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Study found that activated PRAS40 acts not only as a regulator of TGFA (show TGFA Antibodies)-triggered exosome secretion but also as a common regulator of distinct microenvironmental and oncogenic signal-triggered exosome secretion in both normal and tumor cell types. PRAS40 is the first regulator identified for stress-induced exosome secretion.
PRAS40 was downregulated in the DU145 cells following MYO6 (show MYO6 Antibodies) knockdown.
Phosphorylation of S202/203 of AKT1S1 by PKM2 (show PKM2 Antibodies) released AKT1S1 from raptor (show RPTOR Antibodies) and facilitated its binding to 14-3-3 (show YWHAQ Antibodies), resulted in hormonal- and nutrient-signals independent activation of mTORC1 signaling and led accelerated oncogenic growth and autophagy inhibition in cancer cells.
The frameshift mutation detected in the current study would result in a premature stop of amino-acid synthesis in AKT1S1 protein and hence resembles a typical loss-of-function mutation.
Supporting this idea, we identified a downstream target of the TGFb (show TGFB1 Antibodies)-miR (show MLXIP Antibodies)-96 signaling pathway to be AKT1S1 mRNA, whose translated protein is a negative regulator of mTOR (show FRAP1 Antibodies) kinase.
This review discusses the role of PRAS40 and possible feedback mechanisms, and alterations in AKT (show AKT1 Antibodies)/PRAS40/mTOR (show FRAP1 Antibodies) signaling that have been implicated in the pathogenesis of tumor progression. [review]
Findings indicate that dual phosphorylation of PRAS40 by Akt (show AKT1 Antibodies) and mTORC1 promotes formation of a nuclear-specific PRAS40- and RPL11 (show RPL11 Antibodies)-containing complex distinct from mTORC1 that inhibits the RPL11 (show RPL11 Antibodies)-HDM2-p53 (show TP53 Antibodies) pathway.
PRAS40 as a regulator of insulin (show INS Antibodies) sensitivity in hSkMC
PRAS40 contains a functional nuclear export signal. Furthermore, enforced nuclear accumulation of PRAS40 impairs insulin (show INS Antibodies) action, thereby substantiating the function of this protein in the regulation of insulin (show INS Antibodies) sensitivity.
Data suggest that PRAS40 modulates insulin (show INS Antibodies) action in skeletal muscle; knockdown of PRAS40 inhibits insulin (show INS Antibodies) action in cultured myotubes and is associated with up-regulation of IRS1 (insulin receptor substrate 1 (show IRS1 Antibodies)) degradation via proteasome proteolysis.
Overexpression of PRAS40(T246A) in the Proliferative Compartment Suppresses mTORC1 Signaling, Keratinocyte Migration, and Skin Tumor Development
PRAS40 inhibits mTORC1 hyperactivation and plays a key role in protecting cells against neurotoxic prion (show PRNP Antibodies) peptide-induced apoptosis. Thus, PRAS40 is a potential therapeutic target for prion (show PRNP Antibodies) disease.
PRAS40 appears to reduce brain injury following ischemic stroke by converting cell signaling from Akt (show AKT1 Antibodies) to mTOR (show FRAP1 Antibodies)
PRAS40 treatment improves hepatic insulin (show INS Antibodies) sensitivity and reduces systemic hyperglycaemia in obese mice.
PRAS40 phosphorylation acts as a molecular switch allowing mTORC1 activation during physiological growth, opening up unique possibilities for therapeutic regulation of the mTORC1 complex to mitigate pathologic myocardial hypertrophy by PRAS40
Naturally secreted amyloid-beta increases mammalian target of rapamycin (mTOR (show FRAP1 Antibodies)) activity via a PRAS40-mediated mechanism.
These results suggest that a reduction in PRAS40 specifically impairs myoblast protein synthesis, cell cycle, proliferation and differentiation to myotubes.
PRAS phosphorylation and its interaction with pAkt (show AKT1 Antibodies) and 14-3-3 (show YWHAQ Antibodies) might play an important role in neuroprotection mediated by NGF (show NGFB Antibodies) in apoptotic neuronal cell death after transient focal cerebral ischemia
overexpression of SOD1 (show SOD1 Antibodies) may affect the PRAS pathway after transient focal cerebral ischemia by reducing the direct oxidative reaction to pPRAS after reperfusion injury
PRAS40 is an important regulator of insulin (show INS Antibodies) sensitivity of the Akt (show AKT1 Antibodies)-mTOR (show FRAP1 Antibodies) pathway and a potential target for the treatment of cancers, insulin (show INS Antibodies) resistance and hamartoma syndromes.
AKT1S1 is a proline-rich substrate of AKT (MIM 164730) that binds 14-3-3 protein (see YWHAH, MIM 113508) when phosphorylated (Kovacina et al., 2003
AKT1 substrate 1 (proline-rich)
, proline-rich AKT1 substrate 1
, 40 kDa proline-rich AKT substrate
, proline-rich AKT substrate
, PKB/Akt substrate 40