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
- Scrupulous trophoblast invasion is pivotal for successful placentation; its insufficiency results in preeclampsia (PE) and intrauterine growth restriction (IUGR). Although the long non-coding RNA (lncRNA) MALAT1 has been implicated in placental pathologies, its regulatory role in trophoblast biology remains incompletely understood. We demonstrate MALAT1's nuclear predominance in highly invasive mouse trophoblast giant cells (TGC) and human HTR-8/SVneo cells. MALAT1 knockdown (MALAT1) upregulates the proximal gene FRMD8, which stabilizes the membrane-bound sheddase ADAM17 and enhances its proteolytic activity. Paradoxically, this increased protease activity elevates protease inhibitor levels, impairing trophoblast migration and invasion. Mechanistically, RNA pull-down, RIP, and ChIP-PCR assays reveal MALAT1 interacts with Polycomb Repressive Complex 2 (PRC2) components to transcriptionally repress FRMD8. Pharmacological ADAM17 inhibition rescues the anti-invasive phenotype of MALAT1, whereas EZH2 disruption phenocopies MALAT1, establishing a MALAT1-PRC2-FRMD8-ADAM17 axis. Our findings reveal an unconventional epigenetic regulation axis governing trophoblast invasion by fine-tuning protease inhibitor expression, offering mechanistic insights into placental development and identifying potential therapeutic targets for pregnancy-related disorders. - Source: PubMed
Publication date: 2026/04/09
Ghosh MadhubantiAin Rupasri - EGFR signaling, which requires ligand shedding by ADAM proteases, drives the progression of a variety of cancers, including breast, ovarian and lung. We previously reported the generation and characterization of a fully human, affinity-matured anti-ADAM17 monoclonal antibody, D8P1C1, which inhibits both the proliferation of an array of cancer cell lines in vitro as well as breast cancer growth in a mouse xenograft model. Here, we show that the mAb inhibits the shedding of EGFR ligands and EGFR phosphorylation in cancer cell lines, thus explaining its anti-tumor effects. In a xenograft model with a high-grade serous ovarian cancer (HGSOC) cell line, D8P1C1 showed only modest therapeutic effect, without any discernible toxicity. These results suggest that ovarian cancers are less susceptible than breast cancers to therapeutic targeting of ADAM17- or EGFR-dependent signaling. Radioimmuno PET imaging with Zr-DFO-D8P1C1 confirmed tumoral accumulation of the mAb in high-grade and non-high-grade serous ovarian tumor xenografts. Furthermore, we report the generation and preliminary characterization of a bispecific T cell engager derivative of D8P1C1 with improved anti-tumor efficacy in vitro. - Source: PubMed
Publication date: 2026/03/24
Saha NayanenduLee Sang Gyude Stanchina ElisaMendoza Rachelle PVeach Darren RNikolov Dimitar B - Colorectal cancer (CRC) remains a major global health challenge, primarily due to late-stage diagnosis and high metastatic potential. Effective management requires novel diagnostic and prognostic strategies, with a growing focus on molecular biomarkers. A Disintegrin and Metalloproteinase (ADAM) proteins, characterized by unique proteolytic activity, play a fundamental role in tumorigenesis by regulating tumor growth, epithelial-mesenchymal transition (EMT), and metastasis. Based on recent investigations, among all ADAMs, ADAM8, ADAM9, ADAM12, ADAM15, and ADAM17 have been proved to play an important role in the CRC pathogenesis. Thus, this review underscores the potential of selected ADAM family members as promising candidates for biomarkers of CRC. Elevated ADAM8, ADAM9, ADAM12 and ADAM17 levels were observed in CRC tissues and correlated with more advanced tumor stage, while increased serum ADAM15 concentrations associated with the presence distant metastases. Moreover, ADAM9, ADAM12, ADAM15 and ADAM17 levels were associated with poorer survival, whereas ADAM8 overexpression was found to be independent prognostic factor for CRC patients' survival. In addition, the measurement of serum ADAM15 concentrations, especially in combination with well-established tumor marker-CEA improved the diagnosis of patients with this malignancy. In conclusion, selected ADAM are critical contributors to the development and progression of CRC, affecting tumor growth, EMT, and metastasis. ADAM8, ADAM9, ADAM12, ADAM15 and ADAM17 were identified as promising biomarkers for the assessment of CRC progression and proved to be prognostic indicators for patients' survival. Further validation through large prospective studies and standardized assays is necessary to establish their potential in clinical practice. - Source: PubMed
Publication date: 2026/04/01
Romanowicz AdriannaŁukaszewicz-Zając MartaMroczko Barbara - Monocyte chemoattractant protein-induced protein 1 (MCPIP1), encoded by ZC3H12A, is a negative regulator of inflammation and tumorigenesis. While its role has been implicated in various cancers, the function of MCPIP1 in hepatocellular carcinoma (HCC) remains poorly understood. This study explored the contribution of hepatocyte-specific MCPIP1 loss to HCC pathogenesis, highlighting its role in overcoming the inherent tumor resistance observed in female mice. - Source: PubMed
Publication date: 2026/01/29
Kwapisz OliwiaMarona PaulinaGorka JudytaMyrczek RafałGonzalez-Sanchez EsterBertran EstherKotlinowski JerzyGłuc MaciejAlay AniaPydyn NataliaKujdowicz MonikaRamos EmilioFabregat IsabelMiekus Katarzyna - Podocyte injury is a hallmark of chronic kidney disease (CKD) and organ failure, but whether different injury signals perturb unified or distinct molecular targets remains unclear. Using human induced pluripotent stem cell (hiPSC)-derived podocytes, we modeled cellular injury via exposure to diabetic, inflammatory, chemical toxin, biomechanical, and infectious stressors. Transcriptomic analysis revealed both shared and unique changes in gene expression across injury modes. While drug-induced injuries triggered broader transcriptional responses, conserved pathways related to lysosome function, RNA metabolism, and immune activation were identified across models. Importantly, we discovered NEU1, CD82, ABI3BP, and ADAM17 as targets of human podocyte injury. Analysis of multiple kidney disease patient biopsies confirmed enrichment of these targets, underscoring their in vivo relevance and potential as therapeutic targets. These findings highlight the predictive power of human-relevant experimental models and provide insight into podocyte injury responses, offering a framework for future precision medicine approaches. - Source: PubMed
Publication date: 2026/04/02
Barreto Amanda DJiang BowenBurt Morgan ADimitrakakis NikolaosMusah Samira