IndraLab
Statements
reach
"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."
sparser
"Intrinsic or external AKT1 constitutive activation enhances cell survival by blocking the function of pro-apoptotic proteins; in addition, AKT1 activates of the mTOR complex 1 (mTORC1), which is regulated by both nutrients and growth factor signalling and plays an essential role in the cell mass increase."
reach
"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)."
sparser
"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 )."
sparser
"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)."
reach
"The mTOR pathway is considered a central control hub for growth and metabolism (Wullschleger et al., 2006), activated by phosphoinositide-3 kinase (PI3K)/ protein kinase B (Akt) signalling during conditions of ample nutrient and growth factor availability, and inhibited by AMP-activated protein kinase (AMPK) during energy deficiency (Jewell and Guan, 2013)."
reach
"In addition, further research revealed that TrkB activates the downstream of AKT, also named protein kinase B (PKB) and extracellular regulated protein kinase (ERK) mediated mTOR signaling, suggesting that the phosphorylation of ERK and AKT and activation of the common downstream molecular mTOR participate in the antidepressant-like effects of rapastinel in vivo [38, 39]."
reach
"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."
reach
"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."
reach
"Furthermore, over-expression of LINC01605 in HDFs promoted the fibrosis of cells, suggesting that exosomes derived from M2 macrophages could promote fibrosis of cells by transferring LINC01605.Mechanistically, our luciferase reporter assay verified that M2 macrophage-derived exosomes inhibited miR-493-3p in HDF by transferring LINC01605, up-regulating AKT1 levels, and activating the Akt/mTOR signaling pathway."
reach
"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]."
| PMC
reach
"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."
reach
"Cisplatin-upregulated c-Myc could transactive miR-425-3p and promote its transfer via exosomes among NSCLC cells during the treatment.Given stress adaptation of cancer cells, we revealed that exosomal miR-425-3p enhanced autophagic activity in the recipient cells by targeting AKT1 that activates the mTOR complex, exerting an inhibitory role on autophagy."
sparser
"Given stress adaptation of cancer cells, we revealed that exosomal miR-425-3p enhanced autophagic activity in the recipient cells by targeting AKT1 that activates the mTOR complex, exerting an inhibitory role on autophagy. xref In fact, autophagy can be activated by stressful conditions such as drug stress, facilitating the survival of tumor cells and increasing resistance to chemotherapy. xref Previously, we showed that basal autophagy is progressively increased during the development of cisplatin resistance in NSCLC cells and that inhibiting basal autophagy sensitizes NSCLC cells to cisplatin-induced apoptosis. xref , xref The present study showed that autophagy inhibitor BafA1 indeed greatly promoted cisplatin-induced apoptosis in the recipient A549 cells incubated with A549/1.5 exosome or A549/DDP-1000 exosome."
reach
"24
Specifically, the activation of 3T3‐L1 cells via insulin stimulates the insulin receptor substrate 1 (IRS1), PI3K, and AKT1 or AKT2 kinases, which further activate downstream signaling proteins, including CREB, mTOR, and the FOXO family, ultimately leading to the formation of mature adipocytes with distinct lipid droplets (Figure
1a)."
reach
"AKT1 phosphorylation activates the mammalian target of the rapamycin (mTOR) signaling pathway and subsequently enhances sterol regulatory element binding protein 1 (SREBP1), which increases intracellular triacylglycerol content and plays an important role in regulating the de novo synthesis of fatty acids in goat mammary epithelial cells [50]."
reach
"For ovine conceptus development during implantation and placentation, the binding of SPP1 to integrins to alter the cell cytoskeleton, along with the associated effects of integrin activation by SPP1 binding and Arg on cell proliferation, 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 AKT1, TSC1/2 and MTORC1 (cell proliferation and mRNA translation), as well as MTORC2 (cell migration, cell survival and cytoskeletal organization)."
reach
"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."