SCUBA

EIF4EBP2 — Eukaryotic translation initiation factor 4E binding protein 2

EIF4EBP2 belongs to a gene co-expression module in 4 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

EIF4EBP2's module in each cell type

Cell typeModuleShares the module with
EnterocytesCrypt-top colonocyte
Absorption
ALDOC, AQP1, FADS6, GRIK2, RHOBTB2, SLC17A8, SUSD2, TLCD4View in SCUBA
Gamma-delta T cellsRNA Splicing Processing
RNA processing & translation
ABCF2, ACTR1B, ARF3, C1orf35, CDK11B, DCAF8, DDX39B, IDH3B +16 more
Innate lymphoid cellsJAK-STAT Cytokine Signaling
Inflammation
AASDHPPT, ARHGAP9, CHURC1, CIDEB, CSK, DCAF7, DENND2D, EDEM2 +23 moreView in SCUBA
MacrophagesMacrophage Endocytic Signaling
Lysosomal & pahgocytosis
APLP2, ARHGAP30, ARHGEF2, ATF6B, BAG6, CLSTN1, CMTR2, CTBS +20 moreView in SCUBA

About the gene

Chromosome10: 70404145-70428618
Predicted locationIntracellular
Essential geneNo
Protein classPredicted intracellular proteins
Molecular functionProtein synthesis inhibitor
Biological processTranslation regulation

Function

Repressor of translation initiation involved in synaptic plasticity, learning and memory formation. Regulates EIF4E activity by preventing its assembly into the eIF4F complex: hypophosphorylated form of EIF4EBP2 competes with EIF4G1/EIF4G3 and strongly binds to EIF4E, leading to repress translation. In contrast, hyperphosphorylated form dissociates from EIF4E, allowing interaction between EIF4G1/EIF4G3 and EIF4E, leading to initiation of translation. EIF4EBP2 is enriched in brain and acts as a regulator of synapse activity and neuronal stem cell renewal via its ability to repress translation initiation (By similarity). Mediates the regulation of protein translation by hormones, growth factors and other stimuli that signal through the MAP kinase and mTORC1 pathways (By similarity).

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.