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akt inhibitor api-2  (Millipore)


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    Millipore akt inhibitor api-2
    Akt Inhibitor Api 2, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/akt+inhibitor+api-2/api+2/pm40603988-144-0-14
    Average 90 stars, based on 1 article reviews
    akt inhibitor api-2 - by Bioz Stars, 2026-10
    90/100 stars

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    Article Title: Interactions of thyroid hormone and FSH in the regulation of rat granulosa cell apoptosis
    Article Snippet: State Key Laboratory for Agro-Biotechnology, College of Biological Science, China Agricultural University, Beijing 100193, Peoples’ Republic of China, Reproductive Biology Unit, Departments of Cellular and Molecular Medicine, and Obstetrics & Gynaecology, University of Ottawa, Ottawa, Ontario, Canada K1Y 4E9.. Chronic Disease Program, Ottawa Hospital Research Institute, Ottawa, Ontario, Canada, World Class University (WCU) Biomodulation Major, Department of Agricultural Biotechnology, College of Agriculture and Life Sciences, Seoul National University, Seoul 151-921, Republic of Korea

    Article Title: Deregulation of Nrf2/ARE signaling pathway causes susceptibility of dystrophin-deficient myotubes to menadione-induced oxidative stress.
    Article Snippet: Author’s Accepted Manuscript Deregulation of Nrf2/ARE signaling pathway causes susceptibility of dystrophin-deficient myotubes to menadione-induced oxidative stress Su Jin Choi, Hye Sun Kim PII: S0014-4827(18)30087-9 DOI: https://doi.org/10.1016/j.yexcr.2018.02.013 Reference: YEXCR10926 To appear in: Experimental Cell Research Received date: 2 October 2017 Revised date: 12 February 2018 Accepted date: 14 February 2018 Cite this article as: Su Jin Choi and Hye Sun Kim, Deregulation of Nrf2/ARE signaling pathway causes susceptibility of dystrophin-deficient myotubes to menadione-induced oxidative stress, Experimental Cell Research, https://doi.org/10.1016/j.yexcr.2018.02.013 This is a PDF file of an unedited manuscript that has been accepted for publication.. As a service to our customers we are providing this early version of the manuscript.. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form.

    Article Title: EphA2 phosphorylation at Ser897 by the Cdk1/MEK/ERK/RSK pathway regulates M-phase progression via maintenance of cortical rigidity.
    Article Snippet: The ERK inhibitor U0126 (LC Laboratory, Woburn, MA, USA), the RSK inhibitor BI-D1870 (Enzo Life Sciences, Farmingdale, NY,USA), and thePKAinhibitorH89 (AdooQBioScience, Irvine, CA, USA) were used at 10 or 20 mM for 1 h. The Akt inhibitor API-2 (MilliporeSigma) was used at 10 mM for 1 h. The EphB4 inhibitor NVP-BHG712 (AdooQ) was used at 1 mM for 1 h. Detailed protocols are described in each appropriate figure legend.

    Article Title: AKT-mediated enhanced aerobic glycolysis causes acquired radioresistance by human tumor cells.
    Article Snippet: http://dx.doi.org/10.1016/j.radonc.2014.07.015 0167-8140/ 2014 Elsevier Ireland Ltd. All rights reserved.. ⇑ Corresponding author.. Address: Department of Environmental Health, National Institute of Public Health, 2-3-6 Minami, Wako, Saitama 351-0197, Japan.

    Article Title: Activation of the AKT/cyclin D1/Cdk4 survival signaling pathway in radioresistant cancer stem cells
    Article Snippet: An AKT inhibitor, API-2, and a Cdk4 inhibitor, Cdk4-I, were purchased from Calbiochem (San Diego, CA, USA).

    Article Title: Radiation affects glutathione redox reaction by reduced glutathione peroxidase activity in human fibroblasts
    Article Snippet: AKT inhibitor API-2 was purchased from Millipore.

    Article Title: Nuclear accumulation of cyclin D1 following long-term fractionated exposures to low-dose ionizing radiation in normal human diploid cells
    Article Snippet: The AKT inhibitor API-2 was purchased from Calbiochem and dissolved in dimethyl sulfoxide.



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    Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, <t>triciribine;</t> CON, control.
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    Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, <t>triciribine;</t> CON, control.
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    Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, <t>triciribine;</t> CON, control.
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    Tocris api-2 (akt inhibitor)
    Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, <t>triciribine;</t> CON, control.
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    Image Search Results


    Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, triciribine; CON, control.

    Journal: International Journal of Molecular Medicine

    Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

    doi: 10.3892/ijmm.2025.5492

    Figure Lengend Snippet: Cur decreases A/R injury in H9c2 cells via Sirt1. Expression of (A) apoptosis-associated proteins in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (B) Relative protein expression of Bcl2. (C) represents the relative protein expression of Bax. Expression of Sirt1 (D) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (E) Relative protein expression of Sirt1. Apoptosis rate of H9c2 cells was measured by flow cytometry (F and G) illustrates the proportion of apoptotic cells as determined by flow cytometry. (H) caspase 3, (I) LDH activity and (J) viability of A/R injured H9c2 cells after Cur pretreatment, silencing of Sirt1 expression and targeted inhibition of AKT activity. * P<0.05, ** P<0.01, *** P<0.001. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; LDH, Lactate dehydrogenase; si, small interfering; NC, non-targeting control; API-2, triciribine; CON, control.

    Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

    Techniques: Expressing, Inhibition, Activity Assay, Flow Cytometry, Control

    Cur reduces autophagy-dependent ferroptosis in H9c2 cells associated with A/R injury via Sirt1. Expression of autophagy-(A) and ferroptosis-related proteins (B) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Relative protein expression of P62 and the ratio of LC3II/I. (D) Relative protein expression of NCOA4 and FTH1. Detection of (E) total iron ions, (F) MDA, (G) GSSG, (H) GSH, (I) GSH/GSSG and (J) SOD in A/R injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. Fluorescence intensity of (K) lysosomes, (L) ROS and (M) Fe 2+ in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity (magnification, ×200; scale bar, 400 μ m). ** P<0.05, *** P<0.01. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; MDA, malondialdehyde; GSSG, glutathione disulfide; GSH, glutathione; SOD, superoxide dismutase; ROS, reactive oxygen species; NCOA4, nuclear receptor coactivator 4; FTH1, ferritin heavy chain 1; CON, control; si, small interfering; prot, protein; API, triciribine; LC3II, microtubule-associated protein 1 light chain 3 β; NC, non-targeting control.

    Journal: International Journal of Molecular Medicine

    Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

    doi: 10.3892/ijmm.2025.5492

    Figure Lengend Snippet: Cur reduces autophagy-dependent ferroptosis in H9c2 cells associated with A/R injury via Sirt1. Expression of autophagy-(A) and ferroptosis-related proteins (B) in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Relative protein expression of P62 and the ratio of LC3II/I. (D) Relative protein expression of NCOA4 and FTH1. Detection of (E) total iron ions, (F) MDA, (G) GSSG, (H) GSH, (I) GSH/GSSG and (J) SOD in A/R injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. Fluorescence intensity of (K) lysosomes, (L) ROS and (M) Fe 2+ in A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity (magnification, ×200; scale bar, 400 μ m). ** P<0.05, *** P<0.01. Cur, curcumin; A/R, anoxia/reoxygenation; Sirt, silent information regulator 1; MDA, malondialdehyde; GSSG, glutathione disulfide; GSH, glutathione; SOD, superoxide dismutase; ROS, reactive oxygen species; NCOA4, nuclear receptor coactivator 4; FTH1, ferritin heavy chain 1; CON, control; si, small interfering; prot, protein; API, triciribine; LC3II, microtubule-associated protein 1 light chain 3 β; NC, non-targeting control.

    Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

    Techniques: Expressing, Inhibition, Activity Assay, Fluorescence, Control

    Cur mediates nuclear localization of FoxO3a via Sirt1/AKT. (A) Western blot analysis of (B) phosphorylation of AKT and FoxO3a in A/R-injured H9c2 cells after Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Western blot analysis of (D) distribution of FoxO3a in the cytoplasm and nucleus of A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. *** P<0.01. Cur, curcumin; PCNA, proliferating cell nuclear antigen; Sirt, silent information regulator 1; A/R, anoxia/reoxygenation; p-, phosphorylated; si, small interfering; NC, non-targeting control; API, Triciribine; CON, control.

    Journal: International Journal of Molecular Medicine

    Article Title: Curcumin attenuates myocardial ischemia-reperfusion-induced autophagy-dependent ferroptosis via Sirt1/AKT/FoxO3a signaling

    doi: 10.3892/ijmm.2025.5492

    Figure Lengend Snippet: Cur mediates nuclear localization of FoxO3a via Sirt1/AKT. (A) Western blot analysis of (B) phosphorylation of AKT and FoxO3a in A/R-injured H9c2 cells after Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. (C) Western blot analysis of (D) distribution of FoxO3a in the cytoplasm and nucleus of A/R-injured H9c2 cells following Cur pretreatment, Sirt1 silencing and targeted inhibition of AKT activity. *** P<0.01. Cur, curcumin; PCNA, proliferating cell nuclear antigen; Sirt, silent information regulator 1; A/R, anoxia/reoxygenation; p-, phosphorylated; si, small interfering; NC, non-targeting control; API, Triciribine; CON, control.

    Article Snippet: Cur (purity ≥98%, batch no. DC0279-0005) was purchased from Dester Technology Co., Ltd. and Akt inhibitor triciribine (API-2; cat. no. GC15392) was purchased from GLPBIO Technology LLC.

    Techniques: Western Blot, Inhibition, Activity Assay, Control