1 sources retrieved · Most recent: April 2026 · Index updated 14 days ago
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12PubMed Papers
20Diseases
0Drugs
0Pathogenic Variants
FUNCTIONAL ROLETranscription Factor
DATA QUALITY✓ Experimental GO Evidence✓ Swiss-Prot Reviewed
protein bindingnucleusidentical protein bindingnegative regulation of myoblast differentiationdehydrated hereditary stomatocytosisdiabetes mellitus, permanent neonatal 4ghosal hematodiaphyseal dysplasiamaturity-onset diabetes of the young type 13
Based on limited published evidence, EID2B functions as a transcriptional repressor that negatively regulates MYOD-dependent transcription, glucocorticoid receptor signaling, and myoblast differentiation. UniProt and GO annotations indicate EID2B acts as a transcription corepressor localized to the nucleus/nucleoplasm through protein-binding interactions. Recent research demonstrates that exosomal miR-92a-3p targets EID2B in colorectal cancer, where EID2B downregulation promotes M2 macrophage polarization via MAPK/ERK pathway activation, facilitating tumor migration and angiogenesis 1.
1
EID2B is targeted by miR-92a-3p in colorectal cancer exosomes; EID2B negatively correlates with M2 macrophage polarization and MAPK/ERK pathway activation
PMID: 40059261⚠Limited data available — This gene has 1 indexed publication. Summary and analysis may be incomplete.
dehydrated hereditary stomatocytosisOpen Targets
diabetes mellitus, permanent neonatal 4Open Targets
ghosal hematodiaphyseal dysplasiaOpen Targets
maturity-onset diabetes of the young type 13Open Targets
permanent neonatal diabetes mellitus 1Open Targets
22q11.2 deletion syndromeOpen Targets
diabetes mellitus, transient neonatal, 3Open Targets
autosomal recessive hypophosphatemic ricketsOpen Targets
familial pseudohyperkalemiaOpen Targets
osteopetrosis, autosomal recessive 9Open Targets
oligodendrogliomaOpen Targets
pancreatic adenocarcinomaOpen Targets
Alzheimer diseaseOpen Targets
colorectal carcinomaOpen Targets
Parkinson diseaseOpen Targets
No pathogenic variants reported on ClinVar for this gene.