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
The c-Src tyrosine kinase regulates signaling of the human DF3/MUC1 carcinoma-associated antigen with GSK3 beta and beta-catenin.
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c-Src phosphorylates MUC1-CT at YEKV motif and regulates interactions with GSK3β and β-catenin
"c-Src phosphorylates the MUC1 cytoplasmic domain at a YEKV motif located between sites involved in interactions with GSK3 beta and beta-catenin."
The epidermal growth factor receptor regulates interaction of the human DF3/MUC1 carcinoma antigen with c-Src and beta-catenin.
Identification and proteomic profiling of exosomes in human urine.
Human MUC1 oncoprotein regulates p53-responsive gene transcription in the genotoxic stress response.
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MUC1-CT binds p53 and modulates p53-dependent transcription in response to DNA damage
"The MUC1 oncoprotein is aberrantly overexpressed by most human carcinomas. The present work demonstrates that MUC1 associates with the p53 tumor suppressor, and that this interaction is increased by genotoxic stress. The MUC1 cytoplasmic domain binds directly to p53 regulatory domain."
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MUC1 promotes p53-dependent growth arrest while suppressing apoptosis in response to DNA damage
"MUC1 promotes selection of the p53-dependent growth arrest response and suppresses the p53-dependent apoptotic response to DNA damage."
Human colostrum: identification of minor proteins in the aqueous phase by proteomics.
MUC1 oncoprotein blocks nuclear targeting of c-Abl in the apoptotic response to DNA damage.
Molecular cloning and expression of human tumor-associated polymorphic epithelial mucin.
Large-scale proteomics and phosphoproteomics of urinary exosomes.
Characterization of exosome-like vesicles released from human tracheobronchial ciliated epithelium: a possible role in innate defense.
Proteomic analysis of human parotid gland exosomes by multidimensional protein identification technology (MudPIT).
Galectin-3 regulates MUC1 and EGFR cellular distribution and EGFR downstream pathways in pancreatic cancer cells.
Non-cysteine linked MUC1 cytoplasmic dimers are required for Src recruitment and ICAM-1 binding induced cell invasion.
Cooperative interaction of MUC1 with the HGF/c-Met pathway during hepatocarcinogenesis.
In-depth proteomic analyses of exosomes isolated from expressed prostatic secretions in urine.
The mammalian-membrane two-hybrid assay (MaMTH) for probing membrane-protein interactions in human cells.
Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).
Episialin (MUC1) overexpression inhibits integrin-mediated cell adhesion to extracellular matrix components.
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MUC1 overexpression inhibits integrin-mediated cell adhesion to extracellular matrix through steric hindrance
"Episialin (MUC1) is a transmembrane molecule with a large mucin-like extracellular domain protruding high above the cell surface. The molecule is located at the apical side of most glandular epithelial cells, whereas in carcinoma cells it is often present at the entire surface and it is frequently expressed in abnormally large quantities. We have previously shown that overexpression of episialin reduces cell-cell interactions. Here we show that the integrin-mediated adhesion to extracellular matrix of transfectants of a melanoma cell line (A375), a transformed epithelial cell line (MDCK-ras-e) and a human breast epithelial cell line (HBL-100) is reduced by high levels of episialin."
Addition of galactose to Core 6 glycoprotein
C1GALT1 transfers Galactose to the Tn antigen forming Core 1 glycoproteins (T antigens)
Defective GALNT12 does not transfer GalNAc to mucins
Defective GALNT3 does not transfer GalNAc to mucins
A4GNT transfers GlcNAc to core 2 mucins
Defective C1GALT1C1 does not bind C1GALT1
CHST4 transfers SO4(2-) from PAPS to Core 2 mucins
Expression of STAT3-upregulated plasma membrane proteins
GALNTs transfer GalNAc to Mucins to form Tn antigens
Addition of GlcNAc to the Tn antigen via an alpha-1,3 linkage forms a Core 5 glycoprotein
Addition of galactose to the Tn antigen via an alpha-1,3 linkage forms a Core 8 glycoprotein
Addition of GlcNAc to the Tn antigen via a beta-1,6 linkage forms a Core 6 glycoprotein
B3GNT6 transfers GlcNAc to Tn antigen
GCNTs transfer GlcNAc from UDP-GlcNAc to Core 1 mucins
Addition of GalNAc to the Tn antigen via an alpha-1,6 linkage forms a Core 7 glycoprotein
GCNT3 transfers GlcNAc to Core 3 mucin
ST6GAL1 transfers sialic acid to Tn antigens to form sTn antigens
ST3GAL1-4 transfers sialic acid to the T antigen at the alpha 3 position
ST6GALNAC3/4 transfers sialic acid to the sialyl T antigen to form the disialyl T antigen
ST6GALNAC2 transfers sialic acid to Core 1 mucins
Deep research on MUC1 function
Falcon deep research on MUC1 function (Edison Scientific Literature, 2026-05-29)
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MUC1-CT physically interacts with TLR4 and MUC1 deficiency increases TLR4-MyD88 binding, supporting a physical constraint model that attenuates neutrophilic airway inflammation via inhibition of the TLR4/MyD88/NF-κB pathway and NLRP3 inflammasome-mediated pyroptosis
"Mechanism: co-immunoprecipitation indicated MUC1-CT interacts with TLR4 and MUC1 deficiency increases TLR4–MyD88 binding, supporting a physical constraint model."
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MUC1-C sustains antioxidant defenses through an NF-κB/MUC1-C auto-inductive circuit and a MUC1-C→MYC axis regulating GSR, LRP8, and GPX4, conferring ferroptosis resistance in cancer stem cell-like states
"MUC1-C sustains antioxidant defenses through a NF-κB/MUC1-C auto-inductive circuit and a MUC1-C→MYC axis that regulates GSR, LRP8, and GPX4 activity, consistent with glutathione/selenium-dependent ferroptosis control."
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Chronic hypoxia induces durable transcriptional programs persisting after reoxygenation, with MUC1/MUC1-C as a key effector induced by HIF-1α and NF-κB p65 that promotes ROS resistance and metastatic competence; GO-203 inhibition increases mitochondrial ROS in circulating tumor cells and reduces hypoxia-marked metastatic burden by ~53%
"GO-203 pharmacologic inhibition increased mitochondrial ROS in circulating tumor cells (CTCs) and yielded a 53% reduction in the contribution of hypoxia-marked (GFP+) cells to metastatic burden in an in vivo model."
MUC1 attenuates neutrophilic airway inflammation in asthma by reducing NLRP3 inflammasome-mediated pyroptosis through the inhibition of the TLR4/MyD88/NF-κB pathway.
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MUC1-CT physically interacts with TLR4 in airway epithelial cells; MUC1 knockdown increases TLR4-MyD88 binding and downstream NF-κB activation, establishing MUC1 as a negative regulator of TLR4 signaling in vivo
"MUCl-CT interacted with TLR4, and the interaction between TLR4 and MyD88 was significantly increased after MUCl-siRNA transfection."
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MUC1 expression is downregulated in induced sputum from patients with asthma and inversely correlates with TLR4/MyD88/NLRP3/caspase-1/IL-18/IL-1β transcripts and neutrophil proportion, consistent with MUC1 acting as a tonic brake on TLR4-driven inflammasome activity
"MUC1 expression in induced sputum of patients with asthma was downregulated and was related to asthma severity."
MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells.
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MUC1-C sustains a NF-κB/MUC1-C auto-inductive circuit that supports ferroptosis resistance in cancer stem cell-like states; pharmacologic disruption (salinomycin, GO-203) downregulates GSR/LRP8/GPX4 and induces ferroptosis
"We demonstrate that SAL suppresses MUC1-C expression by disrupting a NF-κB/MUC1-C auto-inductive circuit that is necessary for ferroptosis resistance."
Hypoxia induces ROS-resistant memory upon reoxygenation in vivo promoting metastasis in part via MUC1-C.
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MUC1/MUC1-C is upregulated by HIF-1α and NF-κB p65 during chronic hypoxia and sustains superoxide dismutase expression to limit ROS; abrogating MUC1 or inhibiting MUC1-C with GO-203 increases ROS in circulating tumor cells and reduces metastatic burden, linking MUC1-C to hypoxia-driven metastatic competence
"MUC1/MUC1-C is upregulated by both HIF-1α and NF-kB-p65 during chronic hypoxia. Abrogating MUC1 decreases the expression of superoxide dismutase enzymes, causing reactive oxygen species (ROS) production and cell death."