PIP4kγ is a substrate for mTORC1 that maintains basal mTORC1 signaling during starvation
@article{Mackey2014PIP4kIA, title={PIP4kγ is a substrate for mTORC1 that maintains basal mTORC1 signaling during starvation}, author={A. Mackey and Deborah A. Sarkes and I. Bettencourt and J. Asara and L. Rameh}, journal={Science Signaling}, year={2014}, volume={7}, pages={ra104 - ra104} }
A feedback loop involving PIP4kγ and mTORC1 maintains basal mTORC1 activity under nutrient-deprived conditions. Maintaining a Basal Level of Activity Nutrients such as glucose and amino acids activate mammalian target of rapamycin complex 1 (mTORC1), a complex consisting of the kinase mTOR, which couples metabolic signals to pathways that trigger cellular proliferation and growth. When nutrients are limiting, mTORC1 activity is normally suppressed. Mackey et al. found that under nutrient… CONTINUE READING
Topics from this paper
21 Citations
Insulin sensitivity and PIP3 turnover in Drosophila are regulated by phosphatidylinositol 5 phosphate 4-kinase
- Chemistry, Biology
- 2018
- PDF
Deletion of the gene Pip4k2c, a novel phosphatidylinositol kinase, results in hyperactivation of the immune system
- Biology, Medicine
- Proceedings of the National Academy of Sciences
- 2016
- 25
- Highly Influenced
- PDF
Phosphatidylinositol 5 Phosphate 4-Kinase Regulates Plasma-Membrane PIP3 Turnover and Insulin Signaling
- Chemistry, Medicine
- Cell reports
- 2019
- 8
Phosphatidylinositol 5 phosphate 4-kinase regulates plasma-membrane PIP3 turnover and insulin sensitivity in Drosophila
- Chemistry, Biology
- 2018
Dual blockade of the lipid kinase PIP4Ks and mitotic pathways leads to cancer-selective lethality
- Chemistry, Medicine
- Nature Communications
- 2017
- 23
- PDF
PIP4Ks Suppress Insulin Signaling through a Catalytic-Independent Mechanism
- Chemistry, Medicine
- Cell reports
- 2019
- 3
Phosphatidylinositol 5-phosphate 4-kinase γ (PI5P4Kγ), a lipid signalling enigma.
- Medicine, Biology
- Advances in biological regulation
- 2016
- 8
The Mechanistic Target of Rapamycin: The Grand ConducTOR of Metabolism and Aging.
- Biology, Medicine
- Cell metabolism
- 2016
- 255
Adrenoceptor regulation of the mechanistic target of rapamycin in muscle and adipose tissue
- Biology, Medicine
- British journal of pharmacology
- 2019
- 4
Control of Translation at the Initiation Phase During Glucose Starvation in Yeast
- Biology, Medicine
- International journal of molecular sciences
- 2019
- 6
- PDF
References
SHOWING 1-10 OF 58 REFERENCES
The mTOR-Regulated Phosphoproteome Reveals a Mechanism of mTORC1-Mediated Inhibition of Growth Factor Signaling
- Chemistry, Medicine
- Science
- 2011
- 894
- PDF
mTOR Interacts with Raptor to Form a Nutrient-Sensitive Complex that Signals to the Cell Growth Machinery
- Biology, Medicine
- Cell
- 2002
- 2,621
- PDF
hVps34 Is a Nutrient-regulated Lipid Kinase Required for Activation of p70 S6 Kinase*
- Biology, Medicine
- Journal of Biological Chemistry
- 2005
- 539
- PDF
Nutrient regulation of the mTOR Complex 1 signaling pathway
- Biology, Medicine
- Molecules and cells
- 2013
- 185
Ragulator-Rag Complex Targets mTORC1 to the Lysosomal Surface and Is Necessary for Its Activation by Amino Acids
- Chemistry, Medicine
- Cell
- 2010
- 1,730
- PDF
Dissociation of raptor from mTOR is a mechanism of rapamycin‐induced inhibition of mTOR function
- Biology, Medicine
- Genes to cells : devoted to molecular & cellular mechanisms
- 2004
- 297
- Highly Influential
Ku-0063794 is a specific inhibitor of the mammalian target of rapamycin (mTOR)
- Biology, Medicine
- The Biochemical journal
- 2009
- 443
- PDF
A unifying model for mTORC1-mediated regulation of mRNA translation
- Chemistry, Biology
- Nature
- 2012
- 1,029
- PDF
Staurosporine inhibits phosphorylation of translational regulators linked to mTOR
- Biology, Medicine
- Cell Death and Differentiation
- 2001
- 52
- PDF
Phosphatidylinositol 5-phosphate 4-kinase (PIP4K) regulates TOR signaling and cell growth during Drosophila development
- Biology, Medicine
- Proceedings of the National Academy of Sciences
- 2013
- 48
- PDF