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
- 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 - Plasmacytoid dendritic cells (PDCs) represent a crucial bridge between innate and adaptive immunity as they can recognise viruses and viral-infected cells, secrete type I interferon and prime naive T-cell responses. Like naive T cells, PDCs express CD62L, an essential molecule involved in the trans-endothelial migration process, and are supposed to travel directly from blood to lymph nodes to prime naive T cells. We developed a therapeutic PDC line model (PDC*line) derived from a patient with blastic PDC neoplasm, and showing high antigen-presentation capacities. PDC*line-based vaccine was tested in clinical trials in melanoma and lung cancer. Efficient specific T lymphocyte priming was observed suggesting the efficient migration of injected PDC*line-based vaccine to lymph nodes. Here, we investigated the mechanisms involved in this migration and its regulation. In humanised mice, our results demonstrated the efficient migration of the PDC-based vaccine from blood to lymph nodes and its capacity to prime naive T cells. The expression of CD62L was evaluated following irradiation, which was mandatory in the vaccine manufacturing step and possibly important for its efficacy. CD62L was rapidly shed after irradiation of PDC*line cells and primary PDCs but not of NK-T cells, demonstrating the cell specificity of the mechanism. Our results show that p38 MAP kinase, known to be activated in response to irradiation and ADAM17 metalloprotease are involved in the rapid CD62L shedding. This new pathway could participate to the regulation PDC transmigration through High Endothelial Venules and homing to secondary lymphoid organs in cellular stress conditions. - Source: PubMed
Publication date: 2026/09/02
Leplus EstelleKacher JamilaHannani DalilVayssiere GuillaumeMolens Jean-PaulLaulanier KarineGeorgess DanJosserand VéroniqueSaas PhilippePlanel SéverineChaperot LaurencePlumas Joel - Autoimmune diseases affect 5-10% of the global population, with a prevalence of 13% in women and 7% in men. Despite advances in immunology, the molecular basis of immune dysregulation remains limited. Nardilysin (NRD convertase, NRDc), a zinc-dependent metalloendopeptidase, has been identified as an enzyme involved in this dysregulation. Recent studies have identified NRDc dysregulation as a shared feature across type 1 diabetes (T1D), rheumatoid Arthritis (RA), and vitiligo, though the specific mechanism implicated differs by the disease involved. Reported roles for NRDc include modulating the release of the immune checkpoint protein VTCN1 (B7-H4), modulation of pro-inflammatory cytokines, and activation of ADAM17-mediated release of TNF-α and its receptors. While NRDc is recognized for its role in immune signaling, gene transcription, cell differentiation, proliferation, homeostasis, thermogenesis, and metabolism, a unified framework connecting NRDc's multifaceted enzymatic activity to autoimmunity is currently lacking. We review current literature to construct such a framework, positioning it as hypothesis-generating by outlining specific, testable predictions to guide future investigation. Based on the literature, we propose that NRDc functions as a crucial molecular indicator and a therapeutic interface, rather than just a bystander enzyme. - Source: PubMed
Publication date: 2026/08/07
Choudhary YashikaMoutughimou Ben AliUpadhye Vijay JagdishJadeja Shahnawaz DVaishnav Jayvadan