Gene interactions and pathways from curated databases and text-mining

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IGF1 — IGFALS

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Barreca et al., Growth Horm IGF Res 1998 (Sepsis) : By limiting the formation of the 150 kDa complex, this reduction in circulating ALS might contribute to the rapid decline in serum IGF-I observed in sepsis
Silha et al., Adv Exp Med Biol 2005 : Absence of human and also mouse ALS leads to decreased IGF-I levels in circulation and causes mild growth retardation
Kim et al., J Endocrinol 2006 : We conclude that the decline in plasma ALS after parturition is a consequence of hepatic GH resistance and contributes to the associated reduction of plasma IGF-I
Mucci et al., Cancer Epidemiol Biomarkers Prev 2010 (Prostatic Neoplasms) : The acid-labile subunit (ALS) acts in the insulin-like growth ( IGF ) system by binding circulating IGF-I in a ternary complex with binding protein ( IGFBP)-3 to prevent IGF-I from crossing the endothelial barrier
Baxter et al., J Biol Chem 1989 : Pure ALS formed a complex with BP-53 ( Ka approximately 5 x 10 ( 8 ) M-1 ), immunoprecipitable by anti-BP-53 antiserum, only in the presence of IGF-I or IGF-II
Scharf et al., Hepatology 1996 : Insulin, IGF-I , and GH increased ALS expression
Frystyk et al., Endocrinology 1998 : We describe a novel competitive assay for rat insulin-like growth factor (IGF) binding protein-3 ( rIGFBP-3 ) based on the ability of IGFBP-3 to form a ternary complex with the acid labile subunit (ALS) in the presence of IGF
Labarta et al., Clin Endocrinol (Oxf) 1997 (Growth Disorders) : The aims of this investigation were ( a ) to study the presence of immunoreactive forms of the acid-labile subunit (ALS) in different human biological fluids, ( b ) to define the age dependence of serum ALS in normal children and adults and ( c ) to compare the regulation of ALS by GH or IGF-I in children with GH deficiency ( GHD ) and GH receptor deficiency (GHRD) before and after 1 year of therapy with GH or IGF-I, respectively
Frystyk et al., Endocrinology 1998 : We have recently described a competitive binding assay for rat insulin-like growth factor binding protein-3 ( IGFBP-3 ) based on the ability of IGFBP-3 to form a ternary complex with the acid-labile subunit (ALS) in the presence of IGF-I