ADAM9 ELISA kit
- Known as:
- ADAM9 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ADAM9-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ADAM9 ELISA kit
Related genes to: ADAM9 ELISA kit
- Gene:
- ADAM9 NIH gene
- Name:
- ADAM metallopeptidase domain 9
- Previous symbol:
- CORD9
- Synonyms:
- MDC9, KIAA0021, MCMP, Mltng
- Chromosome:
- 8p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-01
- Date modifiied:
- 2016-10-05
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- Hypoxia-inducible factor 1α (HIF-1α) promotes T helper 17 (Th17) differentiation, but whether it regulates ADAM9 expression in Th17 cells during autoimmune nephritis remains unclear. Hypoxia enhanced Th17 differentiation and increased ADAM9 expression in a HIF-1α-dependent manner. HIF-1α deficiency reduced ADAM9 expression and impaired Th17 differentiation in vitro. In anti-glomerular basement membrane nephritis and B6.lpr lupus-prone mice, T cell-specific HIF-1α deletion attenuated renal pathology and reduced kidney-infiltrating CD4 and IL-17A-producing T cells. These findings identify ADAM9 as a HIF-1α-regulated target in Th17 cells that may contribute to autoimmune renal inflammation. - Source: PubMed
Publication date: 2026/09/04
Karino KoheiOba SeiyaImai RuiKono MichihitoPan WenliangTsokos Maria GTsokos George C - Hepatocellular carcinoma (HCC) is characterized by a highly vascularized tumor microenvironment (TME), with VETC being a distinctive, frequent, and prognostically unfavorable type of this vascular TME. VETC HCCs show lymphocyte deprivation and enrichment with large, foamy macrophages distributed close to endothelial cells. - Source: PubMed
Publication date: 2026/06/08
De Carlo CamillaPutignano Anna RitaAkpinar RehaDurante BarbaraViatore MarikaPolidori RebeccaSoldani CristianaFranceschini BarbaraBasso GianlucaProcopio FabioCosta GuidoGrizzi FabioTerracciano Luigi MariaTorzilli GuidoRimassa LorenzaLleo AnaPiscuoglio SalvatoreNg Charlotte K YVilla EricaMarchini SergioMarchesi FedericaDi Tommaso Luca - Collagen XVIIα1, encoded by COL17A1 and historically known as BP180/BPAG2, is a type II transmembrane collagen enriched in hemidesmosomes of basal keratinocytes. Through interactions with integrin α6β4, laminin-332 and other dermal-epidermal junction (DEJ) components, collagen XVIIα1 links the keratin cytoskeleton to the basement membrane. Recent studies indicate that this junctional anchorage supports epidermal homeostasis by preserving stem cell adhesion, polarity and regenerative capacity. During aging, collagen XVIIα1 levels decline and proteolytic processing increases, including ADAM9/ADAM10-dependent ectodomain shedding and cleavage by inflammatory proteases. These changes weaken DEJ integrity and are associated with photoaging and impaired repair. In hair follicles, collagen XVIIα1 is also required for hair follicle stem cell (HFSC) maintenance, and its reduction is linked to HFSC exhaustion, hair aging phenotypes and altered niche signals that may influence melanocyte stem cell-dependent pigmentation. This review summarizes translational approaches targeting collagen XVIIα1 and proposes practical in vivo readouts for target engagement. Key gaps include mechanism attribution, durable functional restoration at the DEJ, persistence within the epidermal-follicular niche and a shortage of rigorous human studies. - Source: PubMed
Publication date: 2026/05/25
He ZixuanZhuo Fenglin - Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality, necessitating identification of novel biomarkers for precision therapy. Herein, we aimed to investigate the role of efferocytosis-related genes (ERGs) in LUAD progression, focusing on ADAM9 as a potential prognostic and therapeutic target. - Source: PubMed
Publication date: 2026/05/25
Lin GuofuLin LanlanZhao JianmingChen Gongping - Cranial neural crest (CNC) cells are a key stem cell like tissue that contribute to most of the facial structures in vertebrates. A disintegrin and metalloproteinase (ADAM) family of proteins is essential for the induction and migration of the CNC. We have shown that Adam13 interacts with the transcription factor Arid3a to regulate gene expression; we show that Adam13 modulates histone modifications in the CNC and that Arid3a binding to the promoter is dependent on the presence of Adam13. These associations promote the expression of a certain variant expressed in the CNC that uniquely activates the expression of genes critical to CNC migration. Furthermore, we show that both Adam13 and human ADAM9 are associated with proteins involved in histone modifications and RNA splicing (a function critically affected by the loss of Adam13). Thus, we propose that ADAMs may act as extracellular sensors to modulate chromatin availability, leading to changes in gene expression and splicing. - Source: PubMed
Publication date: 2026/05/07
Pandey AnkitCousin HeleneKumar ShivTaylor LouisChander AshmitaCoppenrath KelseyShaidani Nikko-IdeenHorb MarkoAlfandari Dominique