ESX1 Antibody
- Known as:
- ESX1 Antibody
- Catalog number:
- GWB-56CD41
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- ESX1 Antibody
Related genes to: ESX1 Antibody
- Gene:
- ESX1 NIH gene
- Name:
- ESX homeobox 1
- Previous symbol:
- ESX1L
- Synonyms:
- ESXR1
- Chromosome:
- Xq22.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-03-14
- Date modifiied:
- 2014-11-19
Related products to: ESX1 Antibody
Related articles to: ESX1 Antibody
- The mycobacterial ESX-1 (Type VII) secretion system is essential for virulence and induces the NLRP3 inflammasome activation. However, the specific bacterial effectors involved in this process, beyond the well-characterized EsxA (ESAT-6), remain largely unidentified. Through systematic screening of ESX-1 effectors, we identified EspF as a potent and evolutionarily conserved activator of the NLRP3 inflammasome across pathogenic mycobacterial species, including , , and . Our results demonstrate that EspF significantly augments the mature IL-1β and IL-18 release, ASC speck formation, caspase-1 activation, and gasdermin D (GSDMD)-mediated pyroptosis in THP-1 cells. Notably, infection with or BCG strain overexpressing EspF significantly enhanced NLRP3 inflammasome activation and pyroptosis, which were completely abolished in NLRP3-deficient cells. Mechanistically, EspF directly interacts with the NACHT and LRR domains of NLRP3. Furthermore, unbiased proteomic screening identified the host E3 ubiquitin ligase TRIM25 as an indispensable binding partner. In THP-1 cells, we confirmed the endogenous interaction and colocalization of the EspF-TRIM25-NLRP3 complex, demonstrating that EspF functions as a molecular scaffold that bridges TRIM25 to NLRP3. This proximity interaction, further validated during mycobacterial infection, facilitates TRIM25-mediated K63-linked ubiquitination of NLRP3. , mice infected with BCG strains overexpressing EspF exhibited exacerbated lung lesions, increased inflammatory cell infiltration, and higher bacterial burdens. Collectively, these findings reveal EspF-TRIM25-NLRP3 axis is a novel mechanism of mycobacterial pathogenesis that drives hyperinflammation to facilitate bacterial survival and dissemination. - Source: PubMed
Publication date: 2026/09/08
Yang YangHan YixinWu LongjianZang XinxinXu WeiLi YunjieXu AhuiJiang HexiangFan JingyanCui LuqingHuang BeiHe GuiqingSong Houhui - The genus exerts a strong selective force, shaping the evolution and structure of innate immune systems across various hosts and revealing overarching, conserved principles of host defense. Despite their phylogenetic distance, amoebae, nematodes, insects, wax moth larvae, and zebrafish share fundamental innate immune strategies while also exhibiting key differences in tissue organization, immune complexity, and the presence or absence of adaptive immunity. This comparative review synthesizes insights from these systems to highlight both the conserved mechanisms that mycobacteria repeatedly exploit and the lineage-specific features that shape host susceptibility. Amoebae demonstrate ancient, cell-autonomous defenses, including nutritional immunity through metal trafficking (Nramp1/zinc intoxication) and membrane repair pathways (ESCRT/autophagy) against the ESX-1 system. Moving to metazoans, the importance of conserved signaling, such as the p38 MAPK (PMK-1) pathway in , becomes evident, which actively suppresses via VHP-1. In other invertebrates, such as , integrated immunometabolism is present, in which disruption of the Akt-FOXO axis causes a conserved wasting syndrome, and mimics chronic TB pathology by forming granuloma-like structures with lipid-accumulating hemocytes and demonstrating innate immune priming. Larval zebrafish, which depend solely on innate immunity, show pathogen-driven granuloma formation and spread, with ESX-1 mediating pro-necrotic cell death and the Asc-dependent inflammasome contributing to restriction. Overall, these cross-species comparisons demonstrate how mycobacteria exploit foundational host mechanisms while revealing the evolutionary breadth and limits of innate immune strategies across the animal kingdom. - Source: PubMed
Publication date: 2025/12/12
Cortacans MarionaCardona Pere-Joan - Spatiotemporal environmental variation results in marked heterogeneity in bacterial infection progression and disease outcome, with vital consequences for treatment success. For the globally important pathogen (Mtb), while the pronounced intra-host spatial heterogeneity in lesion immune cell composition and phenotype has been well-described, the highly complex Mtb cell envelope has presented a particular challenge for the required equivalent insight into bacterial heterogeneity. Here, we develop hybridization chain reaction-fluorescence in situ hybridization (HCR-FISH)-based methodology for Mtb mRNA visualization in the context of intact lung and lesion architecture. In combination with an Mtb transcriptional/translational activity reporter, we reveal spatiotemporal differences in gene expression relating to Mtb lipid metabolism, response to key environmental signals, and the ESX-1 type VII secretion system. Our results establish a framework for in situ analysis of Mtb mRNA, opening the path to elucidating critical bacterial drivers that underlie the marked heterogeneity in Mtb-host interactions. - Source: PubMed
Publication date: 2026/08/12
Lawrence Anna-Lisa ETan Shumin - Eurasian red squirrels were acknowledged as a reservoir for secular leprosy in the British Isles, after detection of in specimens dating back to the 11th century. In order to question the situation of Pallas's squirrels () recently introduced to the European continent, we investigated a series of 522 samples (241 liver, 241 spleen, and 40 faecal samples) collected from 281 deceased specimens by means of controlled quantitative PCR targeting the specific RLEP repetitive element, the RLPM repetitive element, and the most closely related ESX-1 locus gene. Successful amplification of the internal control certified the absence of PCR inhibition in any samples, which all tested negative for complex DNA. Because tissues potentially involved in localized infection were not studied in the absence of clinical signs and the study was geographically restricted, these results cannot be extrapolated beyond dismissed systemic leprosy in tested animals. Nevertheless, the congruency of present data with equally negative ones reported in various continental squirrel populations suggests that, in Europe zoonotic leprosy is restricted to British Islands' red squirrel population. - Source: PubMed
Publication date: 2026/07/20
Souguel SNdiaye A M R AGrine GMakoudi HMaillard J-FBedjaoui SLaidoudi YDavoust BDrancourt M - Tuberculosis (TB) remains a leading cause of infectious disease mortality worldwide, driven by the emergence of drug-resistant Mycobacterium tuberculosis (Mtb) strains and the limited efficacy of current therapeutic strategies. Over the past two decades, Mycobacterium marinum (M. marinum), a close genetic relative of Mtb, has emerged as a powerful surrogate model for investigating conserved mechanisms of TB pathogenesis and accelerating early-stage therapeutic discovery. As a naturally pathogenic mycobacterium, M. marinum shares key virulence determinants with Mtb, including ESX-1-dependent secretion, intracellular survival strategies, lipid-mediated immune modulation, and the ability to induce granulomatous disease. Its compatibility with diverse experimental systems-ranging from macrophage cultures to genetically tractable vertebrate hosts such as zebrafish-enables real-time visualization of host-pathogen interactions, granuloma dynamics, immune regulation, and bacterial dissemination in vivo. In addition to mechanistic pathogenesis studies, M. marinum provides a scalable platform for phenotypic drug screening, host-directed therapeutic discovery, and early in vivo evaluation of antimicrobial candidates, thereby bridging the gap between in vitro assays and mammalian infection models. This review synthesizes recent advances in the use of M. marinum across pathogenesis research, functional genomics, and drug discovery, critically examining its strengths, limitations, and optimal positioning within multi-tiered tuberculosis research pipelines. - Source: PubMed
Publication date: 2026/08/04
Aspatwar Ashok