TACE (C-Terminus) Peptide
- Known as:
- TACE (C-Terminus) Peptide
- Catalog number:
- 1131P
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TACE (C-Terminus) Peptide
Related genes to: TACE (C-Terminus) Peptide
- 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: TACE (C-Terminus) Peptide
Related articles to: TACE (C-Terminus) Peptide
- 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 - The cytokine Interleukin-6 (IL-6) activates its target cells through the membrane-bound IL-6 receptor (IL-6R). IL-6 crucially controls important metabolic functions of the human body. Low-grade inflammation, including increased IL-6 serum levels, contribute to the development of autoimmune diseases like type 2 diabetes (T2D). In this study, we have analyzed the single nucleotide polymorphism of the IL-6R rs2228146 that is associated with T2D and results in the exchange of a single amino-acid residue within the IL-6R protein (p.V385I). We show that the affected amino-acid residue is located within the transmembrane helix of the IL-6R. The IL-6R-V385I variant matures properly and is transported to the cell surface in comparable amounts as the IL-6R-WT, which is clearly distinct from the established IL-6R SNP rs2228145. We further show that IL-6R-V385I can be cleaved by the metalloproteases ADAM10 and ADAM17, generating a soluble IL-6R, and that the membrane-bound form can perform IL-6 classic signaling. - Source: PubMed
Publication date: 2026/09/24
Brüggemann EricGarbers Christoph - Interleukin-6 (IL-6) is a multifunctional cytokine that regulates immunity, tissue repair and metabolic homeostasis, while also driving chronic inflammation in a broad range of diseases. IL-6 exerts its effects through distinct signalling modes, including classic signalling via its membrane-bound receptor (IL-6R) and trans-signalling via the soluble IL-6R (sIL-6R), which expands IL-6 responsiveness to most if not all cell types. Therapeutic targeting of the IL-6 pathway - primarily through monoclonal antibodies neutralizing IL-6 or IL-6R and Janus kinase (JAK) inhibitors targeting downstream signalling - has transformed the treatment of several autoimmune diseases but has also highlighted safety concerns linked to the homeostatic functions of IL-6. Advances in the understanding of IL-6 signalling biology, including endogenous regulation by soluble glycoprotein 130 kDa (sgp130) and the regulation of trans-signalling by a disintegrin and metalloproteinase 17 (ADAM17), have renewed interest in strategies that allow selective pathway modulation. In this Review, we outline the molecular basis of IL-6 signalling, examine the differential roles of classic and trans-signalling in experimental and clinical disease, and compare global and selective IL-6-targeted therapeutic approaches. We focus on the emerging concept of mechanistic and clinical differentiation within the IL-6 pathway and its implications for future drug development. - Source: PubMed
Publication date: 2026/09/23
Rose-John StefanWaetzig Georg HSchreiber Stefan - Intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), contributes to cardiac injury through mechanisms including oxidative stress, inflammation, and immune dysregulation. However, the temporal threshold at which miRNA-mediated transcriptional responses are activated, as well as their immunoregulatory roles in this process, remain unclear. - Source: PubMed
Publication date: 2026/09/23
Dong NaGou PanpanWang CaiyunQiu WanchunWang LeiPu Jiayuan