ADAMTS17
- Known as:
- ADAMTS17
- Catalog number:
- 001169A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADAMTS17
Related genes to: ADAMTS17
- Gene:
- ADAMTS17 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 17
- Previous symbol:
- -
- Synonyms:
- FLJ32769, FLJ16363
- Chromosome:
- 15q26.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-13
- Date modifiied:
- 2016-10-05
Related products to: ADAMTS17
Related articles to: ADAMTS17
- 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 - To investigate the genetic architecture of high myopia. - Source: PubMed
Publication date: 2026/03/19
Morino KazuyaMeguro AkiraNagasaki MasaoMotoike Ikuko NAkiyama MasatoKawaguchi TakahisaNuma ShogoMori YukiYasukura ShotaAkada MasahiroNakao Shin-YaKamei TakuroNakata AiTakeuchi MasakiYamada NorihiroMizuki YukiYoshida TakeshiMomozawa YukihideKamatani YoichiroAnzawa HayatoTabara YasuharuMatsuda FumihikoKinoshita KengoOhno-Matsui KyokoFuse NobuoYamamoto MasayukiTsujikawa AkitakaMizuki NobuhisaMiyake Masahiro
- Source: PubMed
- 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 - Weill–Marchesani syndrome (WMS) is a rare connective tissue disorder. The main clinical features include short stature with a stocky build, brachydactyly, joint stiffness, and microspherophakia. The syndrome can be inherited in an autosomal dominant manner due to heterozygous pathogenic variants in , as well as in an autosomal recessive manner associated with biallelic pathogenic variants in ,, or Despite differences in inheritance patterns, the clinical manifestations are consistent. Therefore, clinical diagnosis requires genetic testing of the proband to determine the genotype, confirm the diagnosis. - Source: PubMed
Publication date: 2026/02/04
Li MengyangBai RongLian YuanyuanShu CanLi HuipingSheng Xunlun