ADAMTS4
- Known as:
- ADAMTS4
- Catalog number:
- 001157A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAMTS4
Related genes to: ADAMTS4
- 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
Related products to: ADAMTS4
Related articles to: ADAMTS4
- 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 - Cerebral amyloid-β (Aβ) deposition is a pathological hallmark of the earliest phases of Alzheimer disease (AD). We previously reported APP669-711 as a novel Aβ-related peptide detectable in human plasma and developed a composite biomarker that combines APP669-711/Aβ1-42 and Aβ1-40/Aβ1-42 ratios to serve as a plasma surrogate of cerebral Aβ burden. We also identified ADAMTS4 (a disintegrin and metalloproteinase with thrombospondin type 1 motif 4) as an APP669-cleaving enzyme that catalyzes the rate-limiting step of APP669-711 production. However, ADAMTS4 accounts for approximately 40% of APP669-site cleavage, leaving the enzymes responsible for the remaining 60% unknown. Here, we identify ADAMTS5 (a disintegrin and metalloproteinase with thrombospondin type 1 motif 5) as a protease with stronger APP669-site cleavage activity in vitro. We further show that the difference in APP669-site cleavage activity between ADAMTS4 and ADAMTS5 is explained by the regulation through the spacer (Sp) domain. Nonetheless, in vivo experiments did not confirm a role for ADAMTS5 in plasma APP669-711 production under healthy conditions. Because ADAMTS5 expression increases in certain pathological states, our results suggest that ADAMTS5 may contribute to plasma APP669-711 production in AD patients with comorbid conditions. - Source: PubMed
Yokoyama MiyabisharaKobayashi HonokaKaneko NaokiNaito HirokiOta KazushiSekiya SadanoriIkemura KentaroOpoku GabrielHirohata SatoshiIwamoto ShinichiTanaka KoichiTomita Taisuke - Intervertebral disc degeneration (IDD) is the main cause of low back pain, which is closely related to an imbalance in extracellular matrix decomposition-anabolism mediated by immune inflammation. Duhuo Jisheng decoction (DHJSD) is effective in treating IDD, but its specific mechanism of action remains unclear and warrants further study. This study aimed to investigate the role of DHJSD in IDD treatment and its underlying mechanisms of action, providing potential therapeutic targets for IDD. - Source: PubMed
Publication date: 2026/03/23
Feng JingXu LeiMiao Hong-YanDu Shi-YangWang Jun-HuiCao XinLiu WeiWang Yun-Tao