Sp600125

Manufactured by Promega

Sourced in United States

SP600125 is a selective inhibitor of the c-Jun N-terminal kinase (JNK) signaling pathway. It acts by blocking the activation of JNK, a key enzyme involved in various cellular processes. This product is primarily used in research applications to study the role of the JNK pathway in biological systems.

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Lab products found in correlation

3 protocols using sp600125

Diabetic Oxidative Stress Modulation

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UDCA was kindly provided by Daewoong Pharmaceutical Co. Ltd. (Seoul, Korea). D-glucose, mannitol, streptozotocin (STZ), pyrrolidine dithiocarbamate (PDTC), and an NF-κB inhibitor were purchased from Sigma-Aldrich (St Louis, MO). SP600125, a selective JNK inhibitor, was from Promega (Madison, WI). Antibodies against phospho-IκB, NF-κB p65, phospho-ERK_1/2, ERK_1/2, phospho-JNK, and JNK were from Cell Signaling Technology (Beverly, MA). Antibodies against RAGE, S100A12, and XBP1 were from Abcam (Cambridge, MA). Anti-phospho-PERK, anti-CHOP, anti-Nrf2, anti-phospho-p38, anti-p38, anti-β-actin, anti-CD68, anti-CD11b/c, anti-GRP78, anti-mouse IgG-R, and anti-rabbit IgG-R antibodies were from Santa Cruz Biotechnology (Santa Cruz, CA). Anti-ATF6 antibody was from IMGENEX (San Diego, CA). Anti-VCAM-1 antibody was from Novus Biologicals. Anti-ICAM-1 antibody was from SouthernBiotech (Birmingham, AL). Anti-rat IgG-R antibody was from Jackson ImmunoResearch (West Grove, PA).

Chung J., An S.H., Kang S.W, & Kwon K. (2016). Ursodeoxycholic Acid (UDCA) Exerts Anti-Atherogenic Effects by Inhibiting RAGE Signaling in Diabetic Atherosclerosis. PLoS ONE, 11(1), e0147839.

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Resveratrol Modulates Egr-1 Expression

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The final concentrations of all the inhibitors were 10 μM except SP 600125 (BIOMOL International, PA), of which the concentration was 20 μM. SB 203580 (Promega, WI) inhibits p38MAPK/SAP2, whereas SP 600125 is a potent JNK inhibitor. U-0126 (Santa Cruz Biotechnology, Inc, TX) is a potent inhibitor of ERK1/2 activity and LY 294002 (Santa Cruz Biotechnology, Inc, TX) blocks PI3K/AKT pathways. Cells were treated with or without 100 μM of resveratrol for another 6 h after 1 h preincubation, and the expression of Egr-1 protein and β-actin (loading control) was examined by western blotting.

Shi Q., Geldenhuys W., Sutariya V., Bishayee A., Patel I, & Bhatia D. (2015). CArG-driven GADD45α activated by resveratrol inhibits lung cancer cells. Genes & Cancer, 6(5-6), 220-230.

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Calycopterin Anticancer Mechanisms in Vitro

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Calycopterin, 5,4′-dihydroxy-3,6,7,8-tetramethoxyflavone was purified from D. kotschyi Boiss and the chemical structure was confirmed in our laboratory as reported previously [20 (link)]. MTT (3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide), dimethylsulfoximine (DMSO), and propidium iodide (PI) were purchased from Sigma (St. Louis, MO, USA). Anti-cell division cycle 25 homolog C (cdc25c), anticyclin B1, anti-Bcl-, anti-Bax, anti-pro-caspase 3, anti-pro-caspase 9, anti-poly ADP-ribose polymerase (PARP), anti-extracellular signal-regulated kinase 1/2 (ERK1/2), anti-c-Jun N-terminal kinase (JNK), anti-p38 MAPK, anti-Akt, anti-phospho-ERK1/2 (Thr202/Tyr204), anti-phospho-JNK (Thr183/Tyr185), anti-phospho-p38 MAPK (Thr180/Try182), anti-phospho-Akt (Ser473), and anti-phospho-phosphatidylinositol-3-kinase (PI3K) (Tyr458/Tyr199) antibodies were purchased from Cell Signaling Technology (Beverly, MA, USA). Benzyloxycarbonyl–Val–Ala–Asp–fluoromethyl ketone (z-VAD-fmk), LY294002, U0126, SP600125, and SB203580 were purchased from Promega (Madison, WI, USA). DMEM cell cultures, fetal bovine serum (FBS) were purchased from Gibco (Gaithersburg, MD, USA). All other reagents were commercial products of the highest available purity grade.

Esmaeili M.A., Farimani M.M, & Kiaei M. (2014). Anticancer effect of calycopterin via PI3K/Akt and MAPK signaling pathways, ROS-mediated pathway and mitochondrial dysfunction in hepatoblastoma cancer (HepG2) cells. Molecular and cellular biochemistry, 397(1-2), 17-31.

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