Human TNF α converting enzyme,TACE ELISA Kit
- Known as:
- Human TNF α converting enzyme,TACE Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-0849
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human TNF α converting enzyme TACE ELISA Kit
Related genes to: Human TNF α converting enzyme,TACE ELISA 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: Human TNF α converting enzyme,TACE ELISA Kit
Related articles to: Human TNF α converting enzyme,TACE ELISA Kit
- 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 - Glioblastoma (GBM) is the most aggressive brain tumor, with a median survival of approximately 15 months despite multimodal therapy. Although ethanol (EtOH) exposure has been associated with tumor-promoting inflammatory and signaling alterations, the molecular mediators linking EtOH to GBM progression remain poorly defined. We used Ingenuity Pathway Analysis (IPA) to construct independent EtOH- and ADAM17-associated molecular networks and identify shared regulatory effectors. Comparison of 921 EtOH-associated and 594 ADAM17-associated molecules identified 97 overlapping molecules, of which 25 were retained as high-confidence shared effectors. IPA disease-association analysis identified GBM as the strongest disease association in both the ADAM17 and integrated EtOH-ADAM17 networks. Computational network perturbation analyses indicated that simulated removal of ADAM17 eliminated the GBM disease association, whereas retention of ADAM17 as the central hub produced only a partial association, supporting its role as a key regulator within the predicted network. Analysis of TCGA-GBM transcriptomic data identified significant upregulation of ADAM17, CAV1, FLNA, and CASP8. Canonical pathway analysis further identified enrichment of ADAM17-associated signaling pathways, including sheddase, EGFR, ERBB4, neuregulin, JAK/IL-6, and matrix metalloproteinase signaling. Collectively, these findings support a candidate EtOH-ADAM17 molecular axis associated with GBM progression, providing a rationale for experimental evaluation of ADAM17 as a therapeutic target. - Source: PubMed
Publication date: 2026/09/01
Arumugam AakashBaik HannahJang NayoungHuang WenfeiChang Sulie L - Adrenocortical carcinoma (ACC) is a rare and aggressive endocrine malignancy. Although immune checkpoint signaling and tumor-infiltrating lymphocytes (TILs) have been implicated in ACC biology, the role of ADAM10 and ADAM17 in the adrenocortical tumor immune microenvironment remains poorly understood. This study aimed to evaluate the expression of ADAM10, ADAM17, PD-L1, CD4, and CD8 in ACC and benign adrenal adenoma (BAA) tissues. - Source: PubMed
Publication date: 2026/09/09
Sözen MehmetDuman Öztürk SedaSelek AlevÇetinarslan BerrinCantürk ZeynepGezer EmreBalcı Sibel - Intracranial aneurysms (IAs) represent a significant and potentially life-threatening category of disease, and there is currently a lack of effective treatment options aimed at preventing the progression of the disease. Accordingly, this study is dedicated to exploring and identifying effective drug targets that can help in the prevention of both the formation and rupture of IAs, along with a detailed examination of the underlying potential mechanisms involved in these processes. The data related to IAs for this research was obtained from the ISGC Biobank and UK Biobank. Then, we investigated the possible biological functions and unintended consequences of targeting the specific genes that were highlighted in IAs by using mediation analysis, virtual knockout experiments, and PW-MR studies. A total of 5 unique potential drug targets for IAs (FKTN, MAP3K1, PSMA4, SLC22A4, ADAM17), 4 unique potential drug targets for SAH (PSMA4, ADAM17, GPR160, SLC22A4), and 2 unique potential drug targets for UIA (SLC22A4, PRCP) were identified across brain or blood samples. Among the various candidates identified, SLC22A4 has emerged as a promising potential drug target, showing significant expression levels in both blood and brain tissues. Additionally, phenome-wide MR of SLC22A4 across 32 selected phenotypes did not identify statistically significant adverse associations after FDR correction. Virtual knockout (KO) experiments on SLC22A4 revealed that SLC22A4 KO disrupted 81 genes, all of which are involved in IAs-related pathways. Besides, we recognized BRD-K85337334 as potential candidates for targeting SLC22A4. This research indicates that an increase in SLC22A4 gene expression within the blood or brain is directly linked to a heightened risk of IAs rupture, which will aid in prioritizing the development of drugs for IAs. - Source: PubMed
Wan XichenWan ZhiYingPeng HaoyangZhang ZeyuHuang YiWang MaoqiWang PengHu WenhaoXiong WeiDing HanXiong YeWu Xiao