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Gf109203x

Manufactured by Cayman Chemical
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Sourced in United States, Germany

GF109203X is a chemical compound that functions as a selective inhibitor of protein kinase C (PKC) enzymes. It has been widely used in scientific research to study the role of PKC in various biological processes.

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Lab products found in correlation

Rapamycin, by LC Laboratories (2 mentions) Go6983, by LC Laboratories (2 mentions) Jte 013, by Cayman Chemical (1 mentions) P creb, by Cell Signaling Technology (1 mentions) P erk1 2, by Cell Signaling Technology (1 mentions) Pd98059, by Cayman Chemical (1 mentions) Vpc23019, by Cayman Chemical (1 mentions) P pkcα, by Cell Signaling Technology (1 mentions) γ 32p atp 3 000, by PerkinElmer (1 mentions) 32p orthophosphate, by PerkinElmer (1 mentions) Chromatin immunoprecipitation chip assay kit, by Beyotime (1 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (1 mentions) 4 6 diamidino 2 phenylindole (dapi), by Merck Group (1 mentions) Erk1 2, by Cell Signaling Technology (1 mentions) Nuclear and cytoplasmic protein extraction kit, by Beyotime (1 mentions) Nvp aew541, by Cayman Chemical (1 mentions) P akt akt, by Cell Signaling Technology (1 mentions) Mk 2206, by Cayman Chemical (1 mentions) Luciferase, by Merck Group (1 mentions) Protein g sepharose bead, by GE Healthcare (1 mentions)

6 protocols using gf109203x

1

HUVEC Sphingosine Kinase Signaling

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[γ-32P]ATP (3,000 Ci/mmol) and [32P]orthophosphate were purchased from PerkinElmer Life Sciences (Turku, Finland). HUVECs were purchased from the Medical Center for Cells, Central South University (Changsha, China). Pertussis toxin (PTX), NS398, and 4′-6-diamidino-2-phenylindole were obtained from Sigma (St. Louis, USA). GF109203X, PD98059, JTE013, and VPC23019 were from Cayman (Michigan, USA). Competitive enzyme immunoassay kit for 6-keto PGF1α, nuclear and cytoplasmic protein extraction kit, and chromatin immunoprecipitation (ChIP) assay kit were obtained from Beyotime Institute of Biotechnology (Haimen, China). Mouse GAPDH was from Boster (Wuhan, China). Rabbit anti-COX-2 antibodies were from Epitomics (Burlingame, USA). Rabbit polyclonal anti-SphK-2 and anti-SphK1 antibodies were from Abcam (Cambridge, USA). P-CREB, ERK1/2, P-ERK1/2, P-PKCα, and PKCα antibodies were from Cell Signaling (Boston, USA). HDL was purchased from Millipore Corporation (Billerica, USA). Lipofectamine 2000 was from Invitrogen (Carlsbad, USA). The small interfering RNA (siRNA) for SphK-2 was obtained from Ruibo Co., Ltd. (Guangzhou, China). RealSuper Mixture (with ROX) was obtained from Cowin Biotech Co., Ltd. (Beijing, China).
Xiong S.L., Liu X, & Yi G.H. (2014). High-density lipoprotein induces cyclooxygenase-2 expression and prostaglandin I-2 release in endothelial cells through sphingosine kinase-2. Molecular and Cellular Biochemistry, 389(1), 197-207.
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2

Ubiquitination Pathway Regulation in Cells

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The primers were synthesized and PAGE purified by IDT DNA. Fugene 6 transfection reagent was purchased from Promega while Lipofectamine RNAiMax was from Life Technologies/Invitrogen. All cell culture reagents including media, antibiotics were from GIBCO/Invitrogen. Antibodies to total Ubiquitin (clone P4D1) was from Santacruz Biotechnology, Luciferase (Millipore), pAKT, AKT (Cell Signaling), Ubiquitin, Lys63 specific (clone Apu3, Millipore), His-tag (clone H3 and C-term, Invitrogen) or Millipore (H8 clone). FLAG tag-HRP antibody (Clone M2) was purchased from Sigma Aldrich. HRP-conjugated and fluorophore-conjugated secondary antibodies were from Jackson ImmunoResearch. ON-TARGET plus siRNA to TRAF6 and scrambled control siRNA were obtained from GE Life Sciences/Dharmacon. D-Luciferin was from Xenogen Corp while GloSensor was from Promega. Erlotinib was a kind gift from Genentech. Tyrphostin AG1478 was obtained from Cayman Chemical. TNF-α antagonist (WP9QY) and IL-1R antagonist were from SantaCruz biotechnology. Recombinant IGF-1, IL-1α were from PepreoTech. CI-1040, GF109203X, NVP-AEW541 and MK2206 (Cayman Chemical), and Linsitinib (LC Laboratories). Protein A and Protein G sepharose beads were from GE HealthCare. Purified NEDD4-1 (Sigma Aldrich), Myc-tagged ubiquitin (Cat. No. U-115) UBE1 (Cat. No. E305), and UBCH5 (Cat. No. E2-616) all were from Boston Biochemicals.
Nyati S., Chaudhry N., Chatur A., Gregg B.S., Kimmel L., Khare D., Basrur V., Ray D, & Rehemtulla A. (2018). A novel reporter for real-time, quantitative imaging of AKT-directed K63-poly-ubiquitination in living cells. Oncotarget, 9(13), 11083-11099.
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3

Postnatal Administration of Pharmacological Inhibitors in Ndufs4-/- Mice

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Rapamycin (LC Laboratories) and GO6983 (LC Laboratories) were dissolved in DMSO and diluted 100-fold in 5% or 30% PEG-400/5% Tween-80 (vehicle), sterile filtered, aliquoted into 1 mL portions, and stored at −80 °C until needed for use. GF109203X (Cayman Chemical) and ruboxistaurin hydrochloride (Synnovator) were directly dissolved in vehicle containing 1% DMSO. Starting at postnatal day 10 (P10), mice were treated daily between 2:00–6:00 p.m. (via intraperitoneal injection with 29 ½ gauge, 300 μL syringes) using 6.66 μL/g body weight of these solutions for final doses of 10 mg/kg/day (ruboxistaurin), 8 mg/kg/day (Rapamycin and GF109203X), or 4 mg/kg/day (GO6983). Control mice were generally treated with vehicle using 6.66 μL/g body weight. For the lifespan experiments control mice were untreated, as it has been reported that untreated Ndufs4−/− mice exhibit identical phenotypes as vehicle-treated Ndufs4−/− mice4 (link), and we also show this here for lifespan, onset of clasping and weight gain (Extended Data Fig. 9).
Martin-Perez M., Grillo A.S., Ito T.K., Valente A.S., Han J., Entwisle S.W., Huang H.Z., Kim D., Yajima M., Kaeberlein M, & Villén J. (2020). PKC downregulation upon rapamycin treatment attenuates mitochondrial disease. Nature metabolism, 2(12), 1472-1481.
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4

Pharmacological Modulation of Synaptic Transmission

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The KCC2 blocker VU0463271(Tocris) (10 µM), the PKC blocker GF-109203X (Cayman) (10 µM), the PKA blocker H89 dihydrochloride (Tocris) (50 µM), The CaMKII specific blocker KN93 (Cayman) (10 µM), the cell-CaMKII penetrating peptide inhibitor, tatCN21 (GL Biochem. Shanghai) (5 µM), the GABAA blocker BMI Tocris) (20 µM), the AMPA receptors blocker DNQX (Cayman) (0.2–20 µM) and NMDA receptors blocker APV (Sigma) (50 µM) were applied via the medium solution. For experiments were the VU0463271 was applied, each neuron was recorded prior to and after the KCC2 blocker application. Each neuron was exposed 30 minutes to the drug, prior to determining its effect on the IPSPs or IPSCs reversal potential.
Kfir A., Awasthi R., Ghosh S., Kundu S., Paul B., Lamprecht R, & Barkai E. (2020). A Cellular Mechanism of Learning-Induced Enhancement of Synaptic Inhibition: PKC-Dependent Upregulation of KCC2 Activation. Scientific Reports, 10, 962.
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5

Dissecting Receptor-Mediated Endocytic Pathways

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The following materials were obtained from the sources indicated: anti-mouse MHC-II antibody (clone 11-5.2) from Biolegend (San Diego, CA, USA); 12-O-tetradecanoyl phorbol 13-acetate (TPA), cytochalasin D, dynasore, chlorpromazine, staurosporine, and piceatannol from Sigma-Aldrich (St. Louis, MO, USA), Fura-2/AM from Dojindo (Kumamoto, Japan), 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM), U-73122, PD98059, SB203580, and SP600125 from Merck Millipore (Darmstadt, Germany), GF 109203X and R406 from Cayman Chemical (Ann Arbor, MI, USA), recombinant murine granulocyte macrophage colony-stimulating factor (GM-CSF) from Peprotech (Rocky Hill, NJ, USA), anti-FcγRII/RIII (clone 2.4G2) antibody and anti-clathrin heavy chain (CHC) antibody from BD Biosciences (San Jose, CA, USA), Alexa Fluor 488-labeled goat anti-mouse IgG1 antibody and Alexa Fluor 546-labeled goat anti-mouse IgG2b antibody from Thermo Fisher Scientific (Waltham, MA, USA). All other chemicals were commercial products of a reagent grade.
Masaki K., Hiraki Y., Onishi H., Satoh Y., Roche P.A., Tanaka S, & Furuta K. (2020). Ligation of MHC Class II Induces PKC-Dependent Clathrin-Mediated Endocytosis of MHC Class II. Cells, 9(8), 1810.
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6

Postnatal Administration of Pharmacological Inhibitors in Ndufs4-/- Mice

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Rapamycin (LC Laboratories) and GO6983 (LC Laboratories) were dissolved in DMSO and diluted 100-fold in 5% or 30% PEG-400/5% Tween-80 (vehicle), sterile filtered, aliquoted into 1 mL portions, and stored at −80 °C until needed for use. GF109203X (Cayman Chemical) and ruboxistaurin hydrochloride (Synnovator) were directly dissolved in vehicle containing 1% DMSO. Starting at postnatal day 10 (P10), mice were treated daily between 2:00–6:00 p.m. (via intraperitoneal injection with 29 ½ gauge, 300 μL syringes) using 6.66 μL/g body weight of these solutions for final doses of 10 mg/kg/day (ruboxistaurin), 8 mg/kg/day (Rapamycin and GF109203X), or 4 mg/kg/day (GO6983). Control mice were generally treated with vehicle using 6.66 μL/g body weight. For the lifespan experiments control mice were untreated, as it has been reported that untreated Ndufs4−/− mice exhibit identical phenotypes as vehicle-treated Ndufs4−/− mice4 (link), and we also show this here for lifespan, onset of clasping and weight gain (Extended Data Fig. 9).
Martin-Perez M., Grillo A.S., Ito T.K., Valente A.S., Han J., Entwisle S.W., Huang H.Z., Kim D., Yajima M., Kaeberlein M, & Villén J. (2020). PKC downregulation upon rapamycin treatment attenuates mitochondrial disease. Nature metabolism, 2(12), 1472-1481.
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