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Mk 2206

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MK-2206 is a small molecule inhibitor that targets the serine/threonine protein kinase AKT. It is designed to inhibit the phosphorylation and activation of AKT, which plays a critical role in cellular processes such as cell growth, proliferation, and survival.

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Lab products found in correlation

Rapamycin, by LC Laboratories (3 mentions) α tubulin sc 23948, by Santa Cruz Biotechnology (2 mentions) Acc antibody 3662, by Cell Signaling Technology (2 mentions) Polyclonal sin1 antibody a300 910a, by Fortis Life Sciences (2 mentions) Oil red o, by Merck Group (2 mentions) Chir99021, by LC Laboratories (2 mentions) Pik 90, by Merck Group (2 mentions) Mln0128, by Active Motif (2 mentions) Sb216763, by Cayman Chemical (1 mentions) Ag1478, by Santa Cruz Biotechnology (1 mentions) Pifithrin α, by Fujifilm (1 mentions) Cdcl2, by Fujifilm (1 mentions) Mek1 2, by Cell Signaling Technology (1 mentions) Ly294002, by Cayman Chemical (1 mentions) Rad001, by Selleck Chemicals (1 mentions) Nvp bez235, by Selleck Chemicals (1 mentions) Ku60019, by Bio-Techne (1 mentions) Gsk2334470, by Selleck Chemicals (1 mentions) Nvp bkm120, by Selleck Chemicals (1 mentions) Ink128, by Active Motif (1 mentions)

14 protocols using mk 2206

1

Investigating mTOR and GSK3 Signaling

Cited 1 time
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All mTOR kinase inhibitors, the GSK3 inhibitor SB216763, the proteasome inhibitor MG132, the protein synthesis inhibitor cycloheximide (CHX) and the antibodies against GSK3α/β, phospho-GSK3α/β (Ser21/9), phospho-Akt (Ser473), Akt, rictor and raptor were the same as described previously 22 (link). The GSK3 inhibitor CHIR99021 was purchased from LC laboratories (Woburn, MA). BKM120 was supplied by Novartis Pharmaceuticals Corporation (East Hanover, NJ). API-1 (NSC177233) was obtained from the National Cancer Institute (Bethesda, MD). MK2206 was purchased from Active Biochem (Maplewood, NJ). Perifosine was supplied by Keryx Biopharmaceuticals, Inc (New York, NY). Oil Red O was purchased from Sigma Chemical Co. (St. Louis, MO). SREBP1 (sc-13551), FASN (sc-55580) and α-tubulin (sc-23948) antibodies were purchased from Santa Cruz Biotechnology, Inc (Santa Cruz, CA). ACC antibody (#3662) was purchased from Cell Signaling Technology, Inc. (Beverly, MA). Polyclonal Sin1 antibody (A300-910A) was purchased from Bethyl Laboratories, Inc. (Montgomery, TX).
Li S., Oh Y.T., Yue P., Khuri F.R, & Sun S.Y. (2015). Inhibition of mTOR complex 2 induces GSK3/FBXW7-dependent degradation of sterol regulatory element-binding protein 1 (SREBP1) and suppresses lipogenesis in cancer cells. Oncogene, 35(5), 642-650.
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2

Investigating Notch Signaling in Cancer Cells

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CdCl2 was obtained from Wako Pure Chemical Industries, Ltd. (Osaka, Japan). LY294002 and SB216763 were obtained from Cayman Chemical Company (Ann Arbor, MI, USA). AG1478 and PPP were obtained from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA). DAPT and pifithrin-α were obtained from Wako. MK-2206 was obtained from Active Biochem (Maplewood, NJ, USA). Antibodies against phospho-EGFR (Tyr1068), total EGFR (D38B1) XP, phospho-Akt (Thr308) (C31E5E), total Akt (pan) (C67E7), phospho-p70 S6 kinase (Thr389) (108D2), phospho-GSK-3α/β (Ser21/9) (37F11), total GSK3-α/β (D75D3) XP, cleaved Notch1 (Val1744) (D3B8), Notch1 (D1E11) XP, Jagged1 (28H8), Jagged2 (C23D2), Snail (C15D3), E-cadherin (24E10), phospho-p53 (Ser15), and MEK1/2 were obtained from Cell Signaling Technology, Inc. (Beverly, MA, USA). p53 (DO-1), Notch1 (C-20), actin (I-19), and lamin A/C (14/LaminAC) antibodies were obtained from Santa Cruz Biotechnology. The siRNAs targeted against the human Notch1 (siRNA-1: Hs_NOTCH1_3 FlexiTube siRNA, SI00119028, siRNA-2: Hs_NOTCH1_4 FlexiTube siRNA, SI00119035), Jagged1 (Hs_JAG1_5 FlexiTube siRNA, SI02780134), Jagged2 (Hs_JAG2_2 FlexiTube siRNA, SI03095764), SNAI1 (siRNA-1: Hs_SNAI1_1 FlexiTube siRNA, SI00083398, siRNA-2: Hs_SNAI1_5 FlexiTube siRNA, SI02636424), and non-target siRNA (AllStars Negative Control siRNA) were purchased from Qiagen (Hilden, Germany).
Fujiki K., Inamura H, & Matsuoka M. (2014). Detrimental effects of Notch1 signaling activated by cadmium in renal proximal tubular epithelial cells. Cell Death & Disease, 5(8), e1378-.
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3

Stock Solution Preparation for Inhibitors

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Stock solutions of NVP-BEZ235, RAD001, NVP-BKM120 and GSK2334470 (Selleckchem, Munich, Germany), MK-2206 and INK128 (Active Biochem, Bonn, Germany), PIK-90 (Merck Chemicals GmbH, Darmstadt, Germany), NU7441 and KU60019 (Tocris Bioscience, Bristol, United Kingdom) were prepared in DMSO. Working concentrations were freshly prepared in medium with control corresponding to highest DMSO concentration.
Sathe A., Chalaud G., Oppolzer I., Wong K.Y., von Busch M., Schmid S.C., Tong Z., Retz M., Gschwend J.E., Schulz W.A, & Nawroth R. (2018). Parallel PI3K, AKT and mTOR inhibition is required to control feedback loops that limit tumor therapy. PLoS ONE, 13(1), e0190854.
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4

MK-2206 Stock Solution Preparation

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MK-2206 (Active Biochem, Bonn, Germany) was stored as a 10 mM stock solution in DMSO and working concentrations were freshly prepared in medium. As a control, DMSO was used corresponding to the DMSO in the highest MK-2206 concentration.
Sathe A., Guerth F., Cronauer M.V., Heck M.M., Thalgott M., Gschwend J.E., Retz M, & Nawroth R. (2014). Mutant PIK3CA controls DUSP1-dependent ERK 1/2 activity to confer response to AKT target therapy. British Journal of Cancer, 111(11), 2103-2113.
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5

Doxycycline-Inducible Mouse Model for mTOR Pathway

Cited 3 times
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C57Bl/6J (B6) mice were bred at the University of California, Irvine, and used at between 6 and 12 weeks of age. All animals were studied in compliance with protocols approved by the Institutional Animal Care and Use Committees of the University of California, Irvine. Mice carrying an AID-GFP reporter on a B6 background were obtained from the Jackson Laboratory (stock number 018421). Mice harboring a transgenic allele encoding a constitutively active form of 4E-BP (4E-BP1M) under a tetracycline-responsive element were described previously (18 (link), 44 (link)). These mice were crossed to a strain harboring an optimized form of rtTA (rtTA-M2) inserted downstream of the Rosa26 promoter, which was purchased from the Jackson Laboratory (stock number 006965). MLN0128 and MK-2206 were purchased from Active Biochem. Rapamycin was purchased from Cell Signaling Technology. S6K1 inhibitor LY294002 was purchased from Tocris Bio. SBI-756 was synthesized as described (19 (link)). Inhibitors were included throughout the indicated cell treatment periods.
Chiu H., Jackson L.V., Oh K.I., Mai A., Ronai Z.A., Ruggero D, & Fruman D.A. (2018). The mTORC1/4E-BP/eIF4E Axis Promotes Antibody Class Switching in B Lymphocytes. Journal of immunology (Baltimore, Md. : 1950), 202(2), 579-590.
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6

IGF-1 Stimulation and PI3K Inhibition

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Cells were stimulated for 20 min with recombinant human IGF-1 (R&D systems) at a final concentration of 100 ng/ml. PI3K inhibitors BKM-120 (Selleck Chemicals), BYL-719 (Selleck Chemicals), A66 (Selleck Chemicals), TGX-221 and IC87114 [gifts from Peter Shepherd, University of Auckland, New Zealand; (54 (link))] were added to cells 15 min prior to IGF-1 stimulation at final concentration of 1 μM. AKT inhibitor MK-2206 (Active Biochem) was added to cells 15 min prior to IGF-1 stimulation at final concentration of 1 μM. NVP-AEW541 (Cayman Chemical) and GSK2334470 (Tocris) were added to cells 15 min prior to growth factor stimulation at final concentration of 1 μM.
Clement E., Inuzuka H., Nihira N.T., Wei W, & Toker A. (2018). Skp2-dependent reactivation of AKT drives resistance to PI3K inhibitors. Science signaling, 11(521), eaao3810.
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7

Preparation of Diverse Pharmacological Compounds

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Stock solutions of Everolimus, Ruxolitinib, Stattic, SH-4-54, Erdafitinib, Axitinib, CI-1040, Roscovitine (Selleckchem, Munich, Germany), MK-2206 (Active Biochem, Bonn, Germany), PIK-90 (Merck Chemicals GmbH, Darmstadt, Germany) were prepared in DMSO while NVP-BEZ235 was in DMF. Palbociclib (Sigma-Aldrich Chemie GmbH, Munich, Germany) stock solution was prepared in water. Working concentrations were freshly prepared in medium.
Tong Z., Sathe A., Ebner B., Qi P., Veltkamp C., Gschwend J.E., Holm P.S, & Nawroth R. (2019). Functional genomics identifies predictive markers and clinically actionable resistance mechanisms to CDK4/6 inhibition in bladder cancer. Journal of Experimental & Clinical Cancer Research : CR, 38, 322.
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8

Investigating mTOR and GSK3 Signaling

Cited 1 time
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All mTOR kinase inhibitors, the GSK3 inhibitor SB216763, the proteasome inhibitor MG132, the protein synthesis inhibitor cycloheximide (CHX) and the antibodies against GSK3α/β, phospho-GSK3α/β (Ser21/9), phospho-Akt (Ser473), Akt, rictor and raptor were the same as described previously 22 (link). The GSK3 inhibitor CHIR99021 was purchased from LC laboratories (Woburn, MA). BKM120 was supplied by Novartis Pharmaceuticals Corporation (East Hanover, NJ). API-1 (NSC177233) was obtained from the National Cancer Institute (Bethesda, MD). MK2206 was purchased from Active Biochem (Maplewood, NJ). Perifosine was supplied by Keryx Biopharmaceuticals, Inc (New York, NY). Oil Red O was purchased from Sigma Chemical Co. (St. Louis, MO). SREBP1 (sc-13551), FASN (sc-55580) and α-tubulin (sc-23948) antibodies were purchased from Santa Cruz Biotechnology, Inc (Santa Cruz, CA). ACC antibody (#3662) was purchased from Cell Signaling Technology, Inc. (Beverly, MA). Polyclonal Sin1 antibody (A300-910A) was purchased from Bethyl Laboratories, Inc. (Montgomery, TX).
Li S., Oh Y.T., Yue P., Khuri F.R, & Sun S.Y. (2015). Inhibition of mTOR complex 2 induces GSK3/FBXW7-dependent degradation of sterol regulatory element-binding protein 1 (SREBP1) and suppresses lipogenesis in cancer cells. Oncogene, 35(5), 642-650.
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9

Pharmacological Inhibitor Acquisition Protocol

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We obtained rapamycin, MLN0128, GDC-0941, and NVP-BEZ235 from LC Laboratories (Woburn, MA, USA); ABT-263, ABT-199, MK2206 and GDC-0980 from Active Biochem (Wan Chai, Hong Kong), and AKT inhibitor VIII from Chemdea (Ridgewood, NJ, USA). InSolution Q-VD-OPh was obtained from EMD Millipore (Billerica, MA, USA), vincristine was obtained from Sigma-Aldrich (St. Louis, MO), dimethyl sulfoxide (DMSO) from Fisher Scientific (Waltham, MA, USA) and doxycycline from Sigma-Aldrich (St. Louis, MO).
Lee J.S., Tang S.S., Ortiz V., Vo T.T, & Fruman D.A. (2015). MCL-1-independent mechanisms of synergy between dual PI3K/mTOR and BCL-2 inhibition in diffuse large B cell lymphoma. Oncotarget, 6(34), 35202-35217.
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10

Brown Preadipocyte Cell Lines Differentiation

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Wild-type (WT), Irs1−/- and Irs2−/- brown preadipocyte cell lines were a kind gift from C. Ronald Kahn [28 (link)]. Cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) containing 10% foetal bovine serum and 1% penicillin-streptomycin (PS), in humidified incubators at 37°C and 5% CO2. For differentiation, pre-adipocytes were grown to confluence (day 0) in culture medium supplemented with 20 nM insulin and 1 nM triiodothyronine (differentiation medium). Confluent cells were incubated for 2 d in differentiation medium further supplemented with 1 μM dexamethasone, 0.5 mM isobutylmethylxanthine and 0.125 mM indomethacin. Subsequently, the cells were maintained in differentiation medium. Culture medium was changed every 2 d, and cell culturing experiments were performed in independent replicates.
For stimulation experiments, cells were starved for 4 h in DMEM with 1% PS and 0.1% bovine serum albumin. Cells were stimulated with 100 nM insulin or IGF-1, or vehicle for 5 min before lysis. For kinase inhibition, cells were pre-treated with 10 μM U0126-EtOH (Selleck Chemicals), 10 μM MK-2206 (Active Biochem) or vehicle (0.1% DMSO) for 1 h before stimulation.
Ardenkjær-Larsen J., Rupar K., Sinkevičiūtė G., Petersen P.S., Villarroel J., Lundh M., Barrès R., Rabiee A, & Emanuelli B. (2020). Insulin-induced serine 22 phosphorylation of retinoid X receptor alpha is dispensable for adipogenesis in brown adipocytes. Adipocyte, 9(1), 142-152.
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