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].
All Product Categories
-
Cadherin Related Products (72)
Related Products (72)
-
Ligusticum cycloprolactam
0 ImagesCat. No.: HY-N17383CAS No.: 2283387-37-9Ligusticum cycloprolactam is a potent, orally active, and CNS-penetrant TLR4/NF-κB inhibitor, exhibiting anti-inflammatory and neuroprotective activity. Ligusticum cycloprolactam reduces FPR1 expression, inhibits NLRP3 inflammasome, TLR4/NF-κB, hepatic MAPK and TGF-β signaling, and selectively activates hepatic FXR. Ligusticum cycloprolactam attenuates pro-inflammatory mediator production, enhances anti-inflammatory cytokine secretion, regulates renal uric acid transporters, and preserves intestinal microbiota composition. Ligusticum cycloprolactam can be used for the research of ischemic stroke, hyperuricemic nephropathy, neuroinflammation, and metabolic dysfunction-associated fatty liver disease.
-
NUAK1-IN-3
0 ImagesCat. No.: HY-182361CAS No.: 3097515-05-1NUAK1-IN-3 is a potent and selective NUAK1 inhibitor with an IC50 of 0.49 nM. NUAK1-IN-3 also inhibits NUAK2 and JAK3 with IC50 values of 265 and 225 nM. NUAK1-IN-3 engages Glu139 of NUAK1, forms a salt bridge between its bicyclic ring nitrogen and Asp142, and uses a fluorine atom to enhance hydrophobic binding interactions. NUAK1-IN-3 attenuates MYPT1 phosphorylation, suppresses the NUAK1-MYPT1 signaling axis, and inhibits proliferation, migration, and invasion of triple-negative breast cancer cells. NUAK1-IN-3 reverses TGF-β1-induced epithelial-mesenchymal transition (EMT) marker alterations, downregulates Snail and N-cadherin, and upregulates E-cadherin in tumor tissues. NUAK1-IN-3 suppresses tumor growth in triple-negative breast cancer xenograft models. NUAK1-IN-3 can be used for the research of triple-negative breast cancer.
-
Salviamarinic acid A
0 ImagesCat. No.: HY-N17650CAS No.: 3038746-92-5Salviamarinic acid A is a water-soluble phenolic acid that can be extracted from Salvia miltiorrhiza with potent anti-pulmonary fibrosis activity. Salviamarinic acid A significantly increases cell viability, cell index, cell motility and E-cadherin expression, and reduces TGF-β1, α-SMA and Collagen I levels. Salviamarinic acid A can be used for pulmonary fibrosis research.
-
OSU-03013
0 ImagesCat. No.: HY-122352CAS No.: 742112-34-1OSU-03013 is a Celecoxib (HY-14398) analog. OSU-03013 can promote apoptosis, up-regulate E-cadherin, and down-regulate β-catenin, c-myc, Wnt1, and N-cadherin. OSU-03013 reduces cell migration and invasion. OSU-03013 regulates both Wnt and mTOR expression to inhibit colon cancer (CC) cell proliferation. OSU-03013 can be used for CC cancer research.
-
SLEC-11
0 ImagesCat. No.: HY-145268CAS No.: 863761-17-5SLEC-11 is a CDH1/E-cadherin modulator that potently inhibits cell death in E-cadherin-deficient cells (EC50=8.2 μM). SLEC-11 can be used to study potential synthetic lethal therapies for gastric cancer.
-
THR-123
0 ImagesCat. No.: HY-P11354THR-123 is an orally active ALK3 peptide agonist. THR-123 has a relatively weak binding to ALK2, but does not bind to ALK6. THR-123 suppresses inflammation, apoptosis and the epithelial-to-mesenchymal transition program and reverses established fibrosis in five mouse models of acute and chronic renal injury. THR-123 can be used for the study of kidney fibrosis.
-
TYMJ-01
0 ImagesCat. No.: HY-181506CAS No.: 3109321-90-3TYMJ-01 is a fluorescent probe and eEF2K degrader. TYMJ-01 induces dose-dependent and specific degradation of eEF2K via the ubiquitin-proteasome pathway, with a DC50 of 82 nM. TYMJ-01 inhibits the proliferation, migration and invasion of triple-negative breast cancer cells. TYMJ-01 enables dynamic fluorescent imaging of eEF2K degradation in triple-negative breast cancer cells; it enhances the anti-tumor activity of Paclitaxel (HY-B0015). TYMJ-01 can be used for the research of triple-negative breast cancer.
-
Apoptosis inducer 44
0 ImagesCat. No.: HY-175815Apoptosis inducer 44 is an apoptosis inducer. Apoptosis inducer 44 triggers apoptosis in MDA-MB-231 cells by increasing the levels of Bax and Cyt C, reducing Bcl-2, and initiating caspase-3 cleavage. Apoptosis inducer 44 suppresses the invasion and migration of MDA-MB-231 cells by down-regulating MMP-2 and MMP-9 expression and up-regulating E-cadherin protein levels. Apoptosis inducer 44 can be used for the study of breast cancer.
-
Sorafenib-d3 tosylate
0 ImagesCat. No.: HY-10201S4CAS No.: 1333386-17-6Synonyms: Donafenib tosylate; Bay 43-9006-d3 tosylateSorafenib-d3 (Donafenib) tosylate is the deuterated-labeled Sorafenib tosylate (HY-10201A). 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.
-
Theophylline-platinum(IV) prodrug-1
0 ImagesCat. No.: HY-175257Theophylline-platinum(IV) prodrug-1 is a PARP-1 inhibitor. Theophylline-platinum(IV) prodrug-1 enhances DNA damage, ROS production, mitochondrial dysfunction, apoptosis and S-phase arrest, along with reducing invasion and metastasis in cells. Theophylline-platinum(IV) prodrug-1 exhibits superior antitumor activity in the xenograft SKOV3-BRCA1-KD tumor model. Theophylline-platinum(IV) prodrug-1 can be used for the study of ovarian cancer.
-
PI3Kα-IN-29
0 ImagesCat. No.: HY-179623PI3Kα-IN-29 is a potent, orally active and selective PI3Kα with an IC50 of 2.5 nM. PI3Kα-IN-29 exhibits >400-fold selectivity over PI3Kβ/δ/γ/mTOR. PI3Kα-IN-29 selectively degrades the H1047R mutant p110α protein and inhibits PI3Kα kinase activity. PI3Kα-IN-29 suppresses PI3K/AKT/mTOR signaling, induces G1 arrest, and inhibits migration. PI3Kα-IN-29 inhibits tumor growth in a T47 mouse model. PI3Kα-IN-29 can be used for the research of breast cancer.
-
N-Cadherin mimic peptide
0 ImagesCat. No.: HY-P11346CAS No.: 1830290-52-2N-Cadherin mimic peptide is a N-cadherin agonist. N-Cadherin mimic peptide promotes N-cadherin homodimerization via enhancing β-catenin signaling, inducing early chondrogenesis and cartilage matrix production in mesenchymal stem cells (MSCs). N-Cadherin mimic peptide is promising for research of MSC-based cartilage regeneration.
-
Hakin-1
0 ImagesCat. No.: HY-176861CAS No.: 346660-34-2Hakin-1 is a E3 Ubiquitin-Ligase Hakai inhibitor. Hakin-1 blocks Hakai-mediated global ubiquitination and specific ubiquitination of E-cadherin and inhibits epithelial-mesenchymal transition (EMT) progression. Hakan-1 inhibits tumor progression and cancer metastasis. Hakin-1 can be used for the study of carcinoma such as colorectal cancer.
-
Black tea extract
0 ImagesCat. No.: HY-N16399Black tea extract is the extract of Black tea. Black tea extract prevents inorganic arsenic (iAs) induced ROS generation, inhibiting uncontrolled proliferation, epithelial to mesenchymal transition (EMT) and metastasis in HaCaT cells. Black tea extract has an anti-fibrotic activity. Black tea extract can be used for skin cancers research.
-
JNK3-IN-11
0 ImagesCat. No.: HY-181993JNK3-IN-11 is a selective JNK3 inhibitor with an IC50 of 2.08 nM. JNK3-IN-11 binds to the JNK3 ATP-binding pocket, forming conserved hydrogen bonds with Met149 and a water-mediated hydrogen bond with Lys93. JNK3-IN-11 suppresses TGF-β1-induced c-Jun phosphorylation, reduces profibrotic markers COL1A1 and PAI-1, restores E-cadherin expression, and has protection against podocyte injure. JNK3-IN-11 can be used for the research of chronic kidney disease.
-
Antimicrobial Peptide YD
0 ImagesCat. No.: HY-P11913CAS No.: 2124174-65-6Antimicrobial Peptide YD is an Antimicrobial peptide. Antimicrobial Peptide YD attenuates the TLR4/MYD88/NF-κB signaling pathway, inhibits ROS production, upregulates the expression of antioxidant enzymes, reduces the levels of inflammation-related factors, and prevents the downregulation of E-cadherin and upregulation of Vimentin. Antimicrobial Peptide YD exhibits activity against Gram-positive bacteria, Gram-negative bacteria, and multidrug-resistant bacteria. Antimicrobial Peptide YD possesses anti-inflammatory, antifibrotic, and antioxidant effects. Antimicrobial Peptide YD can be used in pulmonary fibrosis research.
-
MM129
0 ImagesCat. No.: HY-189206MM129 is an anticancer agent. MM129 inhibits key oncogenic signaling molecules such as AKT, mTOR, and CDK2, and downregulates the expression of PD-L1. MM129 induces cell cycle arrest. MM129 induces Apoptosis. MM129 induces DNA damage. MM129 induces oxidative stress. MM129 exhibits chemosensitizing properties. MM129 restores the expression of E-cadherin. MM129 can be used in the research of colorectal cancer.
-
PEG9MA10-PAB10-GalMA10
0 ImagesCat. No.: HY-184926PEG9MA10-PAB10-GalMA10 is a CD147 LYTAC degrader. PEG9MA10-PAB10-GalMA10 binds to the asialoglycoprotein receptor (ASGPR) via its galactose methacrylate domain, mediating its uptake by hepatoma cells. PEG9MA10-PAB10-GalMA10 induces lysosome-dependent degradation of CD147, resulting in concurrent loss of associated MCT1 and MCT4. PEG9MA10-PAB10-GalMA10 reduces extracellular lactate levels, increases intracellular lactate accumulation, inhibits glycolytic activity, and enhances mitochondrial respiratory capacity. PEG9MA10-PAB10-GalMA10 decreases the secretion of MMP-2 and MMP-9, and upregulates the expression of E-cadherin. PEG9MA10-PAB10-GalMA10 exhibits anti-tumor efficacy in hepatoma models. PEG9MA10-PAB10-GalMA10 can be used for research on liver cancer (hepatocellular carcinoma).
-
TKL002
0 ImagesTKL002 is a blood-brain barrier-permeable inhibitor of the CTH/H2S/NF-κB/EMT signaling axis. TKL002 induces G2/M phase cell cycle arrest and apoptosis in glioblastoma cells. TKL002 inhibits the migration and invasion of glioblastoma cells by upregulating E-cadherin and downregulating N-cadherin and vimentin. TKL002 is applicable to relevant research on glioblastoma.
-
AL-GDa62
0 ImagesCat. No.: HY-145269CAS No.: 2761538-66-1AL-GDa62 is a derivative of the CDH1/E-cadherin modulator SLEC-11 (HY-145268) and induces apoptosis in CDH1-/- cells. AL-GDa62 has an EC50 of 3.2 μM and 2 μM for isogenic mammary epithelial cells MCF10A-WT (wild type) and mutant MCF10A-CDH1-/-, respectively. AL-GDa62 specifically inhibits TCOF1, ARPC5, and UBC9, and suppresses SUMOylation at low micromolar concentrations.
