Article
Inhibition of decidual IGF-1 signaling in response to hypoxia and leucine deprivation is mediated by mTOR and AAR pathways and increased IGFBP-1 phosphorylation.
Molecular and cellular endocrinology
Document Type
Article
Publication Date
7-15-2020
URL with Digital Object Identifier
https://doi.org/10.1016/j.mce.2020.110865
Disciplines
Abstract
Decidual mechanistic target of rapamycin (mTOR) is inhibited, amino acid response (AAR) and protein kinase CK2 are activated, and IGF (insulin-like growth factor) binding protein (IGFBP)-1 is hyperphosphorylated in human intrauterine growth restriction (IUGR). Using decidualized human immortalized endometrial stromal cells (HIESC), we hypothesized that hypoxia and leucine deprivation causing inhibition of decidual IGF-1 signaling is mediated by mTOR, AAR, CK2 and IGFBP-1 phosphorylation. Mass spectrometry demonstrated that hypoxia (1% O
Citation Information
Majida Abu Shehab, Kyle Biggar, Jenica H Kakadia, Manthan Dhruv, et al.. "Inhibition of decidual IGF-1 signaling in response to hypoxia and leucine deprivation is mediated by mTOR and AAR pathways and increased IGFBP-1 phosphorylation." Molecular and cellular endocrinology Vol. 512 (2020) p. 110865 - 110865 Available at: http://works.bepress.com/madhulika-gupta/7/