ArticleMolecular and cellular endocrinology2015
IGFBP-1 hyperphosphorylation in response to leucine deprivation is mediated by the AAR pathway.
Article in Molecular and cellular endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- AMPK-mTORC1 pathway mediates hepatic IGFBP-1 phosphorylation in glucose deprivation: a potential molecular mechanism of hypoglycemia-induced impaired fetal growth.Journal of molecular endocrinology · 2024Article
- IGFBP-1 hyperphosphorylation in response to nutrient deprivation is mediated by activation of protein kinase Cα (PKCα).Molecular and cellular endocrinology · 2021Article
- Mechanistic Target of Rapamycin Complex 1 Signaling Links Hypoxia to Increased IGFBP-1 Phosphorylation in Primary Human Decidualized Endometrial Stromal Cells.Biomolecules · 2021Article
- Significance of highly phosphorylated insulin-like growth factor binding protein-1 and cervical length for prediction of preterm delivery in twin pregnancies.World journal of clinical cases · 2021Article
- Hyperphosphorylation of fetal liver IGFBP-1 precedes slowing of fetal growth in nutrient-restricted baboons and may be a mechanism underlying IUGR.American journal of physiology. Endocrinology and metabolism · 2020Article
- Novel roles of mechanistic target of rapamycin signaling in regulating fetal growth†.Biology of reproduction · 2019Review
- IUGR Is Associated With Marked Hyperphosphorylation of Decidual and Maternal Plasma IGFBP-1.The Journal of clinical endocrinology and metabolism · 2019Observational
- DEPTOR at the Nexus of Cancer, Metabolism, and Immunity.Physiological reviews · 2018Review
- Exposure of decidualized HIESC to low oxygen tension and leucine deprivation results in increased IGFBP-1 phosphorylation and reduced IGF-I bioactivity.Molecular and cellular endocrinology · 2017Article
- Increased IGFBP-1 phosphorylation in response to leucine deprivation is mediated by CK2 and PKC.Molecular and cellular endocrinology · 2016Article
- Hypoxia Increases IGFBP-1 Phosphorylation Mediated by mTOR Inhibition.Molecular endocrinology (Baltimore, Md.) · 2016Article
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Insulin-like growth factor-1 (IGF-I) is the key regulator of fetal growth. IGF-I bioavailability is markedly diminished by IGF binding protein-1 (IGFBP-1) phosphorylation. Leucine deprivation strongly induces IGFBP-1 hyperphosphorylation, and plays an important role in fetal growth restriction (FGR). FGR is characterized by decreased amino acid availability, which activates the amino acid response (AAR) and inhibits the mechanistic target of rapamycin (mTOR) pathway. We investigated the role of AAR and mTOR in mediating IGFBP-1 secretion and phosphorylation in HepG2 cells in leucine deprivation. mTOR inhibition (rapamycin or raptor + rictor siRNA), or activation (DEPTOR siRNA) demonstrated a role of mTOR in leucine deprivation-induced IGFBP-1 secretion but not phosphorylation. When the AAR was blocked (U0126, or ERK/GCN2 siRNA), both IGFBP-1 secretion and hyperphosphorylation (pSer101/pSer119/pSer169) due to leucine deprivation were prevented. CK2 inhibition by TBB also attenuated IGFBP-1 phosphorylation in leucine deprivation. These results suggest that the AAR and mTOR independently regulate IGFBP-1 secretion and phosphorylation in response to decreased amino acid availability.
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