CASP5 ELISA kit
- Known as:
- CASP5 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CASP5-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CASP5 ELISA kit
Related genes to: CASP5 ELISA kit
- Gene:
- CASP5 NIH gene
- Name:
- caspase 5
- Previous symbol:
- -
- Synonyms:
- ICE(rel)III
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-09-13
- Date modifiied:
- 2016-10-05
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- Recent research has identified pyroptosis as a distinct form of programmed cell death that is strongly correlated with tumor outcomes. However, its value as a prognostic biomarker in clear cell renal cell carcinoma (ccRCC) is not yet fully established. - Source: PubMed
Li GuijiaoLi YuerongXu WuYan LingfeiXiang QiLuo YangLiu YufengLi QingLi CuilianWang Tao - Chronic spontaneous urticaria (CSU) involves mast cells and multiple immune pathways, yet mechanisms sustaining disease chronicity remain incompletely defined. - Source: PubMed
Publication date: 2026/04/21
Abboud AlexiaOsakwe AdrienMartinez-Jaramillo ElvisKhoury LaurenVu DonChergui MayLefrançois PhilippeXu LiqinBen-Shoshan MosheOsman MohamedGiménez-Arnau Ana MariaLi YueNetchiporouk Elena - Tuberculous meningitis (TBM), the most severe form of Mycobacterium tuberculosis infection, is characterized by high mortality and neurological sequelae, largely attributed to blood-brain barrier (BBB) disruption. While recent studies identified GSDMD-mediated endothelial pyroptosis as a key mechanism of inflammatory BBB damage, the full molecular landscape in TBM remains unclear. - Source: PubMed
Publication date: 2026/06/03
Luan MengyuChen XiaoyouLu Yu - Sepsis-induced acute lung injury (ALI) is a frequent and life-threatening complication of sepsis, yet clinically actionable transcriptomic biomarkers remain limited. Regulated/programmed cell death (PCD) pathways shape inflammatory injury and barrier dysfunction, but their cell-type-specific transcriptional signatures in sepsis-induced ALI are incompletely defined. - Source: PubMed
Publication date: 2026/06/03
Li XinLiu WeihongZhang YucuiXiang GuohanBi QianyuLin XinLiu YangBa TejinKong LiLiu YangHao Hao - Inflammasomes are signaling platforms that activate inflammatory caspases to initiate innate immune responses. Canonical inflammasomes sense diverse threats and activate CASP1, which cleaves the pro-inflammatory cytokines IL-1β and IL-18 and the pore-forming protein gasdermin D (GSDMD) to induce pyroptosis. In contrast, the non-canonical inflammasome senses bacterial lipopolysaccharide (LPS) through CASP4 and CASP5 to induce pyroptosis. While CASP1 substrates are well defined, those of CASP4 and CASP5 remain less understood. Here, we show that intracellular LPS and the gram-negative bacterial pathogen Salmonella activate CASP4/5 in macrophages to directly cleave and activate CASP3 and CASP7. Activated CASP3 subsequently cleaves gasdermin E (GSDME). Surprisingly, CASP3, but not GSDME, was required for restricting intracellular Salmonella replication, suggesting a protective role for apoptotic signaling. We further find that most GSDMD cleavage during non-canonical signaling is mediated by CASP1. Consistent with this, loss of GSDMD, but not GSDME, reduced LDH release, establishing GSDMD as the primary driver of pyroptosis during LPS transfection. In contrast, during Salmonella infection, cell lysis occurred independently of both GSDMD and GSDME, suggesting the involvement of alternative lytic mechanisms. Finally, we demonstrate that CASP4/5 activation of CASP3/7 and GSDME occurs in human primary macrophages, defining CASP4/5 as dual apoptotic initiator and inflammatory caspases in innate immunity. - Source: PubMed
Publication date: 2026/04/27
Kulkarni MadhuraBourne Christopher MMahale Ashutosh BExconde Patrick MMurphy CeceliaGoodrow Haley TCervantes SofiaKardhashi MatildaKambayashi MiraiYoo WilliamWrong Tristan JPatio Robert CDischer Bohdana MTaabazuing Cornelius Y