Bisindolylmaleimide 1

Manufactured by Merck Group

Sourced in United States

Bisindolylmaleimide I is a small-molecule chemical compound used in biochemical research. It functions as a highly selective and potent inhibitor of protein kinase C (PKC) enzymes.

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Close spelling variants of this product

Bisindolylmaleimide I (Bis1), (4 citations) Bisindolylmaleimide (3 citations) Bisindolylmaleimide I (BIM-I) (2 citations) Bisindolylmaleimide I (Bis) (2 citations)

8 protocols using bisindolylmaleimide 1

Evaluation of Phytochemical Inhibitors

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All phytochemicals (baicalein, Cat# 465119 (>98%); flavone, Cat# F2003 (>99%); genistein, Cat# G6776 (~98%); α-naphthoflavone, Cat# N5757 (>98%); luteolin, Cat# L9283 (>98%); naringenin, Cat# N5893 (>95%); quercetin, Cat# Q0125 (>98%); resveratrol, Cat# R5010 (>99%); chrysin, Cat# C80105 (>97%); hesperetin, Cat# W431300 (>95%); and isoliquiritigenin, Cat# I3766 (>98%)) were obtained from Sigma Chemical (St Louis, MO, USA). The impurities of the phytochemicals could be a confounding factor. Kinase inhibitors, including SB203580 (Cat# 559389, Merck), H-89 (Cat# 371963, Merck), Compound C (Cat# 171260, Merck), Bisindolylmaleimide I (Cat# 203290, Merck), pAKT inhibitor (Cat# 124011, Merck) and U0126 (Cat# 662005, Merck), were purchased from Calbiochem (San Diego, CA, USA). LY333531 (Cat# sc-364215) and HBDDE (Cat# sc-202174) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA). SP600125 (Cat# S5567) and all other chemicals, if not stated, were acquired from Sigma Chemicals (St Louis, MO, USA).

Wong T.Y., Lin S.M, & Leung L.K. (2015). The Flavone Luteolin Suppresses SREBP-2 Expression and Post-Translational Activation in Hepatic Cells. PLoS ONE, 10(8), e0135637.

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Extracellular Vesicle Production Assay

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Cells were resuspended in pre-warmed serum-free RPMI and seeded in triplicate at 3.8 × 10⁵ cells/well in 12-well microtitre plates. EGTA (ethylene glycol-bis(β-aminoethyl ether)-N,N,N′,N′-tetraacetic acid; Sigma-Aldrich) (1.5 mM), bisindolylmaleimide-I (10 µM; Merck Millipore), imipramine (25 µM; Sigma-Aldrich), d-pantethine (1 mM; Sigma-Aldrich), Cl-amidine (50 µM; provided by P.R.Thompson), Y27632 (1 µM; Sigma-Aldrich), calpeptin (25 µM; Sigma-Aldrich), glyburide (10 µM; Sigma-Aldrich), MβCD (10 µM; Sigma-Aldrich), cytochalasin D (10 µM; Sigma-Aldrich), and chlorpromazine (10 µM; Sigma-Aldrich) were added separately and incubated for 24 h at 37 °C/5% CO₂. EMVs released were isolated (4.4) and counted (4.5).

Kosgodage U.S., Trindade R.P., Thompson P.R., Inal J.M, & Lange S. (2017). Chloramidine/Bisindolylmaleimide-I-Mediated Inhibition of Exosome and Microvesicle Release and Enhanced Efficacy of Cancer Chemotherapy. International Journal of Molecular Sciences, 18(5), 1007.

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Regulation of mTOR Signaling by PKC

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All cell lines were purchased from American Tissue Culture Collection (Manassas, VA, USA). Lipofectamine RNAiMAX were from Life Technologies (Grand Island, NY). X-treme GENE 9 were from Roche (Indianapolis, IN). PLD2 inhibitor, VU 0364739 was a kind gift from Dr. Alex Brown (Vanderbilt University, Nashville, TN, USA). PMA, Gö 6976, Bisindolylmaleimide I and U0126 were from EMD Millipore (Billerica, MA). Anti-phospho-p70S6K (Thr389), S6K, mTOR, phospho-ERK1/2 (Thr202/Tyr204), ERK1/2, EGFR, HA antibodies were from Cell Signaling Technology (Danvers, MA) and anti-Actin antibody was purchased from Sigma Aldrich (St. Louis, MO). Anti-LAMP1, LAMP2, PKCδ and PKCε antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA). Anti-EEA1 antibody was from BD Biosciences (San Jose, CA). siRNA for PKCη, PKCδ, PKCε, RAGB, LAMTOR 1, and LAMTOR 3 were from Qiagen (Valencia, CA).

Liu M., Clarke C.J., Salama M.F., Choi Y.J., Obeid L.M, & Hannun Y.A. (2017). Co-ordinated activation of classical and novel PKC isoforms is required for PMA-induced mTORC1 activation. PLoS ONE, 12(9), e0184818.

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Modulation of TRPV1-mediated Knee Pain

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To examine TRPV1 function in rat knee joints, Capsaicin-induced pain-related behavior was evaluated on day 14 after MIA or saline injection. Rats were randomly allocated by body weight and grip strength. Behavioral tests were conducted during the light phase. Capsaicin (SigmaeAldrich) was dissolved into 50 mL 10% ethanol in saline and injected into the articular cavity of the right leg knee joint. Response behavior was measured by duration of flinching and licking behavior for 10 min in a plexiglas cylinder (25 cm diameter, 30 cm high) after Capsaicin injection by a blinded investigator. Bisindolylmaleimide I (PKC inhibitor, EMD Millipore, Billerica, MA, USA) and KT5720 (PKA inhibitor, EMD Millipore) were dissolved in 50 mL of 10% DMSO in saline and administered before Capsaicin injection. Phorbol 12-myristate 13-acetate (PMA) (50 mL, Invivogen, San Diego, CA, USA) was administered before Capsaicin injection. Drugs were administered into the knee joint cavity to examine the effect of those in knee joint. Rats were tested in order of allocated groups.

Koda K., Hyakkoku K., Ogawa K., Takasu K., Imai S., Sakurai Y., Fujita M., Ono H., Yamamoto M., Fukuda I., Yamane S., Morita A., Asaki T., Kanemasa T., Sakaguchi G, & Morioka Y. (2016). Sensitization of TRPV1 by protein kinase C in rats with mono-iodoacetate-induced joint pain. Osteoarthritis and cartilage, 24(7).

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Rat Hippocampal Neuron Treatment Chemicals

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The following chemicals were used to treat rat hippocampal neurons at the indicated concentrations: cytochalasin D (MedChemExpress, Monmouth Junction, NJ, USA; HY-N6682; 2 μM), nocodazole (MedChemExpress, Monmouth Junction, NJ, USA; HY-13520; 3.3 μM), PKI 14-22 (MedChemExpress, Monmouth Junction, NJ, USA; HY-106377A; 0.1 μM), bisindolylmaleimide I (Sigma-Aldrich; #203290; 4 μM), KN-93 (MedChemExpress, Monmouth Junction, NJ, USA; HY-15465; 5 μM), CaMKII Inhibitor XII (Sigma-Aldrich; #208923; 10 μM), PP2 (Sigma-Aldrich; #529573; 10 μM), SP600125 (MedChemExpress, Monmouth Junction, NJ, USA; HY-12041; 25 μM), and PD98059 (Selleck; #S1177; 50 μM). All compounds were dissolved in dimethyl sulfoxide (DMSO) and added to neurons to reach the indicated concentration and a final concentration of 0.2% DMSO.

Chofflet N., Naito Y., Pastore A.J., Padmanabhan N., Nguyen P.T., Poitras C., Feller B., Yi N., Van Prooijen J., Khaled H., Coulombe B., Clapcote S.J., Bourgault S., Siddiqui T.J., Rudenko G, & Takahashi H. (2024). Structural and functional characterization of the IgSF21-neurexin2α complex and its related signaling pathways in the regulation of inhibitory synapse organization. Frontiers in Molecular Neuroscience, 17, 1371145.

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Signaling Pathway Analysis in Cell Culture

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(−)-Noradrenaline, phorbol myristate acetate, lysophosphatidic acid, bisindolylmaleimide I, prazosin, propranolol, and yohimbine were obtained from Sigma-Aldrich Chemical (St. Louis, MO), Dulbecco’s modified Eagle’s medium, fetal bovine serum, trypsin, G418, Lipofectamine 2000, streptomycin, penicillin, amphotericin B, and Fura-2AM were purchased from Invitrogen Life Technologies (Carlsbad, CA). Epidermal growth factor was from Millipore Corporation (Billerica, MA). Polyvinylidene difluoride membranes were from BioRad (Hercules, CA) and SuperSignal West Pico Chemiluminescence kits were from Thermo Fisher Scientific (Waltham, MA). Anti-phospho-p42/44 ERK (extracellular signal-regulated kinases) 1/2 (Thre202/Tyr204), anti-total ERK (p42/44), anti-phospho c-Raf-1 (Ser338), anti-total c-Raf-1, anti-phospho MEK1 (Ser217/Ser221), and anti-total MEK-1 antibodies were obtained from Cell Signaling Technology (Danvers, MA); antitotal ERK2 p42 monoclonal antibody was from Santa Cruz Biotechnology (Santa Cruz, CA).

Alfonzo-Méndez M.A., Castillo-Badillo J.A., Romero-Ávila M.T., Rivera R., Chun J, & García-Sáinz J.A. (2016). Carboxyl terminus-truncated α1D-adrenoceptors inhibit the ERK pathway. Naunyn-Schmiedeberg's archives of pharmacology, 389(8), 911-920.

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Inhibition of Signaling Pathways in HHV-6A Infection

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U87 cells were pretreated with small molecule inhibitors, dissolved in DMSO for 45 min, washed and then stimulated with HHV-6A (MOI = 1) for 5 h. Following inhibitors were used: 5 μM Bisindolylmaleimide I (Protein Kinases C inhibitor, Sigma) (39 (link)) or 5 μM Src Inhibitor-1 (Src kinase inhibitor, Sigma) or 40 μM Apigenin (Casein Kinase 2 inhibitor, Sigma) (40 (link)).

Charvet B., Reynaud J.M., Gourru-Lesimple G., Perron H., Marche P.N, & Horvat B. (2018). Induction of Proinflammatory Multiple Sclerosis-Associated Retrovirus Envelope Protein by Human Herpesvirus-6A and CD46 Receptor Engagement. Frontiers in Immunology, 9, 2803.

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Regulation of hUCB-MSCs by Signaling Pathways

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hUCB-MSCs were obtained from MEDIPOST Co. Ltd (Seoul, Korea). Fetal bovine serum was bought from BioWhittaker Inc. (Walkersville, MO, USA). AA, A23187, bisindolylmaleimide I, BrdU, Indomethacin, LY294002, mitomycin C, Nordihydroguaiaretic acid (NDGA), rapamycin, 1-Aminobenzotriazole (1-ABT), and SB203580 were aquired from the Sigma Chemical Company (St Louis, MO, USA). Phospho-Akt^ser473, phospho-Akt^thr308, Akt1/2/3, β-Actin, collagen1A, collagen3A, collagen5A, fibronectin, phospho-p38, p38, phospho-JNK, JNK, p-ERK1/2, ERK, lamin A/C, MMP-12, pan-cadherin, PKCα, PKCɛ, PKCθ, PKCζ, PKC, Phospho-PKCζ, and Sp1 antibodies were obtained from Santa Cruz Biotechnology (Santa Cruz, CA, USA). Phospho-PKC, phospho-mTOR^ser2481 (mTORC2), phospho-mTOR^ser2448 (mTORC1), and mTOR were purchased from Cell Signaling (Beverly, MA, USA). The Akt inhibitor I was aquired from Calbiochem (La Jolla, CA, USA). The CD34, GPR40, phospho-Sp1, and MT3-MMP antibodies were obtained from Abcam (Cambridge, MA, USA). Mithramycin A was purchased from Tocris (Bristol, UK). Zymogram gels were bought from Novex (San Diego, CA, USA). Horseradish peroxidase-conjugated goat anti-mouse and goat anti-rabbit IgG were obtained from Jackson Immunoresearch (West Grove, PA, USA). All other reagents were used as received and were of the highest purity commercially available.

Oh S.Y., Lee S.J., Jung Y.H., Lee H.J, & Han H.J. (2015). Arachidonic acid promotes skin wound healing through induction of human MSC migration by MT3-MMP-mediated fibronectin degradation. Cell Death & Disease, 6(5), e1750-.

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