Literature summary for 2.7.7.12 extracted from

Balakrishnan, B.; Chen, W.; Tang, M.; Huang, X.; Cakici, D.D.; Siddiqi, A.; Berry, G.; Lai, K.
Galactose-1 phosphate uridylyltransferase (GalT) gene: A novel positive regulator of the PI3K/Akt signaling pathway in mouse fibroblasts (2016), Biochem. Biophys. Res. Commun., 470, 205-212.

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Organism

Organism	UniProt	Comment	Textmining
Mus musculus	A2AMS3	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
fibroblast	primary skin fibroblast	Mus musculus	-

General Information

General Information	Comment	Organism
physiological function	GalT-deficient mice exhibit a subfertility phenotype in adult females and growth restriction in both sexes. The growth potential and the protein levels of the Akt(Thr308), Akt(Ser473), pan-Akt, Pdk1, and Hsp90 proteins are significantly reduced by 62.5%, 60.3%, 66%, 66%, and 50%, respectively in GalT-deficient primary fibroblast cells. Reduced expression of phosphorylated Akt proteins in the mutant cells leads to diminished phosphorylation of Gsk-3b (-74%). Protein expression of BiP and pPten are 276% and 176% higher, respectively in cells with GalT-deficiency. The mRNA abundance of Akt1, Pdpk1, Hsp90aa1 and Pi3kca genes are significantly reduced at least 2.03-, 1.37-, 2.45-, and 1.78fold, respectively in mutant fibroblasts. Both serum-fasted normal and GalT-deficient cells respond to Igf-1-induced activation of Akt phosphorylation at +15 min, but the mutant cells have lower phosphorylation levels. The steady-state protein abundance of Igf-1 receptor is also significantly reduced in mutant cells	Mus musculus

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Release 2023.1 (January 2023)