SCUBA

IGF2 — Insulin like growth factor 2

IGF2 belongs to a gene co-expression module in 1 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.

IGF2's module in each cell type

Cell typeModuleShares the module with
EndothelialYAP Mechanotransduction
migration & adhesion
COBLL1, CREB5, DEPP1, DST, FGL2, FLNC, FN1, GCNT2 +7 moreView in SCUBA

About the gene

SynonymsC11orf43, FLJ44734, IGF-II
Chromosome11: 2129112-2158391
Predicted locationMembrane, Secreted
Essential geneNo
Protein classCancer-related genes, Disease related genes, Human disease related genes, Plasma proteins, Predicted membrane proteins, Predicted secreted proteins, RAS pathway related proteins
Molecular functionGrowth factor, Hormone, Mitogen
Biological processCarbohydrate metabolism, Glucose metabolism, Osteogenesis

Function

The insulin-like growth factors possess growth-promoting activity (By similarity). Major fetal growth hormone in mammals. Plays a key role in regulating fetoplacental development. IGF2 is influenced by placental lactogen. Also involved in tissue differentiation. In adults, involved in glucose metabolism in adipose tissue, skeletal muscle and liver (Probable). Acts as a ligand for integrin which is required for IGF2 signaling. Positively regulates myogenic transcription factor MYOD1 function by facilitating the recruitment of transcriptional coactivators, thereby controlling muscle terminal differentiation (By similarity). Inhibits myoblast differentiation and modulates metabolism via increasing the mitochondrial respiration rate (By similarity). Preptin undergoes glucose-mediated co-secretion with insulin, and acts as a physiological amplifier of glucose-mediated insulin secretion. Exhibits osteogenic properties by increasing osteoblast mitogenic activity through phosphoactivation of MAPK1 and MAPK3

Human Protein Atlas · Open Targets · UniProt

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