Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Cadherin and catenin expression in normal human bronchial epithelium and non-small cell lung cancer.
ARVCF localizes to the nucleus and adherens junction and is mutually exclusive with p120(ctn) in E-cadherin complexes.
Suppression of breast cancer invasion and migration by indole-3-carbinol: associated with up-regulation of BRCA1 and E-cadherin/catenin complexes.
FGF-1 and FGF-2 modulate the E-cadherin/catenin system in pancreatic adenocarcinoma cell lines.
Protein binding and functional characterization of plakophilin 2. Evidence for its diverse roles in desmosomes and beta -catenin signaling.
Galpha12 and Galpha13 negatively regulate the adhesive functions of cadherin.
Structure of internalin, a major invasion protein of Listeria monocytogenes, in complex with its human receptor E-cadherin.
WNT7a induces E-cadherin in lung cancer cells.
A role for Galpha12/Galpha13 in p120ctn regulation.
Rab11 in recycling endosomes regulates the sorting and basolateral transport of E-cadherin.
E-cadherin phosphorylation by protein kinase D1/protein kinase C{mu} is associated with altered cellular aggregation and motility in prostate cancer.
Biosensor-based micro-affinity purification for the proteomic analysis of protein complexes.
E-cadherin-dependent transcriptional control of apolipoprotein A-IV gene expression in intestinal epithelial cells: a role for the hepatic nuclear factor 4.
Plakoglobin, or an 83-kD homologue distinct from beta-catenin, interacts with E-cadherin and N-cadherin.
Regulation of epithelial wound closure and intercellular adhesion by interaction of AF6 with actin cytoskeleton.
The von Hippel-Lindau tumor suppressor gene product represses oncogenic beta-catenin signaling in renal carcinoma cells.
E-cadherin regulates human Nanos1, which interacts with p120ctn and induces tumor cell migration and invasion.
Proteomics analysis of the interactome of N-myc downstream regulated gene 1 and its interactions with the androgen response program in prostate cancer cells.
Helicobacter pylori CagA interacts with E-cadherin and deregulates the beta-catenin signal that promotes intestinal transdifferentiation in gastric epithelial cells.
A limited screen for protein interactions reveals new roles for protein phosphatase 1 in cell cycle control and apoptosis.
Ankyrin-G is a molecular partner of E-cadherin in epithelial cells and early embryos.
Thermodynamically reengineering the listerial invasion complex InlA/E-cadherin.
EPLIN mediates linkage of the cadherin catenin complex to F-actin and stabilizes the circumferential actin belt.
P120-catenin is a novel desmoglein 3 interacting partner: identification of the p120-catenin association site of desmoglein 3.
Smad7 stabilizes beta-catenin binding to E-cadherin complex and promotes cell-cell adhesion.
Molecular basis of actin reorganization promoted by binding of enterohaemorrhagic Escherichia coli EspB to alpha-catenin.
Identification of WNT/beta-CATENIN signaling pathway components in human cumulus cells.
Resolving cadherin interactions and binding cooperativity at the single-molecule level.
The role of N-acetylglucosaminyltransferase III and V in the post-transcriptional modifications of E-cadherin.
CagA associates with c-Met, E-cadherin, and p120-catenin in a multiproteic complex that suppresses Helicobacter pylori-induced cell-invasive phenotype.
Characterizing the initial encounter complex in cadherin adhesion.
Lef-1 isoforms regulate different target genes and reduce cellular adhesion.
The Tensin-3 protein, including its SH2 domain, is phosphorylated by Src and contributes to tumorigenesis and metastasis.
Identification of a physiological E2 module for the human anaphase-promoting complex.
Vinculin regulates cell-surface E-cadherin expression by binding to beta-catenin.
Armus is a Rac1 effector that inactivates Rab7 and regulates E-cadherin degradation.
GATA3 inhibits breast cancer metastasis through the reversal of epithelial-mesenchymal transition.
Hypoxia and cell cycle regulation of the von Hippel-Lindau tumor suppressor.
E-cadherin and plakoglobin recruit plakophilin3 to the cell border to initiate desmosome assembly.
Pharmacologic inhibition of the anaphase-promoting complex induces a spindle checkpoint-dependent mitotic arrest in the absence of spindle damage.
The extracellular architecture of adherens junctions revealed by crystal structures of type I cadherins.
Rack1 promotes epithelial cell-cell adhesion by regulating E-cadherin endocytosis.
Identification of PTPN23 as a novel regulator of cell invasion in mammary epithelial cells from a loss-of-function screen of the 'PTP-ome'.
Nuclear PKM2 regulates β-catenin transactivation upon EGFR activation.
Tumor suppressor Alpha B-crystallin (CRYAB) associates with the cadherin/catenin adherens junction and impairs NPC progression-associated properties.
Structure of a novel phosphotyrosine-binding domain in Hakai that targets E-cadherin.
Non-junctional human desmoglein 3 acts as an upstream regulator of Src in E-cadherin adhesion, a pathway possibly involved in the pathogenesis of pemphigus vulgaris.
Centralspindlin and α-catenin regulate Rho signalling at the epithelial zonula adherens.
The CD46-Jagged1 interaction is critical for human TH1 immunity.
Ideal, catch, and slip bonds in cadherin adhesion.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
Flotillin microdomains stabilize cadherins at cell-cell junctions.
Perturbation of the mutated EGFR interactome identifies vulnerabilities and resistance mechanisms.
Rescue of wild-type E-cadherin expression from nonsense-mutated cancer cells by a suppressor-tRNA.
The mammalian-membrane two-hybrid assay (MaMTH) for probing membrane-protein interactions in human cells.
Intestinal brush border assembly driven by protocadherin-based intermicrovillar adhesion.
Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.
ASPP2 controls epithelial plasticity and inhibits metastasis through β-catenin-dependent regulation of ZEB1.
E-cadherin interactome complexity and robustness resolved by quantitative proteomics.
Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection.
Loss of DLG5 promotes breast cancer malignancy by inhibiting the Hippo signaling pathway.
Blepharocheilodontic syndrome is a CDH1 pathway-related disorder due to mutations in CDH1 and CTNND1.
E-cadherin binds to desmoglein to facilitate desmosome assembly.
Sperm Flagellar 1 Binds Actin in Intestinal Epithelial Cells and Contributes to Formation of Filopodia and Lamellipodia.
Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Regulation of intestinal epithelial intercellular adhesion and barrier function by desmosomal cadherin desmocollin-2.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
A protein interaction landscape of breast cancer.
Identification of Desmoglein-2 as a novel target of Helicobacter pylori HtrA in epithelial cells.
OpenCell: Endogenous tagging for the cartography of human cellular organization.
A physical wiring diagram for the human immune system.
Desmoglein-2 is important for islet function and β-cell survival.
E-cadherin gene mutations provide clues to diffuse type gastric carcinomas.
Caspase-mediated cleavage of E-Cadherin
Interaction of integrin alphaEbeta7 with Cadherin-1
E-cadherin degradation by MMP9, KLK7
Connection of adjacent cells through calcium-dependent trans-dimerization of cadherin
Interaction of cadherin with Beta/gamma catenin, alpha catenin and p120 catenin
E-cadherin degradation by ADAM10, ADAM15
IQGAP1 binds CDH1:CTTNB1:CTTNA1 and MEN1
SRC phosphorylates InlA-bound CDH1 and CTNNB1
CBLL1 binds SRC-phosphorylated CDH1 complex
CBLL1 ubiqutinates the InlA-bound CDH1 complex
Proteasome-dependent degradation of ubiquitinated CDH1
MDM2 mediates CDH1 ubiquitination
miR-9 inhibits CDH1 mRNA translation
miR-10b inhibits CDH1 mRNA translation
CDH1 translocates from ER to Golgi
CDH1 is proteolytically cleaved in Golgi
CDH1 is N-glycosylated on asparagine residues in endoplasmic reticulum
CDH1 translocates to the plasma membrane
CDH1 associates with CTNND1
CDH1:CTNNB1 complex binds CTNNA1
SNAI2 and TBX3 repress CDH1 gene expression during melanocyte development
MITF-M-dependent CDH1 gene expression
Removal of CDH1 signal peptide
MOGS removes terminal glucose from Glu3Man9GlcNAc2-CDH1
Glucosidase II removes glucose residue from Glu2Man9GlucNAc2-CDH1
Glucosidase II removes glucose residue from Glu1Man9GlucNAc2-CDH1
CANX binds Glu1Man9GlcNAc2-CDH1
Cytosolic tail of CDH1 is phosphorylated
CDH1-associated CTNNA1 binds VCL
CDH1:CTNNB1,JUP complex binds to ANK3
CDH1 forms homotypic trans-dimers
CDH1-associated CTNNA1 binds F-actin
The complex of MDM2 and CDH1 translocates to early endosomes
CDH1 is phosphorylated on tyrosine residues
Ubiquitinated CDH1 is endocytosed
Lysosomal degradation of ubiquitinated CDH1
Ubiquitinated CDH1 translocates to lysosomes for degradation
E-cadherin strand dimer degradation by PS1
UniProt record for human CDH1 (P12830)
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Cadherins, including E-cadherin/CDH1, are calcium-dependent cell adhesion proteins.
"Cadherins are calcium-dependent cell adhesion proteins"
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E-cadherin mediates homophilic cell-cell adhesion by preferentially interacting with itself.
"They preferentially interact with themselves in a homophilic manner in connecting cells"
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E-cadherin is a component of an E-cadherin/catenin adhesion complex containing beta-catenin or gamma-catenin, located at adherens junctions.
"beta-catenin/CTNNB1 or gamma-catenin/JUP"
Manual deep research summary for human CDH1 (E-cadherin)
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E-cadherin mediates calcium-dependent homophilic trans-adhesion via strand-swap dimerization between EC1 domains on apposing cells; trans interactions are sufficient for aggregation while cis interactions are additionally required for junction assembly.
"EC1 domains of each protomer closely interact and symmetrically exchange their N-terminal β-strands, which contain a conserved tryptophan residue, Trp2; trans interactions are sufficient to mediate aggregation, while cis interactions are further required for assembly of junctions"
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The cytoplasmic tail of E-cadherin nucleates the cadherin-catenin complex by binding beta-catenin/plakoglobin and p120-catenin, coupling homophilic adhesion to the cortical actin cytoskeleton via alpha-catenin and adaptor proteins.
"Component of an E-cadherin/catenin adhesion complex; the juxtamembrane domain binds CTNND1 (p120-catenin); alpha-catenin links the complex to F-actin via adaptor proteins including EPLIN and AF6/afadin"
Falcon deep research report on CDH1
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E-cadherin is a calcium-dependent cell-cell adhesion molecule that organizes epithelial tissue architecture via homophilic adhesion, supporting epithelial integrity and polarity.
"E‑cadherin is a **calcium-dependent cell–cell adhesion molecule** that organizes epithelial tissue architecture by mediating **homophilic adhesion** and supporting epithelial integrity and polarity"
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The E-cadherin ectodomain is composed of five extracellular cadherin repeats (EC1-EC5) containing calcium-binding sites that rigidify the ectodomain for adhesion.
"extracellular portion contains **five cadherin repeats (EC1–EC5)** with **calcium-binding sites**"
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Homophilic adhesion proceeds through an EC1-mediated X-dimer intermediate to a stable strand-swapped dimer in which a tryptophan from one EC1 inserts into the hydrophobic pocket of the opposing EC1.
"**homophilic trans-binding** is driven primarily by the **EC1 domain** and proceeds through an **X-dimer intermediate** followed by formation of a stable **strand-swapped dimer**, in which a **tryptophan side chain from one EC1 inserts into a hydrophobic pocket** of the opposing EC1"
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In epithelia, E-cadherin is enriched at the plasma membrane and concentrates at adherens junctions, where it maintains epithelial sheet cohesion and tissue architecture.
"In epithelia, E‑cadherin is enriched at the **plasma membrane** and concentrates at **adherens junctions** where it contributes to epithelial sheet cohesion and tissue architecture"
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The E-cadherin cytoplasmic tail is anchored to the actin cytoskeleton through beta-catenin and alpha-catenin, enabling transmission of actomyosin forces across junctions.
"Experimental/biophysical synthesis emphasizes anchoring through **β‑catenin and α‑catenin**, enabling transmission of actomyosin forces across junctions"
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E-cadherin also interacts with p120-catenin, and changes in E-cadherin availability can alter beta-catenin and p120-catenin signaling states.
"Broader mechanistic synthesis also highlights interaction with **p120‑catenin**, and how changes in E‑cadherin availability can alter β‑catenin and p120‑catenin signaling states"
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Adherens junctions formed by E-cadherin act as a mechanosensitive scaffold, transmitting actomyosin-generated pulling forces via beta-catenin/alpha-catenin anchorage rather than functioning as static "glue".
"E‑cadherin-based adhesions transmit **actomyosin-generated pulling forces** through β‑catenin/α‑catenin anchorage, and junction stability can be limited by cytoskeletal anchorage rather than cadherin–cadherin binding strength"
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Loss or downregulation of E-cadherin can release beta-catenin to permit nuclear translocation and Wnt pathway activation, and can alter RhoA/Rac1 signaling via redistribution of p120-catenin.
"a synthesis of cancer-related mechanisms describes that E‑cadherin loss can permit **β‑catenin nuclear translocation** with **Wnt pathway activation** (samardali2025acomprehensiveliterature pages 7-8). The same synthesis notes that redistribution of **p120‑catenin** can influence **RhoA/Rac1** signaling"
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EMT programs repress E-cadherin, and this loss contributes to invasion and metastasis; E-cadherin downregulation is a hallmark of EMT and cancer cell motility changes.
"EMT programs repress E‑cadherin and that such loss contributes to invasion and metastasis"
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Germline CDH1 pathogenic variants are a primary cause of hereditary diffuse gastric cancer (HDGC), with clinical management historically including prophylactic total gastrectomy.
"Germline **CDH1 pathogenic variants** are a primary cause of **HDGC**, and clinical management has historically included **prophylactic total gastrectomy (PTG)**"
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E-cadherin loss is necessary but not sufficient for invasive progression; invasion in HDGC models emerges from the interplay between defective cell-cell junctions, ECM attachment, and 3D tissue architecture.
"invasion in HDGC models emerges from interplay between **defective cell-cell junctions**, **ECM attachment**, and **3D tissue architecture**, rather than from loss of adhesion alone"
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E-cadherin can undergo proteolytic cleavage/shedding, generating soluble E-cadherin fragments; cleavage releases junctional restraint and can free beta-catenin.
"E-cadherin can undergo **proteolytic cleavage/shedding**, generating **soluble E-cadherin fragments**; cleavage releases junctional restraint and can free β-catenin"
E-cadherin and APC compete for the interaction with beta-catenin and the cytoskeleton.
Uvomorulin-catenin complex formation is regulated by a specific domain in the cytoplasmic region of the cell adhesion molecule.
Transformation of cell adhesion properties by exogenously introduced E-cadherin cDNA.
Two-step adhesive binding by classical cadherins.
E-cadherin supports steady-state Rho signaling at the epithelial zonula adherens.