terminal effector differentiation and exhaustion-like signatures, including upregulation of cytotoxic markers (GZMB, GZMK, GZMA), differentiation markers (KLRG1, IL18R1/IL18RAP), and exhaustion-associated genes (EOMES, CD244, TNFSF10, CCR5, PRDM1, RGS16). Gene set enrichment analysis confirmed exhaustion-like CD8 + T-cell phenotype enrichment in active disease, which resolved after treatment. Pathway analysis revealed marked downregulation of mitochondrial respiratory chain components, ATP synthesis, and protein import pathways in active FCGS, with partial post-treatment resolution. Immunofluorescence of draining lymph nodes showed significantly increased CTLA-4 + CD3+ T cells in both FCGS groups versus controls, suggesting persistent immunoregulatory signaling despite clinical improvement. These findings identify overlapping T-cell exhaustion and mitochondrial dysfunction-associated transcriptomic signatures in FCGS, supporting therapeutic strategies targeting immune-metabolic pathways. - Source: PubMed
Publication date: 2026/05/06
Soltero-Rivera MariaWanakumjorn PatrawinChen YihongBarnum SamanthaCharpentier Luis Diego CastilloArzi BoazArzi Natalia VapniarskyKol Amir - Oligoarticular juvenile idiopathic arthritis (oligo JIA) is the most common JIA subtype and is often complicated by uveitis, a potentially sight-threatening comorbidity. Despite its prevalence, the immunopathogenic mechanisms underlying oligo JIA and its extra-articular manifestations remain poorly understood. The objective was to characterize the immune landscape of oligo JIA and identify pathogenic cell populations and regulatory mechanisms associated with the disease and uveitis. - Source: PubMed
Publication date: 2026/04/27
Lopez-Corbeto MireiaGuillén YolandaJiménez-Gracia LauraMoreno-Ruzafa EstefaníaAlvarez-Errico DamianaPalau NúriaMartín-Begué NievesHeyn HolgerJulià AntonioMarsal Sara - This study aimed to systematically search for molecular biomarkers that contribute to the risk of coronary artery disease (CAD). - Source: PubMed
Publication date: 2026/04/09
Nikpay Majid - The efficacy of neoantigen vaccine for advanced hepatocellular carcinoma (HCC) is limited largely due to insufficient T cell mobilization and activation. Herein, we develop a spleen-targeted neoantigen mRNA vaccine (STNvac) with highly efficient spleen-selective mRNA transfection. Using a three-dose vaccination regimen, STNvac demonstrates remarkable therapeutic efficacy in orthotopic HCC model with a high likelihood of complete tumor regression and significantly improved survival rates (p < 0.0001). Notably, we identify a distinct ISG15 CD8 T cell population as crucial mediators of STNvac-induced immunity with potent antigen-processing and cytotoxic capacities. Intriguingly, STNvac promotes the formation of tertiary lymphoid structures (TLSs) through GZMA-F2R-mediated interactions between ISG15 CD8 T cells and antigen-presenting cells (APCs), which is also confirmed in HCC patients. Taken together, our findings demonstrate the potent antitumor efficacy of spleen-targeted mRNA vaccine and reveal its underlying immune cell interactive mechanisms, presenting high potential for clinical translation. - Source: PubMed
Publication date: 2026/04/20
Lin XinyiChen GengTang RuijingWu MingZhang DaLin FangzhouGuan JianhuaYang JingDong XiuqingZheng XiaoyuanQiu LimanYu HaijunCai ZhixiongLiu Xiaolong