ADAMTS4 ELISA kit
- Known as:
- ADAMTS4 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAMTS4-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAMTS4 ELISA kit
Related genes to: ADAMTS4 ELISA kit
- Gene:
- ADAMTS4 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 4
- Previous symbol:
- -
- Synonyms:
- KIAA0688, ADAMTS-2, ADMP-1
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-15
- Date modifiied:
- 2016-10-05
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- Idiopathic pulmonary fibrosis is the most common and aggressive form of interstitial lung disease. Despite extensive research on the pathomechanisms of fibrogenesis, little is known about the mechanisms of fibrosis resolution. Here, lineage tracing of alveolar fibroblasts was carried out during fibrosis development and delayed resolution in aged mice. Histological analyses, single-cell transcriptomics, and ex vivo models including alveolar organoids and precision-cut lung slice cultures were employed. The data reveal that lipofibroblasts contribute to myofibroblast formation during fibrogenesis, with the reverse differentiation trajectory occurring during fibrosis resolution. Importantly, delayed resolution is associated with the persistence of ADAM metallopeptidase with thrombospondin type 1 motif 4-positive (ADAMTS4+) cells. Investigation of human lung transplant tissues, single-cell and spatial transcriptomic datasets, and functional ex vivo interventions reveal strong clinical relevance. Our study underscores the significance of the lipofibroblast-to-myofibroblast reversible switch in fibrosis development and resolution and identifies ADAM metallopeptidase with thrombospondin type 1 motif 4 as a potential therapeutic target in human lung fibrosis. - Source: PubMed
Publication date: 2026/05/08
Zabihi MahsaKhadim AliLingampally ArunVazquez-Armendariz Ana IvonneHadzic StefanPanagiotidis Georgios-DimitriosKalina DanielHalweg JanProcida-Kowalski TaraBartkuhn MarekChu XuranKoepke JanineSamakovlis ChristosBoehm MarioWeissmann NorbertGünther AndreasSeeger WernerBraubach PeterHerold SusanneWygrecka MalgorzataBellusci SaverioEl Agha Elie - A disintegrin and metalloproteinase with thrombospondin motifs 4 (ADAMTS4) has been implicated in arthritis and lung fibroblast activation; however, its role in liver homeostasis and fibrogenesis remains largely unexplored. Here, we investigated the functional significance of ADAMTS4 in liver fibrosis. We found that hepatic ADAMTS4 mRNA expression was significantly elevated in patients with fibrotic steatohepatitis. In mouse models of liver fibrosis, genetic deletion of ADAMTS4 protected against liver fibrogenesis, accompanied by a marked reduction in the recruitment of myeloid-derived infiltrating macrophages. Mechanistically, ADAMTS4-mediated cleavage of versican generated versikine, which promoted macrophage migration and differentiation toward a pro-inflammatory phenotype in vitro. In addition, tumor necrosis factor (TNF)α significantly increased both the mRNA expression and protein secretion of ADAMTS4. Furthermore, ADAMTS4 directly induced collagen accumulation through activation of signal transducer and activator of transcription 3 (STAT3) in LX2 cells. To explore the potential genetic regulation of ADAMTS4 expression, we performed response-eQTL analysis in patients with metabolic dysfunction-associated steatotic liver disease and identified a single-nucleotide polymorphism associated with increased ADAMTS4 expression in a subset of patients carrying a specific genotype. Collectively, our findings identify ADAMTS4 as a critical regulatory factor that promotes the recruitment of myeloid-derived infiltrating macrophages and collagen accumulation during liver fibrogenesis, suggesting that targeting ADAMTS4 may represent a potential therapeutic strategy for liver fibrosis. - Source: PubMed
Publication date: 2026/05/06
Park JeongwooKim TaeeungShim Wan SeobHong Sung EunPark MisoOh SeungseokKoo Bo KyungLee Dong HyeonJoo Sae KyungYoo TaekyeongLee Young JooLim Sung-ChulSeo Seung-YongKim Kyu MinNieto NataliaChoi MurimKim WonKang Keon Wook - Osteosarcoma (OS) is an aggressive bone malignancy characterized by genomic instability and extensive extracellular matrix (ECM) remodeling. Members of the are matrix-associated proteases implicated in tumorigenesis; however, their roles in OS remain poorly defined. This study provides a comprehensive genomic, transcriptomic, and functional analysis of the ADAMTSs in OS, with particular focus on ADAMTS-3. Copy number alterations and mRNA expressions of ADAMTS genes were analyzed using the TCGA datasets. Gene set enrichment analysis and co-expression analyses identified biological processes associated with ADAMTS-3. Mechanistic studies investigated tumor necrosis factor-alpha (TNF-α) regulation of ADAMTS-3 in OS cells. Genomic profiling revealed frequent amplification and high mRNA expression of ADAMTS4, ADAMTS12, ADAMTS16, and ADAMTS17, indicating potential oncogenic activity. ADAMTS-3 was markedly overexpressed in OS tissues and cell lines, showing strong positive correlations with inflammatory (IL6, STAT3, NF-κB) and matrix-remodeling (MMP2, MMP9) genes. Functional enrichment indicated that ADAMTS-3 is associated with ECM organization, immune response regulation, and epithelial-mesenchymal transition. Mechanistically, TNF-α induced ADAMTS-3 transcription via activation of MEK, PI3K, JNK, and NF-κB pathways, with STAT3 and NF-κB by enhancing promoter activity. These findings identify ADAMTS-3 as an inflammation-responsive gene that links inflammatory signaling to ECM remodeling and tumor invasiveness in OS, representing a potential molecular bridge. - Source: PubMed
Publication date: 2026/05/03
Aymaz Ehed MuhammedAlper MeltemSav Feyza NurAydemir TuğşenKöçkar Feray - Postmenopausal female individuals are disproportionately affected by knee osteoarthritis (KOA), experiencing earlier onset and more severe pathology compared to their male counterparts. Despite this clinical disparity, the molecular mechanisms underlying female-specific vulnerability remain poorly defined. - Source: PubMed
Publication date: 2026/04/26
Katz Nicole BKhay Adam MDave Kandarp MCasey EllenAmbrosio FabrisiaIijima Hirotaka - ADAMTS4 is a secretory metalloproteinase involved in the pathogenesis of atherosclerosis. Both in vitro and in vivo model systems are used to study the regulation of ADAMTS4 in atherosclerosis. Here we describe three model systems: in vitro model system of macrophages and foam cells and in vivo model of high-fat-diet-induced atherosclerosis. We can use qPCR for studying the mRNA expression of ADAMTS4, while ELISA and Western blot can be employed to assess its protein expression. - Source: PubMed
Aswani S SBoban P TSaja K