ADA17_HUMAN TACE ELISA tesk kit
- Known as:
- ADA17_HUMAN TACE Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16978
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ADA17_HUMAN TACE ELISA tesk kit
Related genes to: ADA17_HUMAN TACE ELISA tesk kit
- 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: ADA17_HUMAN TACE ELISA tesk kit
Related articles to: ADA17_HUMAN TACE ELISA tesk kit
- Acute respiratory distress syndrome (ARDS) is characterized by endothelial barrier disruption, excessive neutrophil recruitment, and sustained pulmonary inflammation. The A Disintegrin and Metalloproteinase 17 (ADAM17) regulates inflammatory signaling through ectodomain shedding of adhesion molecules and cytokine receptors, yet its endothelial-specific contribution to acute lung injury remains poorly defined. - Source: PubMed
Publication date: 2026/09/28
Biedritzky AnnaKleinmaier CarolinFuhr AnikaHerrmann Lisa MariaNgamsri Kristian-ChristosKonrad FranziskaKoeppen Michael - Respiratory syncytial virus (RSV) infection causes epithelial injury, barrier disruption, and formation of syncytia in human lung tissue; however, the regulatory host defense mechanisms involved remain poorly defined. ADAM17 is a multifunctional sheddase implicated in inflammatory lung disease and is considered a potential therapeutic target during viral infections. Here, we show that RSV infection induces ADAM17 activity through PKC- and ERK-dependent signaling, increasing surface ADAM17 levels and sheddase activity. Genetic loss or pharmacological inhibition of ADAM17 reduced RSV-induced formation of syncytia, post-entry viral spread, and viral titers. This identifies ADAM17 as a host factor that supports viral dissemination. ADAM17 deficiency simultaneously exacerbated RSV-induced epithelial injury, characterized by loss of intercellular cohesion, impaired barrier function, increased paracellular permeability, and enhanced cytotoxicity. RSV-induced ADAM17 activity promoted the release of multiple epithelial growth factor receptor (EGFR) ligands. Supplementation with recombinant amphiregulin partially restored barrier function in infected ADAM17-deficient cells. Consistent with these functional effects, ADAM17 deficiency was associated with the loss of epithelial differentiation-associated transcriptional programs and increased expression of inflammatory genes. These findings indicate that ADAM17 plays a dual role in RSV infection. It facilitates syncytial viral spread, while preserving epithelial integrity through autocrine EGFR signaling. Thus, ADAM17 activity represents a biological trade-off between viral dissemination and tissue protection, indicating that therapeutic ADAM17 inhibition may reduce viral spread at the cost of aggravating epithelial damage.IMPORTANCEDuring respiratory syncytial virus (RSV) infection, the airway epithelium must maintain barrier integrity while responding to virus-induced syncytium formation and tissue damage. It is poorly understood which host factors balance tissue preservation against viral replication and spread. Here, we demonstrate that the host cellular metalloproteinase ADAM17 is activated upon RSV infection. While RSV-induced ADAM17 activity promotes syncytium formation and viral spread, it concurrently controls the maintenance of epithelial barrier integrity, preserves cell survival, and inhibits hyperinflammatory signaling. By demonstrating that ADAM17 has a dual mode of action controlling both viral propagation and epithelial barrier resilience, this work uncovers a central trade-off: the same host factor exploited by RSV for dissemination is essential for protecting airway tissue. Consequently, targeting ADAM17 for antiviral therapy presents major challenges, as blocking viral spread may compromise vital epithelial defenses. - Source: PubMed
Publication date: 2026/09/28
Meineke RobertKnittler Marie-ChristinTagore RajarsheeEngling NeleLudlow MartinOsterhaus Albert D M ERimmelzwaan Guus F - Anastomotic leakage continues to be a severe and prevalent complication in colorectal surgery, leading to elevated morbidity and mortality rates despite modern advancements in surgical and perioperative care. To address this persistent clinical challenge, the aim of the present study was to engineer a biocompatible poly(lactic-co-glycolic acid) (PLGA) matrix designed for the sustained release of melatonin, subsequently evaluating its therapeutic efficacy in promoting colon anastomotic repair. Seventy-two male Wistar albino rats were randomly assigned to three experimental groups: anastomosis (n = 24); anastomosis + matrix (n = 24); and anastomosis + melatonin-loaded matrix (n = 24). Anastomotic segments were harvested on postoperative days 3 and 7, and colonic bursting pressure was measured as a functional indicator of anastomotic integrity. The melatonin-loaded matrix significantly enhanced anastomotic healing on postoperative day 7. Melatonin delivery: (1) markedly reduced the gene expression of pro-inflammatory cytokines; (2) modulated iNOS, COX-2 and MPO expression on both days 3 and 7; (3) decreased HO-1 and catalase expression on day 7; (4) promoted collagen synthesis; (5) enhanced collagen deposition through upregulation of Arg-1; and (6) regulated ADAM10 and ADAM17 gene expression. These results are correlated with the histological analysis findings. Collectively, controlled release of melatonin via a PLGA-based biomaterial matrix promotes colon anastomosis healing. This strategy represents a promising translational approach for reducing postoperative anastomotic complications. - Source: PubMed
Publication date: 2026/09/27
Demir UfukYurtgezen Zekiye GülfemErbil GülfemGökçe Oruç NumanOral AyhanUzun Metehan - Cardiopulmonary bypass (CPB) alters blood flow patterns and may induce endothelial activation; however, the effects of different CPB configurations on endothelial-associated biomarkers remain unclear. In this exploratory pilot study, we compared circulating biomarkers and tissue immunohistochemical findings between beating-heart partial CPB and cardioplegic total CPB in juvenile pigs. Ten 8-week-old female crossbred piglets underwent partial CPB with continued cardiac beating ( = 5) or total CPB with aortic cross-clamping and cardioplegic arrest ( = 5) for 60 min. Serum vascular cell adhesion molecule-1 (VCAM-1), a disintegrin and metalloproteinase-17 (ADAM-17), and thrombospondin-1 (TSP-1) concentrations were measured using an enzyme-linked immunosorbent assay, and tissue VCAM-1 and platelet endothelial cell adhesion molecule-1 (PECAM-1) were assessed immunohistochemically. At the end of the CPB procedure, serum VCAM-1 was higher in the total CPB group than in the partial CPB group (581 [339-759] ng/mL vs. 239 [224-304] ng/mL; |rank-biserial r| = 0.84 (95%CI, 0.36 to 1.00); Hodges-Lehmann estimate of the location shift = 341.7 ng/mL, 95% CI, 5.1-607.0 ng/mL; = 0.03), whereas ADAM-17 and TSP-1 and tissue findings showed no consistent intergroup differences. Total CPB was associated with an early increase in circulating VCAM-1. Because the CPB configurations differed in several physiological and procedural factors, this response should be interpreted as configuration-associated rather than as evidence of an isolated effect of reduced pulsatility. - Source: PubMed
Publication date: 2026/08/25
Udagawa HiromuHamamoto YujiNam EunryelOkamoto MinoruKomatsu MasafumiIsaka Mitsuhiro - Neuroinflammation is increasingly implicated in Alzheimer's disease (AD), but how distinct CSF inflammatory biomarkers relate to AD pathology remains unclear. This study examined whether CSF biomarkers reflecting astrocytic activation (GFAP), microglial activation (TREM2), systemic inflammation (CRP), TNF-related signaling (TNFR2), and inflammatory proteolysis (ADAM17) were associated with CSF Aβ42/40, CSF p-tau181, and cognitive performance across the AD clinical spectrum. Data were obtained from 933 ADNI participants, including 312 cognitively normal (CN) individuals, 471 participants with mild cognitive impairment (MCI), and 150 participants with AD dementia. Analyses were corrected for multiple comparisons using the FDR method. The results showed that CSF neuroinflammatory biomarkers differed across diagnostic groups, with GFAP showing the strongest progressive increase from CN to MCI and AD dementia. Higher GFAP, TREM2, TNFR2, and ADAM17 levels were associated with lower CSF Aβ42/40, higher CSF p-tau181, and poorer cognitive performance, particularly in MCI, whereas CRP showed weaker and less consistent associations. In joint models including all inflammatory and core AD biomarkers, both higher GFAP and higher TNFR2 remained independently associated with worse cognitive function. Mediation analyses showed that lower CSF Aβ42/40 partly mediated the associations of higher GFAP and TREM2 with worse cognitive performance. Higher CSF p-tau181 mediated broader associations linking higher GFAP, TREM2, TNFR2, and ADAM17 levels to worse cognitive performance, with the strongest effects observed in MCI. Overall, higher CSF neuroinflammatory biomarkers may be linked to AD pathology and cognitive impairment; however, given the observational design, causality cannot be established, and longitudinal mechanistic studies are needed to validate these findings. - Source: PubMed
Publication date: 2026/09/25
Alruwaili MubarakTurkistani Areej AhmedShilbayeh Sireen Abdul RahimMirdad Dahlia Soleman AAlmulhim Marwa FareedAlnaaim SaudAlmubarak Muhannad