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AKT1 activates MTOR. 61 / 75
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"It has been validated that the AKT1 activates the downstream protein MTOR through TSC2 and RHEB and simultaneously upregulates TF FOXO1, which is phosphorylated by kinase PHKB [ xref , xref ]."

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"Leptin-induction of VEGF levels in endometrial cancer cells was related to the activation of MAPK/ERK1/2 and mTOR but not to PI-3K and AKT1 signaling pathway."

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"MTOR acts as a central regulator in autophagy induction, and AKT1 modulates the activation of MTOR."

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"Phosphorylated class I PI3K enzymes and protein kinase B (Akt and PKB) can activate mTOR, and then its downstream effector p70S6 kinase as well as initiation factor 4E binding protein (4E-BP1) became activated."

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"While activated RAS inhibits mTOR activity to upregulate autophagy and promote senescence ( xref )(Figure), activated AKT1 was able to activate mTOR even in the presence of activated RAS, likely explaining the ability of mAKT1 to inhibit RASG12V-induced autophagy."

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"Akt1 activates mTOR which plays a crucial role in protein synthesis and cell proliferation."

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"Akt1 activates mTOR which plays a crucial role in protein synthesis and cell proliferation."

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"Interestingly, leptin-induction of VEGF levels in cancer-EEC was related to the activation of MAPK/ERK1/2 and mTOR but not to PI-3K and AKT1 signaling pathway (XREF_FIG and XREF_FIG)."

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"AKT1 independent activation of mTOR has been reported in several cell types, including B-lymphocyte cell lines [XREF_BIBR] and follicular lymphoma cells [XREF_BIBR]."

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"Taken together, these results suggest that the miR-99 family plays an important role in dermal wound healing by concurrently targeting IGF1R, mTOR, and AKT1 (as well as AKT2, to a lesser extent), which in turn modulate the PI3K and AKT and mTOR signaling pathways."

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"In addition, AKT1 strongly activates mTOR signaling pathway."

eidos
"Akt1 activates mTOR which plays a crucial role in protein synthesis and cell proliferation ."

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"For ovine conceptus development during implantation and placentation, integrin activation by SPP1 binding and arginine are proposed to stimulate remodeling of trophectoderm for elongation and adherence to uterine LE/sGE via cytoskeletal reorganization that facilitates cell motility, stabilizes adhesion, and collectively activates MTOR signaling pathways mediated by protein kinase b-alpha (AKT1), tuberous sclerosis 1 and 2 (TSC1 and TSC2) and MTORC1 (cell proliferation and mRNA translation), as well as mTORC2 (cell migration, cell survival and cytoskeletal organization) in trophectoderm cells."

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"An established mechanism for eliciting muscle hypertrophy is through the Akt1 pathway, which activates mTOR and p70s6k and ultimately leads to enhanced protein synthesis."

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"The PI3K effector Akt and protein kinase B has been found to directly phosphorylate tuberin and is thereby thought to activate mTOR through inhibition of the tuberin and hamartin complex."

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"PAkt activates the downstream mTOR and make it phosphorylated, which is followed by down-regulation of phosphorylated p70S6K."

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"Consistent with this idea, in the presence of activated RAS, activated AKT1 activated mTOR, as judged by phosphorylation of mTOR substrates, 4EBP1 and p70S6K (XREF_FIG)."

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"While activated RAS inhibits mTOR activity to upregulate autophagy and promote senescence, activated AKT1 was able to activate mTOR even in the presence of activated RAS, likely explaining the ability of mAKT1 to inhibit RASG12V induced autophagy."

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"Major differences were observed in neonatal monocytes in the mTOR pathway (Supplementary Data 3), including a decreased expression of the upstream mTOR activator RAC-alpha serine/threonine-protein kinase (encoded by the Akt1 gene)."

"Once phosphorylated, Akt can act on a broad spectrum of substrates that can influence cell survival and proliferation and protein synthesis (65). Phosphorylation of mTOR by Akt leads to mTOR activation (40, 52) and the subsequent activation of p70S6K"

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"AKT1 stimulates mTOR kinase, which activates transcription factor HIF1A even at the normoxic conditions [XREF_BIBR]."

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"The benzimidazole anthelmintics usually decreased signaling proteins related to cell proliferation and survival, such as phosphorylated (p) HER2/3, PI3K and protein kinase B (AKT), rapidly accelerated fibrosarcoma (a family of three serine/threonine specific protein kinases) (RAF)/MEK/ERK, mTOR, and Ki-67."

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"UnAG decreased insulin receptor substrate (IRS) phosphorylation, increased protein kinase B (Akt) phosphorylation, and, hence, suppressed mTOR signaling."

sparser
"Akt-1 also activates mTOR, downstream p70, and S6kinase-1 to increase protein synthesis [ xref ]."

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"AKT1 activates mTOR, which in turn initiates protein translation via downstream effectors S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E-binding protein 1 (EIF4EBP1, also known as 4E-BP1) [ xref ]."

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"Sirolimus suppressed the proliferation of TSC2 and TSC2 fibroblasts and selectively stimulated the mTOR-activating protein kinase B (Akt) pathway in TSC2 fibroblasts but not in TSC2 fibroblasts derived from normal skin."

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"AKT, protein kinase B alpha; ER, endoplasmic reticulum; IKKβ, I-kappa-B kinase beta; IKKɛ, I-kappa-B kinase epsilon; IRS1/2, insulin receptor substrate 1; ISRE, interferon-stimulated response element; MAVS, mitochondrial antiviral signaling protein; mTOR, mechanistic target of rapamycin; NF-κB, nuclear factor kappa-light-chain-enhancer of activated B cells; PI-3K, phosphoinositide-3-kinase; STAT1/2/3/4/5/6, signal transducer and activator of transcription 1/2/2/4/5/6; STING, stimulator of interferon genes; TBK1, TANK-binding kinase 1.Fig."

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"The E to K substitution results in constitutive AKT1 activation, which stimulates downstream mTOR signaling."

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"Protein kinase B (Akt) is a major activator of mTOR."

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"In particular, loss of Akt1 decreased mTOR activation by mutant K-ras, because p-S6, p4E-BP1, total 4E-BP1 and total eIF4E were diminished in Akt1 -/- tumors (XREF_FIG)."

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"IGF-1 treatment activated protein kinase B (AKT), which may inhibit autophagy via the AKT and mammalian target of rapamycin signaling pathway."

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"This protein will degrade Cell Division Control Protein 2 (CDC2), resulting in cell arrest in the G2-M phase.63 AKT1 inhibition can also inhibit the activity of proteins that play an important role in cell proliferation such, as Mammalian Target of Rapamycin (mTOR), IkB Kinase (IKK), and Cyclin D1, and increase the activity of antiproliferative proteins such as Glycogen Synthase Kinase 3 Betha (GSK3β) and Forkhead box protein O1 (FOXO1).64When overexpressed, CDK4 causes uncontrolled cell growth and proliferation."

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"Activation of mTOR by AKT1 after irradiation mediates the radioresistance of cancer cells."

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"Phosphorylated Akt1 (pAkt1) indirectly activates mechanistic target of rapamycin (mTOR) by phosphorylating TSC1/2 complex, the inhibitory regulator of mTOR, thereby activating mTOR pathway that culminates in phosphorylation of 4EBP1 at Thr46/47 and S6K at Thr389, both important regulators of cap-dependent protein translation ( xref )."

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"Phosphorylated AKT1 also indirectly activates mTOR, which promotes skeletal muscle hypertrophy ( xref )."

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"Consistent with this idea, in the presence of activated RAS, activated AKT1 activated mTOR, as judged by phosphorylation of mTOR substrates, 4EBP1 and p70S6K ( xref )."

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"Protein kinase B (Akt) and the mitogen activated protein kinase (MAPK) signals activate mTOR through the interaction of tuberous sclerosis complex (TSC) 1/2, v Rheb and the mammalian target of rapamycin complex 1/2 (mTORC1/2)."

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"Consistently, Akt1 mediated mTOR signaling has been shown to be important for priming satellite cells for cell cycle entry [XREF_BIBR] and for the expression of myogenic factor such as myogenin and MyoD (Additional file 8 : Figure S4B) [XREF_BIBR]."

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"Since AKT1 activates mTOR and mTOR is a potent inhibitor of autophagy ( xref ), we hypothesized that activated AKT1 suppresses RASG12V-induced autophagy by activation of mTOR."

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"Note: AKT, protein kinase B; COX-1, cyclooxygenase-1; cPLA2, cytoplasmic phospholipase A2; EIF2α, eukaryotic initiation factor 2 alpha; ER, endoplasmic reticulum; HK-2 cells, human kidney 2 cells; MAPK, mitogen-activated protein kinase; mitoROS, mitochondrial reactive oxygen species; mTOR, mitogen-activated protein kinase; PS-MPs, polystyrene microplastics; ROS, reactive oxygen species."

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"In contrast, leptin-induction of VEGF levels in endometrial cancer cells was related to the activation of MAPK/ERK1/2 and mTOR but not to PI-3K and AKT1 signalling pathway [XREF_BIBR]."

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"Activation of mTOR by AKT1 after irradiation mediates the radioresistance of cancer cells."

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"Mitogen-activated protein kinase (MAPK) and protein kinase B (Akt) activate mTOR via the interaction of tuberous sclerosis complex (TSC) 1/2, Rheb, and the mammalian target of rapamycin complex 1/2 (mTORC1/2)."

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"Although mTOR was activated in PIK3CA mutant cells when deprived of glutamine (XREF_SUPPLEMENTARY), our data suggest that the activation of mTOR does not determine glutamine sensitivity in these cells, because the overexpression of myristoylated AKT1 increased mTOR activity in the PIK3CA WT in the absence of glutamine (XREF_SUPPLEMENTARY)."

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"Besides, the regulatory relationships between Sox2ot and miR-211, miR-211 and MCL-1, as well as between MCL-1 and the protein kinase B (Akt)/mammalian target of the rapamycin (mTOR)/p70 ribosomal S6 protein kinase (p70S6K) signaling pathway were explored."

eidos
"This inhibits negative regulators of mTOR such as tuberous sclerosis complex ( TSC1 / 2 ) and induces mTOR signaling to lead protein translation of key proteins involved in synaptic plasticity , learning , and memory apart from the proteins involved in cell growth mechanisms ."

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"Unexpectedly, AKT1, AKT2, and AKT3 knockdown by shRNAs, whether singly or in combination, enhanced mTOR activation (XREF_SUPPLEMENTARY), and although the mechanism is unclear, these data provide an additional rationale for dual targeting of AKT and mTOR in mesothelioma."

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"Protein kinase B, or Akt, can directly activate mTOR through phosphorylation whilst also repressing the endogenous mTORC1 inhibitor, PRAS40, and thereby augment mTOR downstream effects."

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"Phosphoinositide 3-kinase (PI3K), pyruvate dehydrogenase kinase (PDK), and protein kinase B (PKB; Akt) activation induced by growth factors (GFs) activate the mammalian target of the rapamycin (mechanistic target of rapamycin kinase; mTOR) pathway, which results in elevated HIF-1α transcriptional activity [6]."
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"The present study demonstrates an association between IGF-1R and the phosphatidylinositol 3-kinase (PI3K)/threonine protein kinase B (Akt)/mammalian target of rapamycin mTOR signaling pathway and autophagy."

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"Phospho-Akt1 indirectly activates mTOR function, thereby inhibiting autophagy induction and promoting cell survival."
| PMC

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"Akt-1 also activates mTOR, downstream p70, and S6kinase-1 to increase protein synthesis [XREF_BIBR]."

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"Phosphorylated Akt1 indirectly activates mTOR by phosphorylating TSC1/2 (tuberous sclerosis protein complex 1/2) complex, which is a negative regulator of mTOR there by activating the pathway to phosphorylate 4EBP1 (eukaryotic initiation factor 4E- binding protein-1) at Thr46/47, S6K (p70 Ribosomal S6 kinase) at Thr389 both are important in initiating protein translation downstream (Fig.  xref D)."

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"Mammalian PI 3-kinase induces actin reorganization by Rac- and Rho dependent pathways (Reif et al. 1996) and is also possibly upstream of mTOR (FRAP and RAFT) (Downward 1995)."

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"In vitro studies indicated that Akt1 phosphorylation activated mTOR and subsequently enhanced sterol regulatory element binding protein 1 (SREBP1), thus increasing intracellular triacylglycerol content."

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"Although mTOR signaling in the hypothalamus regulates food intake and absence of S6 K enhances insulin sensitivity and protects against diet- and age related obesity, our findings in Akt1 null mice fed a high-fat diet suggest that Akt, rather than mTOR, is the critical mediator of vascular senescence because mTOR activity was increased to a similar extent by a high-fat diet in WT and Akt1 null mice."

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"We hypothesized that inhibition of histone deacetylase (HDAC) could suppress BPA-induced neuropathic pain through inhibition of transient reception potential (TRP) overexpression and protein kinase B (Akt) mediated mammalian target of rapamycin (mTOR) activation."

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"Normally, the activated PI3K phosphorylates protein kinase B (AKT) and stimulates the mammalian target of rapamycin (mTOR) pathways [76]."

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"Inhibition of mTOR by knockdown or treatment with the small molecule inhibitors rapamycin or torin induces autophagy, and inhibition of upstream kinases such as AKT1 that activate mTOR also results in the induction of autophagy xref ."

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"Moreover, miR-199a-5p downregulated FKBP5, leading to upregulated phosphorylation level of AKT1, which promoted the malignant phenotypes of AGS cells by activating mammalian target of rapamycin complex 1(mTORC1)."

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"Likewise, over-expression of Akt1 up-regulates mTOR and NF-kappaB (data not shown)."