PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29802942-9 2018 The inhibition of cell migration by lipoic acid is accompanied by the downregulation of FAK, ERK1/2 and AKT phosphorylation, and inhibition of nuclear translocation of beta-catenin. Thioctic Acid 36-47 AKT serine/threonine kinase 1 Homo sapiens 104-107 33671655-6 2021 Furthermore, ALA and DHLA upregulated the expression of survival-related proteins mTOR (mammalian target of rapamycin), Akt (protein kinase B), and Nrf2 (nuclear factor erythroid 2-related factor 2) in PC12 cells, which were previously downregulated by metal exposure. Thioctic Acid 13-16 AKT serine/threonine kinase 1 Homo sapiens 120-123 33113440-9 2021 The mRNA expression of spermatogenesis-related genes (ER1, AKT1, and Cav1) were markedly augmented in the ALA group compared with the CON group. Thioctic Acid 106-109 AKT serine/threonine kinase 1 Homo sapiens 59-63 29802942-10 2018 SIGNIFICANCE: Our data demonstrated that lipoic acid inhibited the migration and invasion of metastatic breast cancer cells at least in part through inhibiting ERK1/2 and AKT signaling. Thioctic Acid 41-52 AKT serine/threonine kinase 1 Homo sapiens 171-174 28611356-0 2017 The osteogenesis-promoting effects of alpha-lipoic acid against glucocorticoid-induced osteoporosis through the NOX4, NF-kappaB, JNK and PI3K/AKT pathways. Thioctic Acid 38-55 AKT serine/threonine kinase 1 Homo sapiens 142-145 25460366-0 2015 Alpha-lipoic acid activates eNOS through activation of PI3-kinase/Akt signaling pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 66-69 26781804-0 2016 alpha-Lipoic acid inhibits sevoflurane-induced neuronal apoptosis through PI3K/Akt signalling pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 79-82 22975849-0 2013 alpha-Lipoic acid interaction with dopamine D2 receptor-dependent activation of the Akt/GSK-3beta signaling pathway induced by antipsychotics: potential relevance for the treatment of schizophrenia. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 84-87 24203573-3 2014 We also demonstrated that the Akt/GSK-3beta/beta-catenin pathway is involved in the control of D2R expression levels, but is unlikely implicated in the preventive effects of (+-)-alpha-lipoic acid since co-treatment with haloperidol and (+-)-alpha-lipoic acid exerts synergistic effects on Akt/GSK-3beta activation. Thioctic Acid 237-259 AKT serine/threonine kinase 1 Homo sapiens 30-33 24203573-9 2014 Taken together, our data suggest that (+-)-alpha-lipoic acid exerts synergistic effects with haloperidol on the Akt/GSK-3beta pathway, potentially involved in the therapeutic effects of APs, and antagonism of ERK activation and D2R upregulation, potentially involved in tardive dyskinesia and treatment resistance. Thioctic Acid 38-60 AKT serine/threonine kinase 1 Homo sapiens 112-115 23875003-4 2013 3xTg-AD mice fed 0.23% w/v lipoic acid in drinking water for 4 weeks showed an insulin mimetic effect that consisted of increased brain glucose uptake, activation of the insulin receptor substrate and of the PI3K/Akt signaling pathway. Thioctic Acid 27-38 AKT serine/threonine kinase 1 Homo sapiens 213-216 22975849-4 2013 These findings led us to examine whether the Akt/GSK-3beta pathway was involved in D2R upregulation and oxidative stress elicited by antipsychotics and, in (+-)-alpha-lipoic acid-induced reversal of these phenomena, in SH-SY5Y cells. Thioctic Acid 156-178 AKT serine/threonine kinase 1 Homo sapiens 45-48 22975849-9 2013 These results suggest (1) that the effect of antipsychotics on the Akt/GSK-3beta pathway in SH-SY5Y cells is reminiscent of their in vivo action, (2) that (+-)-alpha-lipoic acid partially synergizes with antipsychotic drugs (APDs) on the same pathway, and (3) that the Akt/GSK-3beta signaling cascade is not involved in the preventive effect of (+-)-alpha-lipoic acid on antipsychotics-induced D2R upregulation. Thioctic Acid 155-177 AKT serine/threonine kinase 1 Homo sapiens 67-70 22975849-9 2013 These results suggest (1) that the effect of antipsychotics on the Akt/GSK-3beta pathway in SH-SY5Y cells is reminiscent of their in vivo action, (2) that (+-)-alpha-lipoic acid partially synergizes with antipsychotic drugs (APDs) on the same pathway, and (3) that the Akt/GSK-3beta signaling cascade is not involved in the preventive effect of (+-)-alpha-lipoic acid on antipsychotics-induced D2R upregulation. Thioctic Acid 155-177 AKT serine/threonine kinase 1 Homo sapiens 269-272 22975849-9 2013 These results suggest (1) that the effect of antipsychotics on the Akt/GSK-3beta pathway in SH-SY5Y cells is reminiscent of their in vivo action, (2) that (+-)-alpha-lipoic acid partially synergizes with antipsychotic drugs (APDs) on the same pathway, and (3) that the Akt/GSK-3beta signaling cascade is not involved in the preventive effect of (+-)-alpha-lipoic acid on antipsychotics-induced D2R upregulation. Thioctic Acid 345-367 AKT serine/threonine kinase 1 Homo sapiens 67-70 22820890-0 2012 alpha-Lipoic acid ameliorates impaired glucose uptake in LYRM1 overexpressing 3T3-L1 adipocytes through the IRS-1/Akt signaling pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 114-117 21362131-0 2012 alpha-Lipoic acid attenuates vascular calcification via reversal of mitochondrial function and restoration of Gas6/Axl/Akt survival pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 119-122 22528396-0 2012 alpha-Lipoic acid protects 3T3-L1 adipocytes from NYGGF4 (PID1) overexpression-induced insulin resistance through increasing phosphorylation of IRS-1 and Akt. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 154-157 21362131-9 2012 Collectively, the findings suggest ALA attenuates vascular calcification by inhibiting VSMC apoptosis through two distinct mechanisms; preservation of mitochondrial function via its antioxidant potential and restoration of the Gas6/Axl/Akt survival pathway. Thioctic Acid 35-38 AKT serine/threonine kinase 1 Homo sapiens 236-239 21362131-7 2012 Moreover, ALA inhibited Pi-induced down-regulation of cell survival signals through the binding of growth arrest-specific gene 6 (Gas6) to its cognate receptor Axl and subsequent Akt activation, resulting in increased survival and decreased apoptosis. Thioctic Acid 10-13 AKT serine/threonine kinase 1 Homo sapiens 179-182 21590646-1 2011 Alpha-lipoic acid (ALA) has been shown to modulate cell death via PI3K/Akt signal pathway in various cells. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 71-74 21590646-1 2011 Alpha-lipoic acid (ALA) has been shown to modulate cell death via PI3K/Akt signal pathway in various cells. Thioctic Acid 19-22 AKT serine/threonine kinase 1 Homo sapiens 71-74 21590646-12 2011 Moreover, these findings imply that ALA may ameliorate ER stress-induced cell death by activating PI3K/Akt signal pathway and attenuating changes of cell death-related proteins in FRTL5 thyroid cells. Thioctic Acid 36-39 AKT serine/threonine kinase 1 Homo sapiens 103-106 11375349-5 2001 alpha-Lipoic acid (2.5 mmol/l) increased PI 3-kinase activity (31-fold) and Akt1 (4.9-fold). Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 76-80 20580704-5 2010 We observed that alpha-lipoic acid is able to scavenge reactive oxygen species in MCF-7 cells and that the reduction of reactive oxygen species is followed by cell growth arrest in the G1 phase of the cell cycle, via the specific inhibition of Akt pathway and the up-regulation of the cyclin-dependent kinase inhibitor p27(kip1), and by apoptosis, via changes of the ratio of the apoptotic-related protein Bax/Bcl-2. Thioctic Acid 17-34 AKT serine/threonine kinase 1 Homo sapiens 244-247 20098578-6 2009 Furthermore, the protein expression of phosphorylated Akt (p-Akt) levels and total Akt, and the mRNA expression of Akt were decreased dose-dependently in cells that were treated with alpha-lipoic acid (P < 0.05). Thioctic Acid 183-200 AKT serine/threonine kinase 1 Homo sapiens 54-57 20098578-6 2009 Furthermore, the protein expression of phosphorylated Akt (p-Akt) levels and total Akt, and the mRNA expression of Akt were decreased dose-dependently in cells that were treated with alpha-lipoic acid (P < 0.05). Thioctic Acid 183-200 AKT serine/threonine kinase 1 Homo sapiens 61-64 20098578-6 2009 Furthermore, the protein expression of phosphorylated Akt (p-Akt) levels and total Akt, and the mRNA expression of Akt were decreased dose-dependently in cells that were treated with alpha-lipoic acid (P < 0.05). Thioctic Acid 183-200 AKT serine/threonine kinase 1 Homo sapiens 61-64 20098578-6 2009 Furthermore, the protein expression of phosphorylated Akt (p-Akt) levels and total Akt, and the mRNA expression of Akt were decreased dose-dependently in cells that were treated with alpha-lipoic acid (P < 0.05). Thioctic Acid 183-200 AKT serine/threonine kinase 1 Homo sapiens 61-64 17360480-0 2007 Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/Akt signaling pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 108-111 17360480-7 2007 Lipoic acid-dependent Akt phosphorylation and inhibition of NF-kappaB activity were abolished by the PI3K inhibitors LY294002 and wortmannin. Thioctic Acid 0-11 AKT serine/threonine kinase 1 Homo sapiens 22-25 18435927-0 2008 Alpha-lipoic acid induces apoptosis in hepatoma cells via the PTEN/Akt pathway. Thioctic Acid 0-17 AKT serine/threonine kinase 1 Homo sapiens 67-70 17566113-0 2007 R-(+)-alpha-lipoic acid inhibits endothelial cell apoptosis and proliferation: involvement of Akt and retinoblastoma protein/E2F-1. Thioctic Acid 0-23 AKT serine/threonine kinase 1 Homo sapiens 94-97 10491755-8 1999 Although tyrosine phosphorylation patterns were not affected by lipoic acid pretreatment, insulin-stimulated protein kinase B/Akt serine 473 phosphorylation and activity were considerably impaired by oxidation but protected by lipoic acid pretreatment. Thioctic Acid 227-238 AKT serine/threonine kinase 1 Homo sapiens 126-129 10491755-10 1999 CONCLUSION/INTERPRETATION: This study shows the ability of lipoic acid to provide partial protection against the impaired insulin-stimulated glucose transporter 4 translocation and protein kinase B/Akt activation induced by oxidative stress, potentially by its capacity to maintain intracellular redox state. Thioctic Acid 59-70 AKT serine/threonine kinase 1 Homo sapiens 198-201