ADAM17 _ TACE Antibody
- Known as:
- ADAM17 _ TACE Antibody
- Catalog number:
- AF1026a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ADAM17 _ TACE Antibody
Related genes to: ADAM17 _ TACE Antibody
- Gene:
- ADAM17 NIH gene
- Name:
- ADAM metallopeptidase domain 17
- Previous symbol:
- TACE
- Synonyms:
- cSVP, CD156B
- Chromosome:
- 2p25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-10
- Date modifiied:
- 2019-04-23
Related products to: ADAM17 _ TACE Antibody
Related articles to: ADAM17 _ TACE Antibody
- Periodontitis is a chronic inflammatory disease driven by dysregulated host responses and failed resolution of inflammation, leading to progressive periodontal tissue destruction. This resolution failure is critically linked to impaired macrophage efferocytosis and a deficiency in endogenous specialized pro-resolving mediators such as Resolvin D (RvD). - Source: PubMed
Publication date: 2026/08/08
Yu Xuan-XuanZhuang Zi-YaoGe Rui-YangLin ShuangRen Jiang-YanZhou Yi-WenZhang Jing-LunLi Zi-XuanLi Ge-FeiJi JunYan FuhuaLi HuangDeng Jie - This study investigated the role of Krüppel-like factor 4 (KLF4) in macrophage-mediated inflammation in type 2 diabetes mellitus (T2DM) with psoriasis. KLF4, tissue inhibitor of metalloproteinases 3 (TIMP3)/a disintegrin and a metalloproteinase domain 17 (ADAM17) levels were measured in skin samples from patients. A diabetic psoriasis-like dermatitis mouse model was established using imiquimod (IMQ) and treated with KLF4-overexpressing lentivirus. Glucose/lipid metabolism, skin pathology, mast cell counts, and inflammatory markers were assessed. Macrophage status was evaluated by F4/80 staining. KLF4 was downregulated in patients with T2DM with psoriasis. In mice with diabetic psoriasis-like dermatitis. KLF4 overexpression improved glucose/lipid metabolism and reduced skin erythema, scaling, thickening, psoriasis area severity index, and mast cell infiltration. KLF4 also decreased inflammation and modulated the TIMP3/ADAM17 pathway. These findings indicate that KLF4 ameliorates IMQ-induced inflammation via the TIMP3/ADAM17 pathway in diabetic psoriasis-like dermatitis. - Source: PubMed
Publication date: 2026/07/31
Jin MeichenLi YiyaoKong YuanCheng XiangyiZhang Jingbin - The family of inactive rhomboid-like proteins (iRhoms) have emerged as essential non-catalytic modulators of membrane protein trafficking and signaling, particularly in inflammation, and cancer, through their selective regulation of the protease A Disintegrin And Metalloproteinase 17 (ADAM17). Serving as obligate cofactors, iRhoms regulate maturation, stability and substrate selectivity of ADAM17, thereby controlling the release of cytokines, growth factors and immunomodulatory receptors. Recent studies have expanded the functional landscape of iRhoms beyond ADAM17 regulation, implicating them in endoplasmic reticulum (ER) stress adaptation, innate immune activation, and the shaping of the tumour microenvironment. Dysregulated iRhom/ADAM17 signaling contributes to chronic inflammatory pathologies, resistance to immunotherapies, and tumour progression across diverse cancer types. Here, we provide insights into the molecular function, trafficking dynamics and regulatory mechanisms of iRhoms. Further, we evaluate their impact on cytokine-dependent signaling networks in inflammation and tumourigenesis. This review positions iRhoms as central coordinators of membrane-proximal signaling events and underscores their emerging relevance as disease modifiers and potential therapeutic targets in inflammatory and malignant disorders. - Source: PubMed
Publication date: 2026/07/28
Chan SherminDmello RhynelleSaad Mohamed I - Congenital heart defects (CHD) constitute a prevalent group of structural birth anomalies, characterised by substantial genetic heterogeneity and diverse clinical phenotypes. - Source: PubMed
Publication date: 2026/07/06
Korobeinikova Anna VPetriaikina Ekaterina STychinin Dmitry IYudin Vladimir SBulaeva Naida IGyulmamedova Sayaly MKhugaev Georgy ASukhacheva Tatiana VSnigir Ekaterina AMitrofanov Sergey IRumyantseva Antonina MSvetlichnyy Dmitry VYudin Sergey MGolukhova Elena ZSkvortsova Veronika I - The overlap between the geographic distribution of COVID-19 outbreaks and pollution levels suggested a strong correlation between exposure to atmospheric particulate matter and an increased risk of developing severe forms of disease. This correlation has been highlighted by several epidemiological studies, indicating the existence of shared molecular mechanisms. Emerging evidence has highlighted the important role of lipid rafts in facilitating viral entry into cells. Specifically, the receptor binding domain of the SARS-CoV-2 spike protein interacts with sialylated glycans of the monosialic ganglioside GM1 and GM2 that are particularly enriched in lipid rafts. This interaction has been proposed to facilitate ACE2 recognition by the spike protein and may contribute to early events involved in viral attachment and entry. Here, we reveal that A549 alveolar lung cells, after DEP exposure, exhibit a significant shift in ACE2 into lipid rafts, accompanied by an increase in the immature form of ADAM17, the sheddase responsible for ACE2 cleavage. Additionally, DEP exposure results in a significant increase in IL-6 release, while no changes were observed in IL-8 and sACE2 release. This treatment does not cause significant alterations in protein levels or membrane redistribution of COX-2 and HO-1, proteins involved in the inflammatory response and oxidative stress following exposure to air pollution, and linked to COVID-19 pathogenesis. Finally, lipidomic analysis by UHPLC-MS revealed that DEP exposure induces a significant increase in GM2 levels, and a concomitant decrease in GM1 and GM3 levels. Together, these results indicate that DEP exposure remodels lipid raft-associated molecular features in A549 cells, including ACE2 membrane redistribution, altered ganglioside composition, and increased IL-6 release. Although these changes may be relevant to cellular mechanisms associated with SARS-CoV-2 susceptibility, the present study does not directly assess viral binding, viral entry, or infection, and further functional studies are required. - Source: PubMed
Publication date: 2026/07/22
Botto LauraMauri MarioSerrao SimoneBulbarelli AlessandraLonati ElenaCazzaniga EmanuelaRatti EdoardoPaglia GiuseppePalestini Paola