Cadherin
Cadherins are a family of calcium-dependent cell adhesion molecules and transmembrane glycoproteins that play a crucial role in maintaining tissue architecture and cellular communication. Key members of the cadherin family include E-cadherin (CDH1), N-cadherin (CDH2), and P-cadherin (CDH3), etc. Cadherins mediate cell-cell adhesion through homophilic interactions, forming adherens junctions that connect to the actin cytoskeleton via catenins, thus influencing cellular signaling pathways related to proliferation, differentiation, and migration[1].
cadherins are involved in various signaling pathways, such as the Wnt and Notch pathways, which are critical for development and tissue homeostasis. Cadherins often bind to β-catenin (CTNNB1) through the catenin-binding domain. The catenin-binding domain of cadherin is crucial in cadherin function and it plays an important role in maintaining epithelial integrity. Dysregulation of cadherin expression is associated with several diseases, particularly cancer, such as pancreatic cancer, melanoma, hepatocellular carcinoma, glioblastoma, breast and gastric cancers. The epigenetic silencing of cadherins through mechanisms like DNA methylation further exacerbates this issue in tumor progression. Understanding cadherins' roles in cellular dynamics provides insights into potential therapeutic targets for cancer and other diseases characterized by altered cell adhesion[1].
cadherins are involved in various signaling pathways, such as the Wnt and Notch pathways, which are critical for development and tissue homeostasis. Cadherins often bind to β-catenin (CTNNB1) through the catenin-binding domain. The catenin-binding domain of cadherin is crucial in cadherin function and it plays an important role in maintaining epithelial integrity. Dysregulation of cadherin expression is associated with several diseases, particularly cancer, such as pancreatic cancer, melanoma, hepatocellular carcinoma, glioblastoma, breast and gastric cancers. The epigenetic silencing of cadherins through mechanisms like DNA methylation further exacerbates this issue in tumor progression. Understanding cadherins' roles in cellular dynamics provides insights into potential therapeutic targets for cancer and other diseases characterized by altered cell adhesion[1].
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Cadherin Related Products (71)
Related Products (71)
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anti-TNBC agent-9
0 ImagesCat. No.: HY-172551anti-TNBC agent-9 (Compound 3as) is an anti-cancer agent for triple-negative breast cancer (TNBC). anti-TNBC agent-9 exhibits significant inhibitory activity against MDA-MB-453 cells with an IC50 value of 8.5 μM. anti-TNBC agent-9 inhibits tumor cell migration by upregulating E-cadherin and downregulating N-cadherin, matrix metalloproteinase 2 (MMP2), and MMP9. anti-TNBC agent-9 induces apoptosis by increasing the expression of the pro-apoptotic protein BAX and decreasing the expression of the anti-apoptotic protein BCL-2, thereby inhibiting tumor cell proliferation.
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NF-κB/STAT3/iNOS-IN-1
0 ImagesCat. No.: HY-184692NF-κB/STAT3/iNOS-IN-1 is a NF-κB/STAT3/iNOS inhibitor. NF-κB/STAT3/iNOS-IN-1 reduces the expression of inflammatory mediators TNF-α, IL-1β, IL-6, IL-8 and COX-2. NF-κB/STAT3/iNOS-IN-1 upregulates the expression of epithelial barrier-related proteins E-cadherin, Occludin and Zonula occludens-1. NF-κB/STAT3/iNOS-IN-1 alleviates disease severity and histopathological damage in mouse colitis models. NF-κB/STAT3/iNOS-IN-1 can be used for the research of inflammatory bowel disease (colitis).
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JNK3-IN-10
0 ImagesCat. No.: HY-181556CAS No.: 3085181-00-3JNK3-IN-10 is a blood-brain barrier-impermeable JNK3 inhibitor (IC50=0.257 nM) with over 400-fold selectivity over JNK1. JNK3-IN-10 blocks the JNK3-mediated signaling pathway downstream of TGF-β1, inhibits TGF-β1-induced phosphorylation of c-Jun, reduces the expression of pro-fibrotic markers, and restores the expression of the epithelial protein E-cadherin. JNK3-IN-10 exhibits low cytotoxicity, anti-fibrotic, cytoprotective and renoprotective effects, and alleviates albuminuria, glomerulosclerosis and podocyte foot process fusion. JNK3-IN-10 can be used for the research of chronic kidney disease, glomerulosclerosis and adriamycin-induced nephropathy.
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VEGFR2 AUTOTAC-1
0 ImagesCat. No.: HY-187534VEGFR2 AUTOTAC-1 is a VEGFR2 AUTOTAC degrader. VEGFR2 AUTOTAC-1 recruits p62, activates the autophagy-lysosome pathway through the p62-LC3 axis cascade, forms a ternary complex with VEGFR2 and p62, and drives UPS-independent post-translational degradation of VEGFR2. VEGFR2 AUTOTAC-1 induces G1 phase arrest and endogenous apoptosis in cells via the mitochondrial and caspase apoptotic pathways, thereby inhibiting cancer cell proliferation, migration and malignant phenotypes; meanwhile, it inhibits endothelial cell tube formation, migration and endothelial-mesenchymal transition by regulating E-cadherin and MMP2. VEGFR2 AUTOTAC-1 is applicable to research related to triple-negative breast cancer.(Pink: VEGFR2 target protein ligand (HY-187558); Blue: p62 ligand (HY-W014292); Black: Linker)
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HAV peptide
0 ImagesCat. No.: HY-P11154CAS No.: 244103-75-1Synonyms: Ac-SHAVSS-NH2HAV peptide (Ac-SHAVSS-NH2) is a peptide containing His-Ala-Val. HAV peptide affects the E-cadherin signaling pathway. HAV peptide regulates intercellular junctions.
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Cystatin B agonist 1
0 ImagesCat. No.: HY-175291Cystatin B agonist 1 is an orally active MMP-2/9 inhibitor. Cystatin B agonist 1 exhibits inhibitory effects with IC50 values of 3.95 and 3.43 μM against U87 and T98G cells, respectively. Cystatin B agonist 1 induces the cell-cycle arrest at S phase, inhibits angiogenesis, and suppresses migration and invasion of MG cells. Cystatin B agonist 1 inhibits tumor growth in U87 MG xenograft model. Cystatin B agonist 1 can be used for the study of malignant glioma (MG).
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Sorafenib tosylate (Standard)
0 ImagesSynonyms: Bay 43-9006 tosylate (Standard)Sorafenib (tosylate) (Standard) (Bay 43-9006 (tosylate) (Standard)) is the analytical standard of Sorafenib (tosylate) (HY-10201A). This product is intended for research and analytical applications. Sorafenib (Bay 43-9006) tosylate is a potent oral active multikinase inhibitor. Sorafenib blocks autophosphorylation and activity of receptor tyrosine kinases (VEGFR-2, VEGFR-3) and RAF family kinases, thereby suppressing the RAF/MEK/ERK and PI3K/Akt pathways, inhibiting STAT3 phosphorylation, and selectively inhibiting the MAPK pathway in cancer cells. Sorafenib tosylate induces cell cycle arrest, autophagy, apoptosis, and PARP cleavage, reduces Bcl-2, Bcl-XL, cyclin D1 levels, and activates Bak and Bax. Sorafenib tosylate inhibits tumor growth and metastasis in mouse and rat models. Sorafenib tosylate can be used for cancer research, such as colon, breast, non-small-cell lung cancer (NSCLC), ovarian, pancreatic, melanoma, colorectal and hepatocellular carcinoma.
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2,5-Epidithia-3,6-dioxopiperazine
0 ImagesCat. No.: HY-177477CAS No.: 21056-79-12,5-Epidithia-3,6-dioxopiperazine (Formula 15) is a derivative of Epidithiodioxopiperazine (ETP). 2,5-Epidithia-3,6-dioxopiperazine improves intracellular penetration and restores the activity of 2-Cys-Prx (especially Peroxiredoxin II (PrxII)) of form simulation in cells. 2,5-Epidithia-3,6-dioxopiperazine inhibits PDGF-induced proliferation and migration in vascular smooth muscle cells while promoting these actions in endothelial cells with VEGF induction. 2,5-Epidithia-3,6-dioxopiperazine effectively inhibits the proliferation and migration and lung metastasis of melanoma cells. 2,5-Epidithia-3,6-dioxopiperazine can be used for vascular diseases such as hypertension, angina pectoris and myocardial infarction research.
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FF-21101
0 ImagesCat. No.: HY-P991341
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DMBT
0 ImagesCat. No.: HY-183377CAS No.: 1260071-76-8DMBT is an orally effective anti-tumor metastasis and anti-angiogenesis agent. DMBT downregulates key molecules such as EGFR/p-Akt/HIF-1α/VEGF/MMP-9, inhibits the HIF-1α/VE-cadherin (cadherin)/MMPs and Nrf2/HO-1 signaling pathways, and reduces hypoxia-induced ROS levels as well as the secretion and activity of MMP-9. DMBT inhibits hypoxia-induced vasculogenic mimicry, cancer cell migration, invasion and metastasis, and exhibits no obvious cytotoxicity to normal cells. DMBT reduces the area of laser-induced choroidal neovascularization lesions. DMBT can be used in studies related to breast cancer, melanoma and macular degeneration.
