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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

AKT1 substrate 1

PRAS40, PKB/Akt substrate 40
Top mentioned proteins: Akt, mTOR, mTORC1, Insulin, p70S6K
Papers on PRAS40
Hydrophobic Motif Site-phosphorylated Protein Kinase CβII between mTORC2 and Akt Regulates High Glucose-induced Mesangial Cell Hypertrophy.
Ghosh Choudhury et al., San Antonio, United States. In Am J Physiol Cell Physiol, Feb 2016
PKCβII via its phosphorylation at Ser-660 regulated phosphorylation of Akt at both catalytic loop and hydrophobic motif sites, resulting in phosphorylation and inactivation of its substrate PRAS40.
Disruption of REDD1 gene ameliorates sepsis-induced decrease in mTORC1 signaling but has divergent effects on proteolytic signaling in skeletal muscle.
Lang et al., State College, United States. In Am J Physiol Endocrinol Metab, Jan 2016
However, Akt and PRAS40 phosphorylation was suppressed in both sham and septic muscle from REDD1(-/-) mice despite unaltered PDK1, PP2A, or TSC2 expression.
A putative biomarker signature for clinically effective AKT inhibition: correlation of in vitro, in vivo and clinical data identifies the importance of modulation of the mTORC1 pathway.
Stronach et al., Houston, United States. In Oncotarget, Jan 2016
GSK2141795 treatment in vitro and in vivo resulted in ~50-90% decrease in phospho-PRAS40 and 20-80% decrease in fluoro-deoxyglucose (FDG) uptake.
Tobacco Smoke Exposure Impairs Brain Insulin/IGF Signaling: Potential Co-Factor Role in Neurodegeneration.
de la Monte et al., Providence, United States. In J Alzheimers Dis, Jan 2016
Correspondingly, CS and CS8+R exposures inhibited expression of proteins and phosphoproteins required for signaling through Akt, PRAS40, and/or p70S6K, increased AβPP-Aβ, and reduced ASPH protein, which is a target of insulin/IGF-1 signaling.
Enabling systematic interrogation of protein-protein interactions in live cells with a versatile ultra-high-throughput biosensor platform.
Fu et al., Atlanta, United States. In J Mol Cell Biol, Dec 2015
We further demonstrate the application of BRET(n) in uHTS format in chemical biology research, including the discovery of chemical probes that disrupt PRAS40 dimerization and pathway connectivity profiling among core members of the Hippo signaling pathway.
Ischemia-Induced Changes of PRAS40 and p-PRAS40 Immunoreactivities in the Gerbil Hippocampal CA1 Region After Transient Cerebral Ischemia.
Lee et al., Ch'unch'ŏn, South Korea. In Cell Mol Neurobiol, Dec 2015
UNASSIGNED: Proline-rich Akt substrate of 40-kDa (PRAS40) is one of the important interactive linkers between Akt and mTOR signaling pathways.
Regulation of mTORC1 by PI3K signaling.
Cantley et al., Boston, United States. In Trends Cell Biol, Sep 2015
Activation of mTORC1 [composed of mTOR, regulatory-associated protein of mTOR (Raptor), mammalian lethal with SEC13 protein 8(mLST8), 40-kDa proline-rich Akt substrate (PRAS40), and DEP domain-containing mTOR-interacting protein (DEPTOR)] depends on the Ras-related GTPases (Rags) and Ras homolog enriched in brain (Rheb) GTPase and requires signals from amino acids, glucose, oxygen, energy (ATP), and growth factors (including cytokines and hormones such as insulin).
Proline-rich AKT substrate of 40-kDa (PRAS40) in the pathophysiology of cancer.
Tiwari et al., Stockton, United States. In Biochem Biophys Res Commun, Aug 2015
The proline-rich AKT substrate of 40-kDa (PRAS40), also known as AKT substrate 1 (AKT1S1), lies at the crossroads of these cascades and inhibits the activity of the mTOR complex 1 (mTORC1) kinase.
Point mutations of the mTOR-RHEB pathway in renal cell carcinoma.
Sudarshan et al., Birmingham, United States. In Oncotarget, Aug 2015
Several of the FAT domain mutants demonstrated a decreased binding of DEPTOR (DEP domain containing mTOR-interacting protein), while a subset of these mutations showed altered binding of the negative regulator PRAS40 (proline rich AKT substrate 40).
Taking aim at Alzheimer's disease through the mammalian target of rapamycin.
Maiese, Newark, United States. In Ann Med, 2014
mTOR modulates multi-faceted signal transduction pathways that involve phosphoinositide 3-kinase (PI 3-K), protein kinase B (Akt), hamartin (tuberous sclerosis 1)/ tuberin (tuberous sclerosis 2) (TSC1/TSC2) complex, proline-rich Akt substrate 40 kDa (PRAS40), and p70 ribosomal S6 kinase (p70S6K) and can interface with the neuroprotective pathways of growth factors, sirtuins, wingless, forkhead transcription factors, and glycogen synthase kinase-3β.
Cardiosphere Conditioned Media Influence the Plasticity of Human Mediastinal Adipose Tissue-Derived Mesenchymal Stem Cells.
De Falco et al., Latina, Italy. In Cell Transplant, 2014
Nonetheless, earlier BAD phosphorylation (Ser112) occurs associated with the CS microenvironment (and to a lesser extent to EDCM), whereas faster phosphorylation of PRAS40 in FBS, and of Akt (Ser473) in EDCM and 5-azacytidine occurs compared to CCM.
Driving neural regeneration through the mammalian target of rapamycin.
Maiese, Newark, United States. In Neural Regen Res, 2014
mTOR through its relationship with phosphoinositide 3-kinase (PI 3-K) and protein kinase B (Akt) and multiple downstream signaling pathways such as p70 ribosomal S6 kinase (p70S6K) and proline rich Akt substrate 40 kDa (PRAS40) promotes neuronal cell regeneration through stem cell renewal and oversees critical pathways such as apoptosis, autophagy, and necroptosis to foster protection against neurodegenerative disorders.
Dual specificity kinase DYRK3 couples stress granule condensation/dissolution to mTORC1 signaling.
Pelkmans et al., Zürich, Switzerland. In Cell, 2013
When DYRK3 is active, it allows stress granule dissolution, releasing mTORC1 for signaling and promoting its activity by directly phosphorylating the mTORC1 inhibitor PRAS40.
Insulin-like growth factor-1 induces the phosphorylation of PRAS40 via the PI3K/Akt signaling pathway in PC12 cells.
Zheng et al., Shiqi, China. In Neurosci Lett, 2012
Taken together, these data demonstrate that IGF-1 stimulates the phosphorylation of PRAS40 at Thr246 in neuronal cells and the effect of IGF-1 is mediated, at least in part, by the PI3K/Akt signaling pathway.
The Akt signaling pathway: an emerging therapeutic target in malignant melanoma.
Robertson et al., United States. In Cancer Biol Ther, 2012
Furthermore, targeting Akt3 and downstream PRAS40 has been shown to inhibit melanoma tumor development in mice.
PRAS40 acts as a nodal regulator of high glucose-induced TORC1 activation in glomerular mesangial cell hypertrophy.
Ghosh Choudhury et al., San Antonio, United States. In J Cell Physiol, 2010
Data identify high glucose-induced phosphorylation and inactivation of PRAS40 as a central node for mesangial cell hypertrophy in diabetic nephropathy.
Increased expression of a proline-rich Akt substrate (PRAS40) in human copper/zinc-superoxide dismutase transgenic rats protects motor neurons from death after spinal cord injury.
Chan et al., Stanford, United States. In J Cereb Blood Flow Metab, 2008
overexpression of SOD1 in the Tg rats results in an increase in endogenous pPRAS40 and a decrease in motor neuron death through the PI3K/Akt pathway.
Insulin signalling to mTOR mediated by the Akt/PKB substrate PRAS40.
Kim et al., Minneapolis, United States. In Nat Cell Biol, 2007
Here, we identify PRAS40 (proline-rich Akt/PKB substrate 40 kDa) as a novel mTOR binding partner that mediates Akt signals to mTOR.
Insulin-mediated phosphorylation of the proline-rich Akt substrate PRAS40 is impaired in insulin target tissues of high-fat diet-fed rats.
Ouwens et al., Leiden, Netherlands. In Diabetes, 2006
effect of in vivo insulin action on phosphorylation of the PKB/Akt substrate 40
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