IGFBP1

Gene Information
 
Gene Symbol
IGFBP1
 
Aliases
AFBP, IBP1, IGF-BP25, PP12, hIGFBP-1
 
Entrez Gene ID
 
Gene Name
Insulin like growth factor binding protein 1
 
Chromosomal Location
7p12.3
 
HGNC ID
 
Summary
This gene is a member of the insulin-like growth factor binding protein (IGFBP) family and encodes a protein with an IGFBP N-terminal domain and a thyroglobulin type-I domain. The encoded protein, mainly expressed in the liver, circulates in the plasma and binds both insulin-like growth factors (IGFs) I and II, prolonging their half-lives and altering their interaction with cell surface receptors. This protein is important in cell migration and metabolism. Low levels of this protein may be associated with impaired glucose tolerance, vascular disease and hypertension in human patients. [provided by RefSeq, Aug 2017]
  e!Ensembl
Gene
Transcript  
Protein

Gene Ontology (GO)

GO ID Ontology Function Evidence Reference
GO:0007165 Biological process Signal transduction TAS 2454104
GO:0043567 Biological process Regulation of insulin-like growth factor receptor signaling pathway IBA 21873635
GO:0090090 Biological process Negative regulation of canonical Wnt signaling pathway TAS 24431302
GO:0005615 Cellular component Extracellular space IBA 21873635
GO:0005102 Molecular function Signaling receptor binding TAS 24431302
Protein Information
 
Protein Name
Insulin-like growth factor-binding protein 1, IBP-1, IGF-binding protein 1, IGFBP-1, alpha-pregnancy-associated endometrial globulin, amniotic fluid binding protein, binding protein-25, binding protein-26, binding protein-28, growth hormone independent-binding protein, placental protein 12
 
Function
IGF-binding proteins prolong the half-life of the IGFs and have been shown to either inhibit or stimulate the growth promoting effects of the IGFs on cell culture. They alter the interaction of IGFs with their cell surface receptors. Promotes cell migration.
 
UniProt
 
PDB
 
Pfam
Pfam Accession Pfam ID
PF00219 IGFBP
PF00086 Thyroglobulin_1
Pathways
 
Reactome
 

 

ATF4 activates genes in response to endoplasmic reticulum stress
Regulation of Insulin-like Growth Factor (IGF) transport and uptake by Insulin-like Growth Factor Binding Proteins (IGFBPs)
Post-translational protein phosphorylation
FOXO-mediated transcription of oxidative stress, metabolic and neuronal genes

Interactions
 
STRING MINT IntAct
ENSP00000370473 P17936 P17936
    View interactions
     

Associated Diseases

Disease groupDisease NameReferences
Congenital, Hereditary, and Neonatal Diseases and Abnormalities
Russell-Silver syndrome
Digestive System Diseases
Biliary Cirrhosis
Liver Fibrosis
Liver Cirrhosis
Endocrine System Diseases
PCOS
References
 
 
PubMed ID Associated gene/s Associated condition Genetic Mutation Diagnostic Criteria Association with PCOS Ethnicity Conclusion
SHBG  
 
 
 
Related 
21 PCO, 18 obese women without menstrual disturbances and 9 Control 
obese women with PCO insulin influence ovarian androgen production and decreases the serum SHBG and IGFBP-1 which could contribute in the augmentation of the symptoms of PCO 
IGF-1 and IGF 
 
 
 
Related 
10 PCOS, 12 hypopituitarism and 10 Control 
Women with PCOS have normal serum IGF-1 concentrations but IGFBP-1 levels, regulated by insulin, are low 
 
 
 
 
Related 
 
Decreased serum level of IGFBP-1 is unlikely to be a mechanism for ovarian hyperandrogenism in PCOS 
Matrix metalloproteinases(MMPs) 
 
 
 
Related 
42 PCOS and 30 Control 
MMPs may be implicated in the pathophysiology of PCOS either by regulating ovarian tissue remodeling or indirectly by facilitating IGF-I bioavailability through proteolysis of IGFBP-1 
Glycodelin  
 
 
PCOS was diagnosed before pregnancy, and defined by oligomenorrhea (eight or fewer menstrual periods annually before pregnancy) and hyperandrogenism (elevated serum free testosterone concentration or hirsutism) 
Related 
72 PCOS and 62 Control 
During the first trimester, serum glycodelin and IGFBP-1 concentrations are markedly decreased in PCOS, implicating endometrial epithelial and stromal dysfunction during periimplantation and early pregnancy as a possible mechanism for EPL in PCOS 

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