ADAMTS9 ELISA kit
- Known as:
- ADAMTS9 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAMTS9-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAMTS9 ELISA kit
Related genes to: ADAMTS9 ELISA kit
- Gene:
- ADAMTS9 NIH gene
- Name:
- ADAM metallopeptidase with thrombospondin type 1 motif 9
- Previous symbol:
- -
- Synonyms:
- KIAA1312
- Chromosome:
- 3p14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-27
- Date modifiied:
- 2015-11-09
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- Lipedema is a common, female-predominant disorder characterized by disproportionate, painful lower-limb adipose tissue, and it still lacks an objective biomarker, a disease-modifying therapy, or consensus on whether its core lesion is inflammatory. Its molecular literature is openly contradictory, reporting both immune enrichment and immune down-regulation in the same gluteofemoral depot. Because the dominant morbidity is pain rather than adipose mass, this ambiguity carries direct clinical cost. We therefore asked the following three questions: whether the reported molecular hallmarks survive control for cell-type composition, whether pain and adipose volume behave as separable endpoints, and what the germline architecture implies about the primary lesion. - Source: PubMed
Publication date: 2026/09/01
Amato Alexandre CAmato Juliana LBenitti Daniel - Multiple myeloma is an incurable hematological malignancy that requires extensive research to understand its biology and identify novel therapeutic strategies. Hypoxia within the tumor microenvironment affects numerous biological processes, including enhancing cellular stress resistance, promoting angiogenesis, shifting metabolism toward anaerobic glycolysis, and modulating gene expression and epigenetic modifications. - Source: PubMed
Publication date: 2026/09/14
Łuczkowska KarolinaStodolak PatrycjaKulig PiotrMachaliński Bogusław - ADAMTS9 mutations cause the ciliopathies nephronophthisis and Joubert syndrome. Here we demonstrated that deletion of ADAMTS9 in the proximal nephron led to polycystic kidney development in mice. In males, Adamts9 deletion caused kidneys to become highly cystic while remaining small without undergoing enlargement. In contrast, female mice developed cystic kidneys at a slower rate. ADAMTS9 deletion disrupted ciliogenesis through the loss of cleavage of the ciliary transition zone (TZ) protein TMEM67, which led to loss of the MKS/B9 module - a key component of the ciliary gate. Functional analysis of all eight ciliopathy patient variants of ADAMTS9 identified to date showed TMEM67 C-terminus failed to localize to the TZ, thus disrupting a key regulatory mechanism in patient renal ciliogenesis. Modeling ADAMTS9-mediated TMEM67 cleavage utilizing TMEM67-cleavage deficient mice revealed loss of TZ formation, but not elevated canonical Wnt signaling as the underlying mechanism driving cystogenesis. Adamts9 deletion led to comparatively intense interstitial collagen deposition, which likely restricted kidney enlargement and resulted in the characteristically small kidney phenotype seen in nephronophthisis. By comparative analysis of four interconnected polycystic kidney models, in addition to Pkd1 and Pkd2 deleted kidneys, we identified differential collagen homeostasis as a principle factor determining cystic kidney size and type. - Source: PubMed
Publication date: 2026/09/24
Fischer SydneyRobert Karyn LAhmed ManuKane Griffin IKavanaugh Matthew AWang WeiTran Pamela VAtukorale Prabhani UNandadasa Sumeda - Carotid atherosclerosis is a major etiologic substrate for ischemic stroke. Although imaging can characterize stenosis and plaque morphology, circulating biomarkers may better support screening and scalable risk stratification, yet reliable serum protein markers for carotid plaque, particularly for plaque instability, remain limited. - Source: PubMed
Guo ShuaiweiCui ShengyanZhang XiaoXing ZixuanSun YixinQin MingqianMa XiaoyingLi XiangyuMa YanGao PengChen YanfeiWang YabingYang BinChen JianChen FeiLu XiaJin JiaqiJiao LiqunWang Tao - Obesity is an important risk factor for Type 2 Diabetes (T2D) as approximately 90% of T2D patients are obese. The single nucleotide polymorphisms (SNPs) rs4607103 (C˃T) in the ADAMTS9 gene and rs7578597 (T˃C) in the THADA gene were identified as two novel T2D risk loci. However, studies investigating the associations of these variants with T2D and obesity are limited, and little is known about the mechanisms underlying their association with T2D. Therefore, we aimed to evaluate the association between THADA and ADAMTS9 gene variants and T2D, taking into account the presence or absence of obesity. - Source: PubMed
Publication date: 2026/06/19
Erkoç-Kaya DuduArikoglu HilalGokturk FatmaIscioglu FundaIpekci Suleyman Hilmi