ATS1_RAT ADAM-TS1 ELISA tesk kit
- Known as:
- ATS1_RAT ADAM-TS1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15881
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ATS1_RAT ADAM-TS1 ELISA tesk kit
Related genes to: ATS1_RAT ADAM-TS1 ELISA tesk kit
- Gene:
- ADAMTS1 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 1
- Previous symbol:
- -
- Synonyms:
- C3-C5, METH1, KIAA1346
- Chromosome:
- 21q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-19
- Date modifiied:
- 2015-11-09
- Gene:
- ADAMTS5 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 5
- Previous symbol:
- -
- Synonyms:
- ADMP-2, ADAMTS11
- Chromosome:
- 21q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-23
- Date modifiied:
- 2015-11-09
- Gene:
- ADAMTS16 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 16
- Previous symbol:
- -
- Synonyms:
- ADAMTS16s
- Chromosome:
- 5p15.32
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-13
- Date modifiied:
- 2016-10-05
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- The purpose of this study is to compare the natural history of clinical and radiologic features in patients with acromelic dysplasias. Twelve patients from nine families with genetically confirmed dysplasia types with acromelia were included in the study, and eight of them were followed-up for a median of 8.1 years. Monoallelic disease-causing variants were identified in FBN1 (acromicric dysplasia, n = 3) and GNAS (Albright hereditary osteodystrophy (AHO), n = 1). Biallelic disease-causing variants in ADAMTSL2 (geleophysic dysplasia type 1, n = 4), ADAMTS10 (Weill-Marchesani syndrome type 1 (WMS1), n = 3), and ADAMTS17 (Weill-Marchesani syndrome type 4 (WMS4), n = 1) were identified. Five novel variants were detected. Short stature was present in all patients. In all patients with geleophysic dysplasia, height normalized during follow-up, and in two, initial acromelia and broad phalanges on hand radiographs resolved over time. Pseudomuscular build, joint limitations, tiptoe walking, and delayed bone age were common findings in geleophysic dysplasia, while patients with WMS1 also had pseudomuscular build, joint limitations, and delayed bone age. Acromicric dysplasia showed mild joint limitation. Intellectual disability was observed only in the WMS4 patient. Spherophakia was specific to patients with WMS. Heterotopic ossification was present in the AHO patient. - Source: PubMed
Publication date: 2026/05/19
Güneş NTürk SOnur HGür KYüksel Elgin CÇifçi Sunamak EUludağ Alkaya DEroğlu A GülerTüysüz B
- 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 - Weill-Marchesani syndrome (WMS) is characterized by severe short stature, joint contractures, tight skin, heart valve and eye anomalies. WMS is caused by biallelic mutations in , , or , or mono-allelic mutations in Because bone growth is driven by chondrocyte proliferation and hypertrophy in the growth plates, the genetics of WMS suggests that the affected extracellular matrix (ECM) proteins contribute to chondrocyte and growth plate function. Here, we show that ; double knockout (DKO) mice have significant postnatal lethality and exacerbated bone shortening, which correlated with a narrower hypertrophic zone in their growth plates. Potential ADAMTS17 substrates identified by N-terminomics and yeast-2-hybrid screening revealed the ECM proteins fibronectin () and collagen VI (). In primary ADAMTS10- and ADAMTS17-deficient skin fibroblasts, fibronectin deposition was impaired concomitant with aberrant intracellular accumulation of fibrillin-1. These findings support a role for ADAMTS17 in ECM protein secretion and assembly. Mechanistically, ADAMTS17 appears to be a critical regulator of ECM protein secretion or pericellular matrix assembly, whereas ADAMTS10 likely modulates ECM formation at later stages. - Source: PubMed
Publication date: 2025/10/01
Taye NandarajKaroulias Stylianos ZBalic ZerinaWang Lauren WWillard Belinda BMartin DanielRichard DanielOkamoto Alexander SCapellini Terence DApte Suneel SHubmacher Dirk