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A484954

Manufactured by Merck Group
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Sourced in Germany

A484954 is a laboratory instrument designed for performing various analytical and research tasks. The core function of this product is to facilitate efficient and precise measurements and analyses within a controlled laboratory environment. No further details on the intended use or specific applications are provided.

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Lab products found in correlation

Propranolol hydrochloride, by Merck Group (2 mentions) Bacl2, by Merck Group (2 mentions) Isoproterenol hydrochloride, by Merck Group (1 mentions) L phenylephrine hydrochloride, by Merck Group (1 mentions) Streptomycin, by Thermo Fisher Scientific (1 mentions) Penicillin, by Thermo Fisher Scientific (1 mentions) Cyto id autophagy detection kit, by Enzo Life Sciences (1 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (1 mentions) Chloroquine, by Merck Group (1 mentions) H9c2 rat cardiomyoblast cell line, by American Type Culture Collection (1 mentions) Ex527, by Bio-Techne (1 mentions) L name, by Dojindo Laboratories (1 mentions) P erk, by Cell Signaling Technology (1 mentions) P egfr, by Cell Signaling Technology (1 mentions) P akt, by Cell Signaling Technology (1 mentions) Protein a g plus agarose, by Santa Cruz Biotechnology (1 mentions) Stattic, by Merck Group (1 mentions) P jak1, by Cell Signaling Technology (1 mentions) P jak2, by Cell Signaling Technology (1 mentions) P pdgfr, by Cell Signaling Technology (1 mentions)

8 protocols using a484954

1

Vasoactive Compound Reagent Sources

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Reagent sources were as follows: A484954 (Merck, Darmstadt, Germany),
noradrenaline (NA), adrenaline, isoproterenol, angiotensin (Ang) II, and (±)-propranolol
hydrochloride (Sigma-Aldrich, St. Louis, MO, U.S.A.).
KODAMA T., OKADA M, & YAMAWAKI H. (2019). Eukaryotic elongation factor 2 kinase inhibitor, A484954 potentiates β-adrenergic receptor agonist-induced acute decrease in diastolic blood pressure in rats. The Journal of Veterinary Medical Science, 81(10), 1509-1514.
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2

Pharmacological Evaluation of Cardioactive Agents

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A484954 (Merck, Darmstadt, Germany), 1-benzyl-3-cetyl-2-methylmidazolium iodide (NH125) (Cayman, Ann Arbor, MI, U.S.A.), noradrenaline (NA), (±)-propranolol hydrochloride, L-phenylephrine hydrochloride, isoproterenol hydrochloride, BaCl2 (Sigma-Aldrich, St. Louis, MO, U.S.A.).
KODAMA T., OKADA M, & YAMAWAKI H. (2018). Eukaryotic elongation factor 2 kinase inhibitor, A484954 inhibits noradrenaline-induced acute increase of blood pressure in rats. The Journal of Veterinary Medical Science, 81(1), 35-41.
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3

Tunicamycin-Induced Cell Death in H9c2 Cells

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The H9c2 rat cardiomyoblast cell line was purchased from ATCC (n° CRL-1446). Cells were cultured in DMEM medium supplemented with 100 U/mL penicillin, 100 mg/mL streptomycin, and 10% FBS (ThermoFisher Scientific, Les Ulis, France) at 37 °C under 5% CO2/95% air. EX527 was from Tocris (49843-98-3), STAC-3, and Endothall were from Santa Cruz (sc-222315 and sc-201325), A484954 was from Merck Chemicals (324516). Chloroquine and 3-Methyladednine were purchased from Sigma-Aldrich (C6628 and M9281). Cyto-ID® Autophagy detection kit was from Enzo Life Sciences (ENZ-51031). Pilot experiments revealed that after 48 h of incubation, the LD50 of tunicamycin (concentration causing 50% cell death) was 10 µg/mL. This dose was thus used throughout this work.
Pires Da Silva J., Monceaux K., Guilbert A., Gressette M., Piquereau J., Novotova M., Ventura-Clapier R., Garnier A, & Lemaire C. (2020). SIRT1 Protects the Heart from ER Stress-Induced Injury by Promoting eEF2K/eEF2-Dependent Autophagy. Cells, 9(2), 426.
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4

Evaluating Vasodilation Mechanisms

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Reagent sources were as follows: A484954 (Merck, Darmstadt, Germany) and L-NAME (Dojindo,
Kumamoto, Japan).
KODAMA T., OTANI K., OKADA M, & YAMAWAKI H. (2023). Eukaryotic elongation factor 2 kinase inhibitor, A484954 induced diuresis via nitric oxide production in spontaneously hypertensive rats. The Journal of Veterinary Medical Science, 85(12), 1314-1318.
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5

Lung Cancer Cell Line Characterization

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The human lung cancer A549 cells were purchased from Shanghai Cell Bank, Chinese Academy of Science. A549 cells, H1299 cells and A549 cells containing either non-targeting control or eEF2K-targeted shRNA (referred to as A549 shNC and A549 sheEF2K; or referred to as siNC and sieEF2K) were cultured in F12K medium. HEK293 cells used for virus packaging were maintained in Dulbecco’s modified Eagle medium (DMEM). All mediums were supplemented with 10% FBS, 100 units/ml penicillin and 0.1 mg/ml streptomycin. Cells were maintained at 37 °C in a humidified cell incubator containing 5% CO2 and 95% air.
A484954, BS3, Gefitinib and Stattic were purchased from Sigma-Aldrich. Antibodies For EGFR (#2646), p-EGFR (#3777), ERK (#4695), p-ERK (#4370), PDGFR (#3174), p-PDGFR (#3124), JAK1 (#3344), p-JAK1 (#74129), JAK2 (#3230), p-JAK2 (#3771), p-PI3K (#4228), AKT (#4685), p-AKT (#9614), Src (#12109), p-Src (#12432), STAT3 (#12640), p-STAT3 (#9145), eEF2K (#3692), eEF2 (#2332), p-eEF2 (#2331), c-Myc(#2729), and PKM2 (#4053) were obtained from Cell Signaling Technology. β-Actin, Tubulin, goat anti-rabbit and goat anti-mouse secondary antibodies were all purchased from Hangzhou HuaAn Biotechnology Co. (PCNA antibody(#101118-T46) was purchased from Sino Biolgical. Protein A/G plus agarose was purchased from Santa Cruz Biotechnology.
Xiao M., Xie J., Wu Y., Wang G., Qi X., Liu Z., Wang Y., Wang X., Hoque A., Oakhill J., Proud C.G, & Li J. (2020). The eEF2 kinase-induced STAT3 inactivation inhibits lung cancer cell proliferation by phosphorylation of PKM2. Cell Communication and Signaling : CCS, 18, 25.
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6

Pharmacological Modulation of Hippocampal Synaptic Plasticity

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A-484954 (Sigma–Aldrich, SML0861), TTX (Sigma–Aldrich, T8024), Bicuculline (Tocris, 2503), Anisomycin (Sigma–Aldrich, A9789), Cycloheximide (Sigma–Aldrich, C1988), KN-93 (Sigma–Aldrich, K1385), Gö 6983 (Sigma–Aldrich, G1918), KT5720 (Tocris, 1288), Thapsigargin (Sigma–Aldrich, T9033), 2-APB (Sigma–Aldrich, D9754), Dantrolene (Sigma–Aldrich, D9175), U0126 (Sigma–Aldrich, U120), LY294002 (Sigma–Aldrich, L9908), SB203580 (Sigma–Aldrich, S8307), CsCl (Sigma–Aldrich, C3032), TEA (Sigma–Aldrich, T2265), BaCl2 (Sigma–Aldrich, 342920), and Fluoxetine (Sigma–Aldrich, F132) were added to ACSF as indicated.
Hippocampal slices were pretreated with these drugs for 1 h, and fEPSPs were recorded in stratum radiatum of CA1 area. A-484954 was applied after at least 20-min stable baseline.
Weng W., Chen Y., Wang M., Zhuang Y, & Behnisch T. (2016). Potentiation of Schaffer-Collateral CA1 Synaptic Transmission by eEF2K and p38 MAPK Mediated Mechanisms. Frontiers in Cellular Neuroscience, 10, 247.
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7

eEF2K Inhibitor Efficacy in Mice

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For all eEF2K inhibitor experiments, mice received A-484954 (Sigma, 324516) daily (10mg/kg body weight; IP) for 15 days.
Jana S., Brahma S., Arora S., Wladyka C.L., Hoang P., Blinka S., Hough R., Horn J.L., Liu Y., Wang L.J., Depeille P., Smith E., Montgomery R.B., Lee J.K., Haffner M.C., Vakar-Lopez F., Grivas P., Wright J.L., Lam H.M., Black P.C., Roose J.P., Ryazanov A.G., Subramaniam A.R., Henikoff S, & Hsieh A.C. (2023). Transcriptional-translational conflict is a barrier to cellular transformation and cancer progression. Cancer cell, 41(5), 853-870.e13.
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8

eEF2K Inhibitor Efficacy in Mice

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For all eEF2K inhibitor experiments, mice received A-484954 (Sigma, 324516) daily (10mg/kg body weight; IP) for 15 days.
Jana S., Brahma S., Arora S., Wladyka C.L., Hoang P., Blinka S., Hough R., Horn J.L., Liu Y., Wang L.J., Depeille P., Smith E., Montgomery R.B., Lee J.K., Haffner M.C., Vakar-Lopez F., Grivas P., Wright J.L., Lam H.M., Black P.C., Roose J.P., Ryazanov A.G., Subramaniam A.R., Henikoff S, & Hsieh A.C. (2023). Transcriptional-translational conflict is a barrier to cellular transformation and cancer progression. Cancer cell, 41(5), 853-870.e13.
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