PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 33858507-8 2021 Mechanistically, ATO mitigated venetoclax-induced upregulation of Mcl-1 by the inhibition of AKT and ERK, along with activation of GSK-3beta. Arsenic Trioxide 17-20 AKT serine/threonine kinase 1 Homo sapiens 93-96 32184170-7 2020 Submicromolar-concentration As2O3 dose-dependently triggered C2C12 myotube atrophy and increased the protein expressions of atrogenes Atrogin1 and MuRF1 and inhibited the upstream phosphorylated proteins Akt and FoxO1, while As2O3 dose-dependently increased AMPK phosphorylation in myotubes. Arsenic Trioxide 28-33 AKT serine/threonine kinase 1 Homo sapiens 204-207 32184170-8 2020 Akt activator SC79 could significantly reverse the As2O3-induced myotube atrophy. Arsenic Trioxide 51-56 AKT serine/threonine kinase 1 Homo sapiens 0-3 29442453-0 2017 Transcriptomic analysis of the PI3K/Akt signaling pathway reveals the dual role of the c-Jun oncogene in cytotoxicity and the development of resistance in HL-60 leukemia cells in response to arsenic trioxide. Arsenic Trioxide 191-207 AKT serine/threonine kinase 1 Homo sapiens 36-39 32169580-0 2020 Activation of PPARgamma intensified the effects of arsenic trioxide in acute promyelocytic leukemia through the suppression of PI3K/Akt pathway: Proposing a novel anticancer effect for pioglitazone. Arsenic Trioxide 51-67 AKT serine/threonine kinase 1 Homo sapiens 132-135 32305283-0 2020 Arsenic trioxide-induced p38 MAPK and Akt mediated MCL1 downregulation causes apoptosis of BCR-ABL1-positive leukemia cells. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 38-41 32305283-2 2020 ATO-induced apoptotic death in K562 cells was characterized by ROS-mediated mitochondrial depolarization, MCL1 downregulation, p38 MAPK activation, and Akt inactivation. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 152-155 32305283-3 2020 ATO-induced BCR-ABL1 downregulation caused Akt inactivation but not p38 MAPK activation. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 43-46 32305283-5 2020 Inhibition of p38 MAPK activation or overexpression of constitutively active Akt increased MCL1 expression and promoted the survival of ATO-treated cells. Arsenic Trioxide 136-139 AKT serine/threonine kinase 1 Homo sapiens 77-80 32305283-9 2020 Collectively, our data indicate that ATO-induced p38 MAPK- and Akt-mediated MCL1 downregulation triggers apoptosis in K562 and MEG-01 cells, and that p38 MAPK activation is independent of ATO-induced BCR-ABL1 suppression. Arsenic Trioxide 37-40 AKT serine/threonine kinase 1 Homo sapiens 63-66 30213730-0 2018 The suppressive effect of arsenic trioxide on TET2-FOXP3-Lyn-Akt axis-modulated MCL1 expression induces apoptosis in human leukemia cells. Arsenic Trioxide 26-42 AKT serine/threonine kinase 1 Homo sapiens 61-64 30213730-5 2018 In addition, ATO-treated U937 cells showed ROS-mediated inhibition of TET2 transcription, leading to downregulation of FOXP3 expression and in turn, suppression of FOXP3-mediated activation of Lyn and Akt. Arsenic Trioxide 13-16 AKT serine/threonine kinase 1 Homo sapiens 201-204 30213730-8 2018 Further, ATO-induced Akt inactivation promoted GSK3beta-mediated degradation of MCL1. Arsenic Trioxide 9-12 AKT serine/threonine kinase 1 Homo sapiens 21-24 30213730-9 2018 Transfection of constitutively active Akt expression abrogated ATO-induced MCL1 downregulation. Arsenic Trioxide 63-66 AKT serine/threonine kinase 1 Homo sapiens 38-41 30213730-11 2018 Thus, our data suggest that ATO induces mitochondria-mediated apoptosis in U937 cells through its suppressive effect on TET2-FOXP3-Lyn-Akt axis-modulated MCL1 transcription and protein stabilization. Arsenic Trioxide 28-31 AKT serine/threonine kinase 1 Homo sapiens 135-138 30554581-7 2018 Conclusion silencing SOX9 gene expression enhances apoptosis of laryngeal squamous cell carcinoma cells induced by As2O3, which is related to increasing the intacellular ROS content and down-regulating the PI3K/AKT signaling pathway. Arsenic Trioxide 115-120 AKT serine/threonine kinase 1 Homo sapiens 211-214 30250637-8 2018 ATO also synergizes with FLT3 TKIs to inactivate FLT3 autophosphorylation and phosphorylation of its downstream signaling targets, including STAT5, AKT and ERK. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 148-151 29574283-4 2018 In the current study, the potential of a subtoxic dose (0.2 muM) of arsenic trioxide (ATO) in combination with VS-5584 (a highly potent PI3K/mTOR dual inhibitor) was tested for blocking of the PI3K/Akt/mTOR pathway, inhibition of NF-kappaB activation and induction of apoptosis and cell-cycle arrest. Arsenic Trioxide 68-84 AKT serine/threonine kinase 1 Homo sapiens 198-201 29574283-7 2018 We also showed that concomitant treatment of VS-5584 and the subtoxic dose of ATO significantly inhibited phosphorylation of NF-kappaB inhibitor alpha (IkappaBalpha) and S6 ribosomal protein (S6) as the downstream proteins of the PI3K/Akt/mTOR pathway. Arsenic Trioxide 78-81 AKT serine/threonine kinase 1 Homo sapiens 235-238 29442453-3 2017 OBJECTIVES: The aim of this study was to investigate the role of the PI3K/Akt signaling pathway in ATOtreated human acute myeloid leukemia (HL-60) cells and in ATO-resistant clones. Arsenic Trioxide 99-102 AKT serine/threonine kinase 1 Homo sapiens 74-77 29442453-10 2017 CONCLUSIONS: The overall results indicate that CCND1, FOXO1, and JUN may contribute to the induction of resistance to ATO, and that the C-Jun N-terminal kinase (JNK) signaling pathway may have greater significance than the phosphoinositide 3-kinase (PI3K)/Akt pathway in mediating the cytotoxic effects of ATO and the development of resistance to ATO in the HL-60 cell line. Arsenic Trioxide 118-121 AKT serine/threonine kinase 1 Homo sapiens 256-259 27189198-9 2016 Vorinostat + ATO resulted in lower levels of Akt protein compared with either drug alone. Arsenic Trioxide 13-16 AKT serine/threonine kinase 1 Homo sapiens 45-48 28355296-10 2017 Interestingly, a specific phosphoinositide 3-kinase (PI3K)/Akt inhibitor (LY294002) augmented the As4O6 induced cell death; whereas p38 mitogen-activated protein kinases (p38 MAPK) inhibitor (SB203580) abrogated the cell death. Arsenic Trioxide 98-103 AKT serine/threonine kinase 1 Homo sapiens 59-62 28355296-11 2017 Thus, the present study provides the first evidence that As4O6 induced G2/M arrest, apoptosis and autophagic cell death through PI3K/Akt and p38 MAPK pathways alteration in SW620 cells. Arsenic Trioxide 57-62 AKT serine/threonine kinase 1 Homo sapiens 133-136 28024471-6 2016 CONCLUSION: The combination treatment of HHT and As2O3 can synergistically inhibit the growth of U937 cells through inhibition of PI3K/Akt signal way and MCL-1 protein. Arsenic Trioxide 49-54 AKT serine/threonine kinase 1 Homo sapiens 135-138 25416439-0 2015 Arsenic trioxide potentiates the anti-cancer activities of sorafenib against hepatocellular carcinoma by inhibiting Akt activation. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 116-119 25869069-0 2015 Arsenic trioxide synergistically potentiates the cytotoxic effect of fludarabine in chronic lymphocytic leukemia cells by further inactivating the Akt and ERK signaling pathways. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 147-150 25791921-0 2015 TG-interacting factor transcriptionally induced by AKT/FOXO3A is a negative regulator that antagonizes arsenic trioxide-induced cancer cell apoptosis. Arsenic Trioxide 103-119 AKT serine/threonine kinase 1 Homo sapiens 51-54 25791921-9 2015 Furthermore, blockage of the AKT pathway enhanced ATO-induced CDKN1A expression and resultant apoptosis in cancer cells, but overexpression of AKT1 inhibited CDKN1A expression. Arsenic Trioxide 50-53 AKT serine/threonine kinase 1 Homo sapiens 29-32 25791921-10 2015 Therefore, we suggest that TGIF is transcriptionally regulated by the c-Src/EGFR/AKT pathway, which plays a role as a negative regulator in antagonizing ATO-induced CDKN1A expression and resultant apoptosis. Arsenic Trioxide 153-156 AKT serine/threonine kinase 1 Homo sapiens 81-84 26359868-11 2015 Furthermore, As2O3 inhibited the phosphorylation of Akt. Arsenic Trioxide 13-18 AKT serine/threonine kinase 1 Homo sapiens 52-55 26359868-12 2015 Insulin-like growth factor-1 significantly reversed the inhibitory effect of As2O3 on Akt phosphorylation and cell proliferation in the myoblasts. Arsenic Trioxide 77-82 AKT serine/threonine kinase 1 Homo sapiens 86-89 26359868-13 2015 These results suggest that submicromolar concentrations of As2O3 alter cell cycle progression and reduce myoblast proliferation, at least in part, through a ROS-independent Akt inhibition pathway. Arsenic Trioxide 59-64 AKT serine/threonine kinase 1 Homo sapiens 173-176 25758096-6 2015 In U937 cells, rapamycin alone increased the activity of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and the addition of ATO decreased the level of phosphorylated ERK, Ser473 phosphorylated Akt and anti-apoptotic Mcl-1 protein. Arsenic Trioxide 159-162 AKT serine/threonine kinase 1 Homo sapiens 228-231 26038719-13 2015 SAHA and ATO combined therapy showed lower levels of Akt and pAkt protein expression than SAHA or ATO alone. Arsenic Trioxide 9-12 AKT serine/threonine kinase 1 Homo sapiens 53-56 26062301-4 2015 The PI3K/Akt signaling pathway was detected by Western Blot in co-cultured AML cells cultured alone or treated with As2O3 alone or in combination with LY294002. Arsenic Trioxide 116-121 AKT serine/threonine kinase 1 Homo sapiens 9-12 25416439-2 2015 Arsenic trioxide (ATO) is a currently clinically used anticancer drug and displays its anticancer activities by inhibiting Akt activation. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 123-126 25416439-2 2015 Arsenic trioxide (ATO) is a currently clinically used anticancer drug and displays its anticancer activities by inhibiting Akt activation. Arsenic Trioxide 18-21 AKT serine/threonine kinase 1 Homo sapiens 123-126 25416439-4 2015 The results have demonstrated that ATO synergized with sorafenib to inhibit the proliferation and promote the apoptosis of HCC cells by diminishing the increased activation of Akt by sorafenib. Arsenic Trioxide 35-38 AKT serine/threonine kinase 1 Homo sapiens 176-179 25416439-5 2015 ATO was shown to inhibit the expression or activation of Akt downstream factors, including glycogen synthase kinase (GSK)-3beta, mammalian target of rapamycin (mTOR), ribosomal protein S6 kinase (S6K), and eukaryotic translation initiation factor 4E-binding protein 1 (4EBP1), which regulate cell apoptosis and were upregulated or activated by sorafenib. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 57-60 24482137-0 2014 Inactivation of Akt by arsenic trioxide induces cell death via mitochondrial-mediated apoptotic signaling in SGC-7901 human gastric cancer cells. Arsenic Trioxide 23-39 AKT serine/threonine kinase 1 Homo sapiens 16-19 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 101-106 AKT serine/threonine kinase 1 Homo sapiens 32-35 25506699-10 2014 Apoptosis generation by etomoxir plus 2-deoxy-D-glucose was further increased by co-incubation with ATO, which is apparently explained by the capacity of ATO to attenuate Akt and ERK activation. Arsenic Trioxide 100-103 AKT serine/threonine kinase 1 Homo sapiens 171-174 25506699-10 2014 Apoptosis generation by etomoxir plus 2-deoxy-D-glucose was further increased by co-incubation with ATO, which is apparently explained by the capacity of ATO to attenuate Akt and ERK activation. Arsenic Trioxide 154-157 AKT serine/threonine kinase 1 Homo sapiens 171-174 24482137-2 2014 The present study assessed the role of Akt in the cell death induced by As2O3. Arsenic Trioxide 72-77 AKT serine/threonine kinase 1 Homo sapiens 39-42 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 101-106 AKT serine/threonine kinase 1 Homo sapiens 48-51 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 101-106 AKT serine/threonine kinase 1 Homo sapiens 48-51 24482137-9 2014 These results demonstrated that inhibition of PI3K/Akt signaling was involved in As2O3-induced apoptosis of gastric cancer SGC-7901 cells. Arsenic Trioxide 81-86 AKT serine/threonine kinase 1 Homo sapiens 51-54 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 0-5 AKT serine/threonine kinase 1 Homo sapiens 32-35 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 0-5 AKT serine/threonine kinase 1 Homo sapiens 48-51 24482137-7 2014 As2O3 decreased the levels of p-Akt (Ser473), p-Akt (Thr308) and p-GSK-3beta (Ser9), suggesting that As2O3 inactivated Akt kinase. Arsenic Trioxide 0-5 AKT serine/threonine kinase 1 Homo sapiens 48-51 24307199-8 2014 Finally, 3-BrP was seen to cooperate with antitumor agents like arsenic trioxide and curcumin in causing cell death, a response apparently mediated by both the generation of oxidative stress induced by 3-BrP and the attenuation of Akt and ERK activation by curcumin. Arsenic Trioxide 64-80 AKT serine/threonine kinase 1 Homo sapiens 231-234 24791595-0 2014 The effect to IL-3Ralpha, downstream PI3k/Akt signaling of all-trans retinoic acid and arsenic trioxide in NB4 cells. Arsenic Trioxide 87-103 AKT serine/threonine kinase 1 Homo sapiens 42-45 24791595-5 2014 In contrast to ATRA, As2O3 reduces both mRNA and protein expression of IL-3Ralpha and inhibits the activity of PI3K/Akt after 24 h, 48 h, and 72 h of exposure. Arsenic Trioxide 21-26 AKT serine/threonine kinase 1 Homo sapiens 116-119 24392034-0 2013 Arsenic trioxide overcomes rapamycin-induced feedback activation of AKT and ERK signaling to enhance the anti-tumor effects in breast cancer. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 68-71 24750786-4 2014 Metformin and ATO induce autophagy and apoptosis in glioma cells by inhibiting and stimulating the PI3K/Akt and the mitogen-activated protein kinase pathways, respectively. Arsenic Trioxide 14-17 AKT serine/threonine kinase 1 Homo sapiens 104-107 24392034-3 2013 Previously, we published that arsenic trioxide (ATO) inhibits AKT activity and in some cases, decreases AKT protein expression. Arsenic Trioxide 30-46 AKT serine/threonine kinase 1 Homo sapiens 62-65 24392034-3 2013 Previously, we published that arsenic trioxide (ATO) inhibits AKT activity and in some cases, decreases AKT protein expression. Arsenic Trioxide 30-46 AKT serine/threonine kinase 1 Homo sapiens 104-107 24392034-3 2013 Previously, we published that arsenic trioxide (ATO) inhibits AKT activity and in some cases, decreases AKT protein expression. Arsenic Trioxide 48-51 AKT serine/threonine kinase 1 Homo sapiens 62-65 24392034-3 2013 Previously, we published that arsenic trioxide (ATO) inhibits AKT activity and in some cases, decreases AKT protein expression. Arsenic Trioxide 48-51 AKT serine/threonine kinase 1 Homo sapiens 104-107 24392034-4 2013 Therefore, we propose that combining ATO and rapamycin may circumvent the AKT feedback loop and increase the anti-tumor effects. Arsenic Trioxide 37-40 AKT serine/threonine kinase 1 Homo sapiens 74-77 24161621-0 2013 Differential sensitivity of p44/p42-MAPK- and PI3K/Akt-targeted neuroblastoma subtypes to arsenic trioxide. Arsenic Trioxide 90-106 AKT serine/threonine kinase 1 Homo sapiens 51-54 23542114-5 2013 ATO inhibited the phosphorylation and activation of AKT and STAT3 through Notch signaling blockade. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 52-55 23911876-0 2013 Characterization of arsenic trioxide resistant clones derived from Jurkat leukemia T cell line: focus on PI3K/Akt signaling pathway. Arsenic Trioxide 20-36 AKT serine/threonine kinase 1 Homo sapiens 110-113 23911876-1 2013 In this study the role of PI3K/Akt signaling pathway in arsenic trioxide (ATO)-treated parental Jurkat cells and also in derived ATO-resistant clones grown in the presence of given ATO concentration was investigated. Arsenic Trioxide 56-72 AKT serine/threonine kinase 1 Homo sapiens 31-34 23911876-1 2013 In this study the role of PI3K/Akt signaling pathway in arsenic trioxide (ATO)-treated parental Jurkat cells and also in derived ATO-resistant clones grown in the presence of given ATO concentration was investigated. Arsenic Trioxide 74-77 AKT serine/threonine kinase 1 Homo sapiens 31-34 23911876-1 2013 In this study the role of PI3K/Akt signaling pathway in arsenic trioxide (ATO)-treated parental Jurkat cells and also in derived ATO-resistant clones grown in the presence of given ATO concentration was investigated. Arsenic Trioxide 129-132 AKT serine/threonine kinase 1 Homo sapiens 31-34 23911876-1 2013 In this study the role of PI3K/Akt signaling pathway in arsenic trioxide (ATO)-treated parental Jurkat cells and also in derived ATO-resistant clones grown in the presence of given ATO concentration was investigated. Arsenic Trioxide 129-132 AKT serine/threonine kinase 1 Homo sapiens 31-34 23911876-6 2013 Akt1/2, AktV or wortmannin inhibitors decreased viability of ATO-resistant clones grown in the presence of ATO, with no effect on ATO-treated parental cells. Arsenic Trioxide 61-64 AKT serine/threonine kinase 1 Homo sapiens 0-4 23911876-6 2013 Akt1/2, AktV or wortmannin inhibitors decreased viability of ATO-resistant clones grown in the presence of ATO, with no effect on ATO-treated parental cells. Arsenic Trioxide 107-110 AKT serine/threonine kinase 1 Homo sapiens 0-4 23911876-6 2013 Akt1/2, AktV or wortmannin inhibitors decreased viability of ATO-resistant clones grown in the presence of ATO, with no effect on ATO-treated parental cells. Arsenic Trioxide 107-110 AKT serine/threonine kinase 1 Homo sapiens 0-4 23911876-7 2013 Flow cytometry analysis showed that ATO decreased the level of p-Akt in ATO-treated parental cells, while the resistant clones exhibited higher levels of p-Akt immunostaining than parental Jurkat cells. Arsenic Trioxide 36-39 AKT serine/threonine kinase 1 Homo sapiens 65-68 23911876-7 2013 Flow cytometry analysis showed that ATO decreased the level of p-Akt in ATO-treated parental cells, while the resistant clones exhibited higher levels of p-Akt immunostaining than parental Jurkat cells. Arsenic Trioxide 72-75 AKT serine/threonine kinase 1 Homo sapiens 65-68 23911876-8 2013 Expression analysis of 84 genes involved in the PI3K/Akt pathway revealed that this pathway was predominantly active in ATO-resistant clones. Arsenic Trioxide 120-123 AKT serine/threonine kinase 1 Homo sapiens 53-56 23980369-11 2013 In addition, the combination therapy of HHT at 40 ng/mL and ATO at 8.5 micromol/L inhibited phosphorylation of AKT in a time-dependent manner. Arsenic Trioxide 60-63 AKT serine/threonine kinase 1 Homo sapiens 111-114 23548265-6 2013 Comparable ATO-sensitizing effects were also found with PI3K/AKT and mitogen-activated protein/extracellular signal-regulated kinase (MEK) inhibitors, suggesting an essential role of the EGFR-mediated downstream signaling pathway in cancer cell protection against ATO. Arsenic Trioxide 11-14 AKT serine/threonine kinase 1 Homo sapiens 61-64 23201927-7 2013 Conversely, blocking Akt activation with the PI3K inhibitor LY294002 effectively suppressed the protective effect of Sal B against ATO-induced cell apoptosis. Arsenic Trioxide 131-134 AKT serine/threonine kinase 1 Homo sapiens 21-24 23352504-0 2013 Inhibition of AKT enhances mitotic cell apoptosis induced by arsenic trioxide. Arsenic Trioxide 61-77 AKT serine/threonine kinase 1 Homo sapiens 14-17 23352504-4 2013 We show that AKT was activated by ATO in HeLa-S3 cells. Arsenic Trioxide 34-37 AKT serine/threonine kinase 1 Homo sapiens 13-16 23352504-5 2013 Inhibition of AKT by inhibitors of the phosphatidyl inositol 3-kinase/AKT pathway significantly enhanced cell sensitivity to ATO by elevating mitotic cell apoptosis. Arsenic Trioxide 125-128 AKT serine/threonine kinase 1 Homo sapiens 14-17 23352504-5 2013 Inhibition of AKT by inhibitors of the phosphatidyl inositol 3-kinase/AKT pathway significantly enhanced cell sensitivity to ATO by elevating mitotic cell apoptosis. Arsenic Trioxide 125-128 AKT serine/threonine kinase 1 Homo sapiens 70-73 23352504-6 2013 Ectopic expression of the constitutively active AKT1 had no effect on ATO-induced spindle abnormalities but reduced kinetochore localization of BUBR1 and MAD2 and accelerated mitosis exit, prevented mitotic cell apoptosis, and enhanced the formation of micro- or multi-nuclei in ATO-treated cells. Arsenic Trioxide 279-282 AKT serine/threonine kinase 1 Homo sapiens 48-52 23352504-8 2013 In addition, AKT1 activation upregulated the expression of aurora kinase B (AURKB) and survivin, and depletion of AURKB or survivin reversed the resistance of AKT1-activated cells to ATO-induced apoptosis. Arsenic Trioxide 183-186 AKT serine/threonine kinase 1 Homo sapiens 13-17 23352504-8 2013 In addition, AKT1 activation upregulated the expression of aurora kinase B (AURKB) and survivin, and depletion of AURKB or survivin reversed the resistance of AKT1-activated cells to ATO-induced apoptosis. Arsenic Trioxide 183-186 AKT serine/threonine kinase 1 Homo sapiens 159-163 23352504-9 2013 Thus, AKT1 activation suppresses ATO-induced mitotic cell apoptosis, despite the presence of numerous spindle abnormalities, probably by upregulating AURKB and survivin and attenuating spindle checkpoint function. Arsenic Trioxide 33-36 AKT serine/threonine kinase 1 Homo sapiens 6-10 23352504-10 2013 Inhibition of AKT therefore effectively sensitizes cancer cells to ATO by enhancing mitotic cell apoptosis. Arsenic Trioxide 67-70 AKT serine/threonine kinase 1 Homo sapiens 14-17 23255002-6 2013 We also found that the HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) or arsenic trioxide (ATO) in combination with rapamycin markedly inhibited the growth of MCF-7 cells and 17-AAG or ATO suppressed rapamycin-induced phosphorylation of Akt. Arsenic Trioxide 90-106 AKT serine/threonine kinase 1 Homo sapiens 254-257 23255002-6 2013 We also found that the HSP90 inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) or arsenic trioxide (ATO) in combination with rapamycin markedly inhibited the growth of MCF-7 cells and 17-AAG or ATO suppressed rapamycin-induced phosphorylation of Akt. Arsenic Trioxide 108-111 AKT serine/threonine kinase 1 Homo sapiens 254-257 22751450-7 2013 Both ERK and AKT inhibitors decreased Mcl-1 levels and enhanced ATO-induced apoptosis in HL-60 cells. Arsenic Trioxide 64-67 AKT serine/threonine kinase 1 Homo sapiens 13-16 23178716-0 2013 SnoN/SkiL expression is modulated via arsenic trioxide-induced activation of the PI3K/AKT pathway in ovarian cancer cells. Arsenic Trioxide 38-54 AKT serine/threonine kinase 1 Homo sapiens 86-89 23178716-4 2013 As2O3 activates Src(Y416) whose activity (inhibited by PP2) modulates EGFR activation, its interaction with Shc/Grb2, and p-AKT. Arsenic Trioxide 0-5 AKT serine/threonine kinase 1 Homo sapiens 124-127 23178716-7 2013 Collectively, As2O3 mediates an initial rise in pY-Src(416) to regulate the PI3K/AKT pathway which increases SnoN and cell survival; these early events may counter the cell death response associated with increased pY-EGFR/MAPK activation. Arsenic Trioxide 14-19 AKT serine/threonine kinase 1 Homo sapiens 81-84 23041229-5 2012 Surprisingly 2-DG causes cell line-specific decrease in LKB-1/AMPK phosphorylation/activation, and also causes Akt/mTOR/p70S6K and MEK/ERK activation, which is prevented by co-treatment with ATO. Arsenic Trioxide 191-194 AKT serine/threonine kinase 1 Homo sapiens 111-114 20622048-1 2010 Simultaneous targeting of the phosphoinositide 3-kinase (PI3K)/Akt pathway increases arsenic trioxide (ATO)-dependent cytotoxicity of chronic lymphocytic leukemia (CLL) cells, whereas it has no significant effects on normal lymphocytes. Arsenic Trioxide 85-101 AKT serine/threonine kinase 1 Homo sapiens 63-66 23239002-0 2012 Synergism between carnosic acid and arsenic trioxide on induction of acute myeloid leukemia cell apoptosis is associated with modulation of PTEN/Akt signaling pathway. Arsenic Trioxide 36-52 AKT serine/threonine kinase 1 Homo sapiens 145-148 21947421-7 2012 Furthermore, the co-treatment of oridonin and As2O3 induced ROS-mediated down-regulation of Akt and XIAP, and inhibition of NF-kappaB activation. Arsenic Trioxide 58-63 AKT serine/threonine kinase 1 Homo sapiens 104-107 21889928-7 2011 In addition, lonidamine elicits ERK and Akt/mTOR pathway activation, as indicated by increased ERK, Akt, p70S6K and rpS6 phosphorylation, and these effects are reduced by co-treatment with ATO. Arsenic Trioxide 189-192 AKT serine/threonine kinase 1 Homo sapiens 40-43 21649584-11 2011 Collectively, we propose that the EGFR/PI3K/Akt pathway may regulate the post-transcriptional regulation of TGIF expression to antagonize ATO-induced apoptosis in HCC. Arsenic Trioxide 138-141 AKT serine/threonine kinase 1 Homo sapiens 44-47 20862710-6 2010 Low-dose ATO produced reactive oxygen species (ROS), and activated the p38 MAPK, Akt, and ERK1/2 pathways at different time points within 60 min. Arsenic Trioxide 9-12 AKT serine/threonine kinase 1 Homo sapiens 81-84 20862710-8 2010 Inhibiting the activation of Akt and ERK1/2, but not p38 MAPK, decreased the ATO-induced expression of cyclin D1 protein. Arsenic Trioxide 77-80 AKT serine/threonine kinase 1 Homo sapiens 29-32 20862710-9 2010 This study reports for the first time that p38 MAPK/Akt/ERK1/2 activation is required for the protein stabilization of CDC6 in addition to cyclin D1 in ATO-induced cell proliferation and cell cycle modulation from G1 to S phase. Arsenic Trioxide 152-155 AKT serine/threonine kinase 1 Homo sapiens 52-55 20534739-0 2010 Induction of B-chronic lymphocytic leukemia cell apoptosis by arsenic trioxide involves suppression of the phosphoinositide 3-kinase/Akt survival pathway via c-jun-NH2 terminal kinase activation and PTEN upregulation. Arsenic Trioxide 62-78 AKT serine/threonine kinase 1 Homo sapiens 133-136 22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Arsenic Trioxide 89-105 AKT serine/threonine kinase 1 Homo sapiens 213-216 22391160-2 2012 This study was purposed to investigate the effects of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3) on the expression of CD44v6 and the associated signal pathway phosphatidylinositol 3-kinase (PI3K)/Akt in acute promyelocytic leukemia (APL) cell line NB4 cells. Arsenic Trioxide 107-112 AKT serine/threonine kinase 1 Homo sapiens 213-216 22391160-5 2012 In As2O3-induced apoptosis, both the transcriptional level and translational level of CD44v6 were remarkably reduced, and the PI3K/Akt pathway was inhibited. Arsenic Trioxide 3-8 AKT serine/threonine kinase 1 Homo sapiens 131-134 21594580-7 2011 The mechanisms of ATO-induced autophagy and apoptosis were mediated by the inhibition of PI3K/Akt and the activation of MAPK signaling pathways. Arsenic Trioxide 18-21 AKT serine/threonine kinase 1 Homo sapiens 94-97 21594580-8 2011 The ATO treatment of U118-MG cells pre-treated with specific chemical inhibitors of PI3K/AKT and MAPK significantly changed the cytotoxicity and the expression of survivin, suggesting that survivin plays a pivotal role in ATO-induced cell death. Arsenic Trioxide 4-7 AKT serine/threonine kinase 1 Homo sapiens 89-92 21180886-6 2011 ATO decreased the viability of HL60 cells and induced cellular apoptosis, which was accompanied by transient activation of Akt. Arsenic Trioxide 0-3 AKT serine/threonine kinase 1 Homo sapiens 123-126 21655183-0 2011 BIM-mediated AKT phosphorylation is a key modulator of arsenic trioxide-induced apoptosis in cisplatin-sensitive and -resistant ovarian cancer cells. Arsenic Trioxide 55-71 AKT serine/threonine kinase 1 Homo sapiens 13-16 21655183-4 2011 Our data demonstrated that ATO induced cell apoptosis by decreasing levels of phosphorylated AKT (p-AKT) and activating caspase-3 and caspase-9. Arsenic Trioxide 27-30 AKT serine/threonine kinase 1 Homo sapiens 93-96 21655183-4 2011 Our data demonstrated that ATO induced cell apoptosis by decreasing levels of phosphorylated AKT (p-AKT) and activating caspase-3 and caspase-9. Arsenic Trioxide 27-30 AKT serine/threonine kinase 1 Homo sapiens 100-103 21655183-8 2011 Moreover, the activation of caspase-3 by ATO treatment improved AKT dephosphorylation, not only by cleaving the regulatory A subunit of protein phosphatase 2A (PP2A), but also by increasing its activation. Arsenic Trioxide 41-44 AKT serine/threonine kinase 1 Homo sapiens 64-67 20622048-1 2010 Simultaneous targeting of the phosphoinositide 3-kinase (PI3K)/Akt pathway increases arsenic trioxide (ATO)-dependent cytotoxicity of chronic lymphocytic leukemia (CLL) cells, whereas it has no significant effects on normal lymphocytes. Arsenic Trioxide 103-106 AKT serine/threonine kinase 1 Homo sapiens 63-66 20622048-2 2010 Combinations of ATO with small molecules that target PI3K and/or Akt may provide a novel approach for the treatment of CLL. Arsenic Trioxide 16-19 AKT serine/threonine kinase 1 Homo sapiens 65-68 19457607-0 2009 Arsenic trioxide induces apoptosis and G2/M phase arrest by inducing Cbl to inhibit PI3K/Akt signaling and thereby regulate p53 activation. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 89-92 20657188-8 2010 All these results may provide a rationale for improving the efficacy of As2O3 as a therapeutic agent through combination treatment with stathmin inhibition or PI3K/Akt inhibitors. Arsenic Trioxide 72-77 AKT serine/threonine kinase 1 Homo sapiens 164-167 19457607-7 2009 The PI3K/Akt inhibitor LY294002 significantly increased the amount of p53 protein and ATO-induced apoptosis in both cell lines and decreased G2/M phase arrest of MGC803 cells. Arsenic Trioxide 86-89 AKT serine/threonine kinase 1 Homo sapiens 9-12 19457607-9 2009 Inhibition of Cbl with the proteasome inhibitor Ps341 decreased apoptosis in NB4 cells and increased the G2/M phase arrest of MGC803 cells, and it also prolonged the activation of PI3K/Akt by ATO. Arsenic Trioxide 192-195 AKT serine/threonine kinase 1 Homo sapiens 185-188 19457607-11 2009 These results demonstrate that inhibition of PI3K/Akt signaling by Cbl is involved in both ATO-induced apoptosis of NB4 cells and ATO-induced G2/M phase arrest of gastric cancer cells. Arsenic Trioxide 91-94 AKT serine/threonine kinase 1 Homo sapiens 50-53 19457607-11 2009 These results demonstrate that inhibition of PI3K/Akt signaling by Cbl is involved in both ATO-induced apoptosis of NB4 cells and ATO-induced G2/M phase arrest of gastric cancer cells. Arsenic Trioxide 130-133 AKT serine/threonine kinase 1 Homo sapiens 50-53 18359480-5 2008 Quercetin and chrysin, alone or with ATO, decreased Akt phosphorylation as well as intracellular GSH content. Arsenic Trioxide 37-40 AKT serine/threonine kinase 1 Homo sapiens 52-55 19242099-0 2009 Combination treatment with arsenic trioxide and irradiation enhances autophagic effects in U118-MG cells through increased mitotic arrest and regulation of PI3K/Akt and ERK1/2 signaling pathways. Arsenic Trioxide 27-43 AKT serine/threonine kinase 1 Homo sapiens 161-164 18937079-8 2009 This FOXO3a accumulation correlated well with the As(2)O(3)-induced reduction of active Akt. Arsenic Trioxide 50-59 AKT serine/threonine kinase 1 Homo sapiens 88-91 18937079-5 2009 Furthermore, we study the Akt activation after As(2)O(3) treatment and the HCC cells proliferation after combination of As(2)O(3) with PI3K inhibitor Wortmannin. Arsenic Trioxide 47-56 AKT serine/threonine kinase 1 Homo sapiens 26-29 18491231-6 2008 ATRA and ATO-induced expression of DAP5/p97 was associated with inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. Arsenic Trioxide 9-12 AKT serine/threonine kinase 1 Homo sapiens 119-122 18491231-9 2008 Together, our data reveal new roles for DAP5/p97 in ATRA-induced differentiation and ATO-induced apoptosis in APL and suggest a novel regulatory mechanism by which PI3K/Akt/mTOR pathway inhibition mediates ATRA- and ATO-induced expression of DAP5/p97. Arsenic Trioxide 85-88 AKT serine/threonine kinase 1 Homo sapiens 169-172 16434995-4 2006 Arsenic trioxide led to increased cell surface expression of DR5 (death receptor 5), inhibition of the serine/threonine kinase Akt and downregulation of the short isoform of FLIP (FLICE-inhibitory protein, FLIPS). Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 127-130 18048359-3 2008 Using cells with targeted disruption of both the Akt1 and Akt2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhanced in the absence of these kinases, suggesting that Akt1/Akt2 are activated in a negative feedback regulatory manner, to control generation of As(2)O(3) responses. Arsenic Trioxide 97-113 AKT serine/threonine kinase 1 Homo sapiens 49-53 18048359-3 2008 Using cells with targeted disruption of both the Akt1 and Akt2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhanced in the absence of these kinases, suggesting that Akt1/Akt2 are activated in a negative feedback regulatory manner, to control generation of As(2)O(3) responses. Arsenic Trioxide 97-113 AKT serine/threonine kinase 1 Homo sapiens 204-208 18048359-3 2008 Using cells with targeted disruption of both the Akt1 and Akt2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhanced in the absence of these kinases, suggesting that Akt1/Akt2 are activated in a negative feedback regulatory manner, to control generation of As(2)O(3) responses. Arsenic Trioxide 295-304 AKT serine/threonine kinase 1 Homo sapiens 204-208 18048359-8 2008 Altogether, these data provide evidence for a key regulatory role of the Akt/mTOR pathway in the generation of the effects of As(2)O(3), and suggest that targeting this signaling cascade may provide a novel therapeutic approach to enhance the anti-leukemic properties of As(2)O(3). Arsenic Trioxide 126-135 AKT serine/threonine kinase 1 Homo sapiens 73-76 18048359-8 2008 Altogether, these data provide evidence for a key regulatory role of the Akt/mTOR pathway in the generation of the effects of As(2)O(3), and suggest that targeting this signaling cascade may provide a novel therapeutic approach to enhance the anti-leukemic properties of As(2)O(3). Arsenic Trioxide 271-280 AKT serine/threonine kinase 1 Homo sapiens 73-76 17537996-0 2007 Low-dose arsenic trioxide sensitizes glucocorticoid-resistant acute lymphoblastic leukemia cells to dexamethasone via an Akt-dependent pathway. Arsenic Trioxide 9-25 AKT serine/threonine kinase 1 Homo sapiens 121-124 17537996-6 2007 Expression of dominant-active Akt, reduction of Bad expression by RNA interference, or overexpression of XIAP abrogated the sensitizing effect of ATO. Arsenic Trioxide 146-149 AKT serine/threonine kinase 1 Homo sapiens 30-33 16434995-0 2006 TRAIL sensitisation by arsenic trioxide is caspase-8 dependent and involves modulation of death receptor components and Akt. Arsenic Trioxide 23-39 AKT serine/threonine kinase 1 Homo sapiens 120-123 18566239-0 2008 Arsenic trioxide decreases AKT protein in a caspase-dependent manner. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 27-30 18566239-4 2008 AKT inhibits several steps in this pathway; therefore, we postulated that As2O3 might decrease its activity. Arsenic Trioxide 74-79 AKT serine/threonine kinase 1 Homo sapiens 0-3 18566239-5 2008 Indeed, As2O3 decreases not only AKT activity but also total AKT protein, and sensitivity to As2O3 correlates with the degree of AKT protein decrease. Arsenic Trioxide 8-13 AKT serine/threonine kinase 1 Homo sapiens 33-36 18566239-5 2008 Indeed, As2O3 decreases not only AKT activity but also total AKT protein, and sensitivity to As2O3 correlates with the degree of AKT protein decrease. Arsenic Trioxide 8-13 AKT serine/threonine kinase 1 Homo sapiens 61-64 18566239-5 2008 Indeed, As2O3 decreases not only AKT activity but also total AKT protein, and sensitivity to As2O3 correlates with the degree of AKT protein decrease. Arsenic Trioxide 8-13 AKT serine/threonine kinase 1 Homo sapiens 61-64 18566239-7 2008 We found that As2O3 regulates AKT protein stability without significant effects on its transcription or translation. Arsenic Trioxide 14-19 AKT serine/threonine kinase 1 Homo sapiens 30-33 18566239-8 2008 We show that As2O3 decreases AKT protein via caspase-mediated degradation, abrogated by caspase-6, caspase-8, caspase-9, and caspase-3 inhibitors but not proteosome inhibitors. Arsenic Trioxide 13-18 AKT serine/threonine kinase 1 Homo sapiens 29-32 18566239-9 2008 Furthermore, As2O3 enhances the ability of a heat shock protein 90 inhibitor to decrease AKT expression and increase growth inhibition. Arsenic Trioxide 13-18 AKT serine/threonine kinase 1 Homo sapiens 89-92 18566239-10 2008 This suggests that As2O3 may be useful in combination therapies that target AKT pathways or in tumors that have constitutively active AKT expression. Arsenic Trioxide 19-24 AKT serine/threonine kinase 1 Homo sapiens 76-79 18566239-10 2008 This suggests that As2O3 may be useful in combination therapies that target AKT pathways or in tumors that have constitutively active AKT expression. Arsenic Trioxide 19-24 AKT serine/threonine kinase 1 Homo sapiens 134-137 16482209-5 2006 Mechanistic studies revealed that ATO exerted cytotoxic action by reactive oxygen species generation, and activated Akt survival pathway. Arsenic Trioxide 34-37 AKT serine/threonine kinase 1 Homo sapiens 116-119 16115127-6 2005 Upon prolonged exposure to As2O3, we isolated a NB-4 cell clone that was resistant to As2O3 and displayed high levels of active Akt. Arsenic Trioxide 27-32 AKT serine/threonine kinase 1 Homo sapiens 128-131 16115127-0 2005 Phosphoinositide 3-kinase/Akt inhibition increases arsenic trioxide-induced apoptosis of acute promyelocytic and T-cell leukaemias. Arsenic Trioxide 51-67 AKT serine/threonine kinase 1 Homo sapiens 26-29 16115127-7 2005 LY294002 treatment of acute promyelocytic primary blasts with elevated Akt phosphorylation levels resulted in an increased sensitivity to As2O3. Arsenic Trioxide 138-143 AKT serine/threonine kinase 1 Homo sapiens 71-74 16115127-5 2005 Overexpression of a constitutively active Akt cDNA rendered NB-4 cells less susceptible to As2O3. Arsenic Trioxide 91-96 AKT serine/threonine kinase 1 Homo sapiens 42-45 16115127-8 2005 These results may provide a rationale for the development of combined or sequential treatment with PI3K/Akt inhibitors to improve the efficacy of As2O3 on acute leukaemias and also to overcome As2O3 resistance. Arsenic Trioxide 146-151 AKT serine/threonine kinase 1 Homo sapiens 104-107 16115127-8 2005 These results may provide a rationale for the development of combined or sequential treatment with PI3K/Akt inhibitors to improve the efficacy of As2O3 on acute leukaemias and also to overcome As2O3 resistance. Arsenic Trioxide 193-198 AKT serine/threonine kinase 1 Homo sapiens 104-107 15316930-0 2005 Phosphoinositide 3-kinase/Akt involvement in arsenic trioxide resistance of human leukemia cells. Arsenic Trioxide 45-61 AKT serine/threonine kinase 1 Homo sapiens 26-29 15316930-1 2005 The purpose of this study was to evaluate the possible involvement of the phosphoinositide 3-kinase (PI3K)/Akt survival pathway in determining resistance to arsenic trioxide (As2O3)-induced apoptosis. Arsenic Trioxide 157-173 AKT serine/threonine kinase 1 Homo sapiens 107-110 15316930-1 2005 The purpose of this study was to evaluate the possible involvement of the phosphoinositide 3-kinase (PI3K)/Akt survival pathway in determining resistance to arsenic trioxide (As2O3)-induced apoptosis. Arsenic Trioxide 175-180 AKT serine/threonine kinase 1 Homo sapiens 107-110 15316930-4 2005 Selective pharmacological inhibitors of the PI3K/Akt axis (LY294002, wortmannin) were employed to influence the sensitivity to As2O3. Arsenic Trioxide 127-132 AKT serine/threonine kinase 1 Homo sapiens 49-52 15316930-7 2005 Also in U937 and K562 cells, inhibitors of the PI3K/Akt axis caused a decrease in As2O3 resistance. Arsenic Trioxide 82-87 AKT serine/threonine kinase 1 Homo sapiens 52-55 15316930-8 2005 Overexpression of constitutively active Akt in HL60PT cells caused the induction of resistance to 2.5 microM As2O3. Arsenic Trioxide 109-114 AKT serine/threonine kinase 1 Homo sapiens 40-43 15316930-9 2005 Conversely, forced expression of a dominant negative Akt in HL60AR cells resulted in a decrease in As2O3 resistance. Arsenic Trioxide 99-104 AKT serine/threonine kinase 1 Homo sapiens 53-56 15316930-11 2005 Taken together our findings suggest that a constitutive activation of the PI3K/Akt pathway, which is increasingly detected in some types of acute myeloid leukemia, may contribute to As2O3 resistance, most likely through NF-kappaB activation. Arsenic Trioxide 182-187 AKT serine/threonine kinase 1 Homo sapiens 79-82 34880920-15 2021 In the arsenic trioxide-target-pathway-HCC network, targets such as AKT1, RAF1, RELA, TP53, and PTEN had a higher degree. Arsenic Trioxide 7-23 AKT serine/threonine kinase 1 Homo sapiens 68-72 15665116-0 2005 Pharmacologic inhibitors of PI3K/Akt potentiate the apoptotic action of the antileukemic drug arsenic trioxide via glutathione depletion and increased peroxide accumulation in myeloid leukemia cells. Arsenic Trioxide 94-110 AKT serine/threonine kinase 1 Homo sapiens 33-36 15665116-8 2005 These results, which indicate that glutathione is a target of PI3K/Akt in myeloid leukemia cells, may partially explain the selective increase of As2O3 toxicity by PI3K/Akt inhibitors, and may provide a rationale to improve the efficacy of these inhibitors as therapeutic agents. Arsenic Trioxide 146-151 AKT serine/threonine kinase 1 Homo sapiens 67-70 15665116-8 2005 These results, which indicate that glutathione is a target of PI3K/Akt in myeloid leukemia cells, may partially explain the selective increase of As2O3 toxicity by PI3K/Akt inhibitors, and may provide a rationale to improve the efficacy of these inhibitors as therapeutic agents. Arsenic Trioxide 146-151 AKT serine/threonine kinase 1 Homo sapiens 169-172 12168106-0 2002 Arsenic trioxide-induced apoptosis in U937 cells involve generation of reactive oxygen species and inhibition of Akt. Arsenic Trioxide 0-16 AKT serine/threonine kinase 1 Homo sapiens 113-116 12168106-9 2002 These data indicate that arsenic trioxide can cause cell damage by inactivating the Akt-related cell survival pathway and generating the reactive oxygen species, providing a new mechanism for arsenic trioxide-induced apoptosis. Arsenic Trioxide 25-41 AKT serine/threonine kinase 1 Homo sapiens 84-87 12168106-9 2002 These data indicate that arsenic trioxide can cause cell damage by inactivating the Akt-related cell survival pathway and generating the reactive oxygen species, providing a new mechanism for arsenic trioxide-induced apoptosis. Arsenic Trioxide 192-208 AKT serine/threonine kinase 1 Homo sapiens 84-87 11368438-4 2001 Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity. Arsenic Trioxide 24-29 AKT serine/threonine kinase 1 Homo sapiens 114-117 11368438-4 2001 Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity. Arsenic Trioxide 24-29 AKT serine/threonine kinase 1 Homo sapiens 137-140 34749590-9 2021 Notably, interferon alpha and/or arsenic trioxide inhibited megakaryocytes proliferation and reduced JAK2, STAT3, STAT5 and AKT phosphorylation in mutant JAK2-expressing iPSCs compared with those without induction. Arsenic Trioxide 33-49 AKT serine/threonine kinase 1 Homo sapiens 124-127