Ask about this productRelated genes to: GZMA antibody
- 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 antibody
Related articles to: GZMA antibody
- IgG4-related disease (IgG4-RD) predominantly affects middle-aged and elderly individuals; however, the impact of aging on lesional immune architecture remains poorly understood. - Source: PubMed
Publication date: 2026/09/04
Yamamoto MotohisaKamekura RyutaUehara MasaakiIchii YutaTakano Kenichi - Perfluorooctanoic acid (PFOA) has been associated with damage to multiple organs, and its effects on the gastrointestinal system have attracted increasing attention. However, the mechanism underlying PFOA-induced intestinal toxicity remains unclear. In this study, we found that PFOA disrupted the intestinal barrier and induced intestinal inflammation in mice, accompanied by increased GzmA expression. Mechanistically, GzmA upregulation promoted intestinal inflammation through the GzmA-PAR1 signaling axis, which enhanced the interaction between caveolin-1 and β-catenin and facilitated the nuclear accumulation of β-catenin. Nuclear β-catenin subsequently upregulated TBX3, which bound to an upstream regulatory of IL24 and promoted IL24 expression following PFOA exposure. To validate the role of GzmA, we knocked down GzmA in normal colonic epithelial cells (NCM460). The results confirmed that GzmA upregulated IL24 expression through the PAR1/β-catenin/TBX3 pathway following PFOA exposure. These findings provide mechanistic insight into PFOA-induced colonic inflammation and highlight the potential utility of this toxicant-based model for investigating molecular targets relevant to intestinal inflammatory diseases. - Source: PubMed
Publication date: 2026/09/03
Li Ya-NanWang XuemeiZhang LeiWang Peng-PuZhang Jian-QiangFang XinCheng Yu-YaoZhao Xing-YuWang Feng-Hong - Periodontitis (PD) is a chronic inflammatory disease characterized by dysregulated immune responses and periodontal tissue destruction. While T lymphocytes are implicated in PD pathogenesis, the roles of specific T cell subsets remain unclear. - Source: PubMed
Publication date: 2026/08/24
Ren FukaiLiu XiqianYan Bin - Neurodegenerative diseases are increasingly recognized as disorders shaped not only by intrinsic neuronal vulnerability, but also by chronic neuroinflammation mediated by maladaptive neuroimmune signaling. Granzymes, a family of serine proteases classically studied for their cytotoxic roles in anti-viral and anti-tumor immunity, are emerging as important mediators of central nervous system (CNS) pathology. In addition to their canonical intracellular functions, granzymes can act extracellularly to cleave the extracellular matrix (ECM), activate cell-surface receptors, disrupt epithelial barrier function, amplify inflammatory cascades, and alter glial and neuronal responses to injury. In this review, we synthesize current knowledge on the roles of Granzyme A (GzmA), Granzyme B (GzmB), Granzyme H (GzmH), and Granzyme K (GzmK) in neurodegeneration and neuroinflammation across diverse CNS disease and injury contexts, such as Alzheimer's disease (AD), multiple sclerosis (MS), stroke, spinal cord injury (SCI), and age-related macular degeneration (AMD). GzmB is the most extensively characterized, with evidence supporting both intracellular neurotoxicity and extracellular pathogenic functions mediated through protease-activated receptor signaling, ECM cleavage, outer blood-retina barrier disruption, angiogenesis, fibrosis, and chronic inflammation. GzmA is implicated in tau proteolysis and structural destabilization of neurons and astrocytes, while GzmK has emerged as a context-dependent regulator of neuroinflammation through PAR-1 activation, microglial modulation, and complement cascade activation. GzmH remains the least understood but may contribute to nerve injury through mechanisms that are only beginning to be defined. We also discuss endogenous and pharmacological granzyme inhibition, highlighting the therapeutic promise of selective extracellular granzyme targeting, particularly for GzmB, while emphasizing the current lack of selective inhibitors for GzmA, GzmK, and GzmH. Collectively, these findings position granzymes as underappreciated neuroimmune effectors and potential therapeutic targets in neurodegenerative diseases and CNS injury. - Source: PubMed
Publication date: 2026/08/18
Yoo Hyung-SukYu PhilipZhou CeresHosseini AmirGranville David JMatsubara Joanne A - Allergic rhinitis (AR) is a prevalent condition characterized by an immunoglobulin E (IgE)-mediated immune response. T follicular helper (TFH) cells regulate B-cell differentiation and antibody production, and circulating TFH2 cells are closely associated with type 2 humoral immunity and IgE-related responses in AR. However, whether AR is marked by isolated TFH2 expansion or broader remodeling of circulating TFH (cTFH) subsets, including TFH1-related heterogeneity, remains unclear. - Source: PubMed
Publication date: 2026/07/30
He JiejunSun YueqiChen YangLai YinyanLei HanShi JianboGao Wenxiang