ADAMTS6
- Known as:
- ADAMTS6
- Catalog number:
- 001159A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAMTS6
Related genes to: ADAMTS6
- Gene:
- ADAMTS6 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 6
- Previous symbol:
- -
- Synonyms:
- ADAM-TS6
- Chromosome:
- 5q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-06
- Date modifiied:
- 2016-10-05
Related products to: ADAMTS6
Related articles to: ADAMTS6
- The ADAMTS family are extracellular matrix (ECM) proteins and enzymes involved in regulating tissue structure and function. The ECM is a network of proteins and polysaccharides surrounding the cells that provide support and maintain cellular function. Mutations to proteins in the ECM lead to systemic connective tissue disorders by disrupting the structural integrity and maintenance of the ECM, resulting in ocular, musculoskeletal, skin, and cardiovascular abnormalities. Mutations that arise from the ADAMTS family lead to specific connective tissue disorders with distinct clinical characteristics. Here, we detail these distinct clinical features of major connective tissue disorders that arise from mutations in the ADAMTS family proteins. These include Ehlers Danlos syndrome arising from mutation in , Geleophysic Dysplasia from 2, Weill-Marchesani Syndrome from and , Ectopia lentis from , thoracic aortic aneurysms and dissection from , valvular disease in , and a further connective tissue disorder from mutations in This review details the mechanisms in which mutations to these genes impair the structure of the ECM, leading to the variety of phenotypic outcomes seen in connective tissue disorders. - Source: PubMed
Publication date: 2026/03/31
Alcocer Ana DRush Elizabeth HMead Timothy J - A disintegrin and metalloproteinase with thrombospondin motifs 6 (ADAMTS6) is an extracellular matrix (ECM) protease that promotes the invasion of lung adenocarcinoma (LUAD) cells. Herein, we investigate its role in epithelial-mesenchymal transition (EMT), a process that drives metastasis and drug resistance in LUAD. Re-analysis of microarray and RNA sequencing data from LUAD cells revealed that during EMT, TGF-β1 increased expression, presumably through the SMAD pathway, as SMAD2 loss completely blocked this effect. Moreover, was shown to occupy hub positions within TGF-β1-associated gene networks. Using additional datasets, we found that expression increased under other EMT-inducing conditions, including IL-1β induction and acquired gefitinib resistance, but decreased upon knockdown of Twist1, a master regulator of EMT. Knockout of repressed colony formation, migration, invasion, and doxorubicin resistance but enhanced cell-ECM adhesion in A549 cells. This effect was mediated by EMT inhibition, evidenced by upregulation of E-cadherin and downregulation of N-cadherin, vimentin, and Twist1, and was accompanied by suppressed nuclear translocation of the NF-κB p65 subunit. Re-analysis of transcriptomic data from patient tumors demonstrated that high expression correlated with the expression of EMT markers, further supporting the -EMT link. Moreover, high expression was associated with worse survival prognosis. Overall, promotes EMT in LUAD cells and may be considered a marker of this process, as well as a potential therapeutic target for its inhibition. - Source: PubMed
Publication date: 2025/12/08
Odarenko Kirill VMatveeva Anastasiya MStepanov Grigory AZenkova Marina AMarkov Andrey V - Prior analysis of mouse embryos homozygous for a point mutation (p.Ser149Arg) that abrogated secretion of the protease, ADAMTS6, showed that it is essential for cardiovascular and limb development. Because mice do not survive past birth, it is currently not feasible to investigate ADAMTS6 in specific cellular lineages postnatally. Therefore, we generated a conditional allele using CRISPR-Cas9-mediated genome editing to insert unidirectional loxP sites flanking the first coding exon in , resulting in a frameshift mutation after loxP recombination. Mice homozygous for the unrecombined floxed allele ( ) are viable, fertile, and without overt phenotype. embryos, generated upon constitutive recombination induced by a -Cre transgene, also do not survive past birth and have identical defects in the heart and limbs as embryos, demonstrating efficient transgene recombination. In addition to previous defects in cardiovascular and limb development, embryos have reduced airway branching, thereby identifying a role for ADAMTS6 in lung maturation. This newly generated allele makes feasible analysis of ADAMTS6 secreted by cells of different lineages and during specified temporal windows during developmental processes as well as in disease models. - Source: PubMed
Publication date: 2025/11/19
Sirek Jessica MRush Elizabeth HDarodkar AditiApte Suneel SMead Timothy J - Perfluoroundecanoic acid (PFUnA) is a long-chain perfluoroalkyl substance. However, whether PFUnA affects liver development during puberty is still unclear. Male 35-day-old Sprague-Dawley rats were gavaged with 0 (corn oil), 1, 5, and 10 mg/kg/day of PFUnA for 21 days. Liver weight was remarkably increased by PFUnA at ≥1 mg/kg, while serum alanine aminotransferase levels were higher at 5 and 10 mg/kg. PFUnA upregulated the expression of , and and downregulated the expression of , and . These changes were also confirmed at the protein level. It increased the release of inflammatory factors (IL-1β, IL-6, and TNF-α). It also downregulated the fibrosis-related gene expression of and . Similar results were obtained in HepG2 cells treated with 50 μM PFUnA in vitro. PFUnA induced oxidative stress and perturbed lipid metabolism. Overall, PFUnA may induce oxidative stress and disrupt lipid metabolism to have an inhibitory influence on pubertal liver development. - Source: PubMed
Publication date: 2025/10/15
Li ZengqiangGuo ChaoqunYe XinyiXu QiangWeng LijunGao YouguangGe Ren-ShanLin Xianzhong - A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) protease family involves a critical member ADAMTS6, which is implicated in the pathogenesis of various cancers. This study explores the function of ADAMTS6 in tumor growth and angiogenesis in gastric carcinoma (GC). Using the TCGA-STAD dataset, key genes closely associated with GC prognosis were screened, and their correlation with the angiogenesis pathway was evaluated. In vitro, a GC cell model with ADAMTS6 knockdown was established, and cell proliferation, migration, invasion, and apoptosis were systematically assessed. The regulatory effect of ADAMTS6 on the angiogenic capacity of human umbilical vein endothelial cells (HUVECs) was determined via tube formation assay. In vivo, a GC xenograft mouse model was established to monitor tumor growth, and the effects of ADAMTS6 knockdown on tumor proliferation, apoptosis, and angiogenesis were comprehensively evaluated using immunohistochemistry, TUNEL staining, immunofluorescence, and Western blot analysis. ADAMTS6 was highly expressed in GC tissues and cell lines, and its expression was positively correlated with poor prognosis and tumor angiogenesis. Silencing ADAMTS6 significantly inhibited GC cell proliferation, migration, and invasion, while inducing apoptosis and attenuating the pro-angiogenic effect on HUVECs in vitro. Consistently, in vivo experiments confirmed that ADAMTS6 knockdown markedly suppressed tumor growth, as evidenced by reduced tumor volume and weight. Moreover, the expression of angiogenesis-related markers was downregulated following ADAMTS6 silencing. ADAMTS6 facilitates tumor growth and angiogenesis in GC and might act as a valuable biomarker for prognosis and a candidate target for anti-angiogenic therapeutic approaches. - Source: PubMed
Publication date: 2025/10/27
Luo KangningHu Bingbing