Sp600125

Manufactured by Cayman Chemical

Sourced in United States

SP600125 is a selective inhibitor of the c-Jun N-terminal kinase (JNK) pathway. It acts by blocking the activation of JNK, which is involved in various cellular processes. This compound is commonly used in research settings to investigate the role of the JNK signaling pathway in different biological systems.

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Lab products found in correlation

49 protocols using sp600125

Modulation of Immune Cell Signaling

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Purified anti-CD3 (145–2 C11) and anti-CD28 (37.51), PE-conjugated antiphosphorylated-ATM (Ser1981), and PE-conjugated anti-FoxP3 were purchased from Biolegend. Antimouse-specific polyclonal phosphorylated antibodies to ERK, P38, and JNK, rabbit polyclonal antibodies to P53 and P21, and PE-conjugated donkey antirabbit IgG or PE-conjugated goat antimouse IgG secondary antibodies were purchased from Cell Signaling Technology. PE-conjugated phospho-CHK2 (Thr68) monoclonal antibody was purchased from eBioscience. MAPK signaling inhibitors U0126, SB203580, LY2228820, and SP600125 were purchased from Cayman Chemical. ATM inhibitor KU55933 was purchased from Sigma and Cayman Chemical. PE-Annexin V and 7-amino-actinomycin (7-AAD) apoptosis detection kit and Foxp3 staining buffer set were purchased from Biolegend.

Liu X., Si F., Bagley D., Ma F., Zhang Y., Tao Y., Shaw E, & Peng G. (2022). Blockades of effector T cell senescence and exhaustion synergistically enhance antitumor immunity and immunotherapy. Journal for Immunotherapy of Cancer, 10(10), e005020.

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Intrathecal Catheter Implantation and Pharmacological Interventions in Rats

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A polyethylene PE10 catheter was implanted in the lumbar subarachnoid space in each rat under isoflurane-induced anesthesia according to the method described previously (Chen & Pan 2006a (link)). Briefly, each animal was placed prone on a stereotaxic frame, and a small incision was made at the back of the neck. The catheter was inserted after a small puncture was made in the atlanto-occipital membrane of the cisterna magna. The caudal tip of the catheter was then advanced and reached the lumbar enlargement of the spinal cord. To minimize animal’s suffering, 1% lidocaine was injected around the incision site during the brief surgery. The animals were allowed to recover for 7 days before intrathecal injection, and no other medications were administered. Rats exhibiting neurological deficits (e.g., paralysis) or poor grooming were promptly killed via CO₂ asphyxiation. In 43 rats instrumented with intrathecal catheters, 4 rats were killed due to motor weakness and impairment. U0126 (5 μg; EMD-Calbiochem, La Jolla, CA), 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imidazole (SB203580, 5 μg; EMD-Calbiochem), and SP600125 (30 μg; Cayman Chemical, Ann Arbor, MI) were dissolved in DMSO and intrathecally injected 20 min before morphine administration on each testing day (days 1–8).

Deng M., Chen S.R., Chen H., Luo Y., Dong Y, & Pan H.L. (2018). Mitogen-Activated Protein Kinase Signaling Mediates Opioid-induced Presynaptic NMDA Receptor Activation and Analgesic Tolerance. Journal of neurochemistry, 148(2), 275-290.

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CRISPR-engineered PDAC cell lines

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The human PDAC cell lines MIA PaCa-2 and PANC-1 were obtained from the American Type Culture Collection. We used two lines of RalGAPβ-deficient MIA PaCa-2 cells (KO1 and KO2) and PANC-1 cells (KO1 and KO2) previously established by the CRISPR-Cas9 system (9 (link)). Cell lines obtained by the same CRISPR treatment but have no indel mutations in the RalGAPβ genomic region were used as controls. All cells were cultured in Dulbecco’s modified Eagle medium (DMEM; Fujifilm Wako Pure Chemical) containing 10% (v/v) fetal bovine serum (FBS; Gibco), 100 U/ml penicillin, and 100 μg/ml streptomycin in a humidified atmosphere with 5% CO₂ at 37 °C. In some experiments, RalGAPβ-WT, RalGAPα2-WT, and RalGAPα2-N1742K mutant (RalGAPα2-MUT) lacking GAP activity were stably expressed in MIA PaCa-2 and PANC-1 cells using lentivirus expression system as described (14 (link)). The type I TGF-β receptor inhibitor SB431542 (Cayman Chemical) and the JNK inhibitor SP600125 (Cayman Chemical) were dissolved in dimethyl sulfoxide and used at indicated concentrations. Unless otherwise specified, all other chemicals were purchased from Sigma-Aldrich or Fujifilm Wako Pure Chemical. All experiments with DNA recombination in this study were approved by the Committees of Tohoku University.

Cao M., Li X., Trinh D.A., Yoshimachi S., Goto K., Sakata N., Ishida M., Ohtsuka H., Unno M., Wang Y., Shirakawa R, & Horiuchi H. (2023). Ral GTPase promotes metastasis of pancreatic ductal adenocarcinoma via elevation of TGF-β1 production. The Journal of Biological Chemistry, 299(6), 104754.

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Pharmacological Inhibitor Assays

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All pharmacological inhibitors were purchased from Sigma-Aldrich (Shanghai, China), reconstituted in sterile DMSO (Sigma-Aldrich, Shanghai, China), and utilized at varying concentrations. The pharmacological inhibitors included the ERK signaling inhibitor U-0126 (10 mM), the NF-κB signaling inhibitor PDTC (20 mM), and the JNK signaling inhibitor SP600125 (20 mM) (Cayman Chemical, Ann Arbor, MI, USA). DMSO, at a concentration of 0.1%, was used as the vehicle control. In the inhibitory experiments, cells were treated with a given inhibitor for 30 min before treatment with Ms_YrbE3A and BCG_YrbE3A. Culture supernatants were then harvested at 8 h after stimulation with Ms_YrbE3A and BCG_YrbE3A and assayed for cytokine concentrations [15 (link)].

Wang J., Zhu X., Peng Y., Zhu T., Liu H., Zhu Y., Xiong X., Chen X., Hu C., Chen H., Chen Y, & Guo A. (2020). Mycobacterium tuberculosis YrbE3A Promotes Host Innate Immune Response by Targeting NF-κB/JNK Signaling. Microorganisms, 8(4), 584.

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Inhibition of Signaling Pathways in Cell Viability Assay

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3-(5′-hydroxymethyl-2′-furyl)-1-benzylindazole (YC-1), sGC inhibitor ODQ, non-competitive selective PDE inhibitor IBMX, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) were purchased from Sigma-Aldrich (St. Louis, MO, USA). The PKA inhibitor H89 were purchased from Enzo Life Sciences (Farmingdale, NY, USA). The sGC activator BAY 41-2272 and NF-κB inhibitor Ro 106-9920 were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). The extracellular regulated MAP kinase (ERK) inhibitor U0126, p38 MAP kinases inhibitor SB202190, c-Jun N-terminal kinases (JNK) inhibitor SP600125, HIF-1α inhibitor CAY10585, p38 activator anisomycin, and phosphatidylinositol-3-kinases (PI3K) inhibitor wortmannin were purchased from Cayman Chemical (Ann Arbor, MI, USA).

Hsieh K.Y., Wei C.K, & Wu C.C. (2019). YC-1 Prevents Tumor-Associated Tissue Factor Expression and Procoagulant Activity in Hypoxic Conditions by Inhibiting p38/NF-κB Signaling Pathway. International Journal of Molecular Sciences, 20(2), 244.

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Bilateral Carotid Artery Occlusion in Rats

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Male Sprague-Dawley rats, weighing 230–250 g, were purchased from the experimental animal center of Shanghai Sippr-BK Laboratory Animals Ltd. (Shanghai, China). Prior to experiments, the rats were housed for 12 weeks in climate-controlled facilities on a 12:12 h light–dark cycle (lights on from 08:30–20:30) at constant temperature (23 ± 1 °C) and humidity (60%) with free access to food and water. After 1 week of acclimatization, rats were randomly divided into six groups (5 rats per group) as follows: (1) Sham-operated; (2) Bilateral common carotid artery’s occlusion (BCCAo); (3) BCCAo+ the autophagy inhibitor 3-methyladenine (3-MA; Sigma, St. Louis, MO, USA); (4) BCCAo+c-Jun N-terminal kinase (JNK) inhibitor SP600125 (Sigma, St. Louis, MO, USA); (4) BCCAo+URB (Cayman Chemicals, Tallinn, Estonia); (5) BCCAo+URB+3-MA; (6) BCCAo+URB+SP600125. After 12 weeks, rats were sacrificed, and their brain were immediately removed for experiments or stored at −70 °C for later use.
Experimental protocols were performed in compliance with international guidelines and Chinese legislation on the use and care of laboratory animals, and were approved by the Animal Laboratory Center of Tongji University School of Medicine.

Su S.H., Wu Y.F., Wang D.P, & Hai J. (2018). Inhibition of excessive autophagy and mitophagy mediates neuroprotective effects of URB597 against chronic cerebral hypoperfusion. Cell Death & Disease, 9(7), 733.

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Endothelial Cell Culture and Stimulation

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HUVECs were obtained from the Cell Resource Center of Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences. Cells were cultured in RPMI 1640 medium (Invitrogen, Carlsbad, CA, USA) supplemented with 10% foetal bovine serum (FBS, HyClone), streptomycin (100 mg/ml; Sigma‐Aldrich, Saint Louis, Missouri, USA) and penicillin (100 units/ml; Sigma‐Aldrich) and maintained at 37 °C under a humidified atmosphere containing 5% CO₂. The cells were seeded into 6‐ or 96‐well plates, stimulated by various drugs for different desired time intervals and then collected for further analysis. The drugs used to stimulate the cells were as follows: SC‐560 (COX‐1 inhibitor); NS‐398 (COX‐2 inhibitor); SC51322 (EP1 antagonist); AH6809 (EP2 antagonist); L798106 (EP3 antagonist); L‐161982 (EP4 antagonist); PD98059 (ERK inhibitor); SB203580 and SB202190 (p38 MAPK inhibitors); SP600125 (JNK inhibitor); Y27632 (ROCK inhibitor); cicaprost, PGE₂, and AA (Cayman Chemical, Ann Harbor, MI, USA); TCDD (Cambridge Isotope Laboratories, Tewksbury, MA, USA).

Yu Y., Liu Q., Guo S., Zhang Q., Tang J., Liu G., Kong D., Li J., Yan S., Wang R., Wang P., Su X, & Yu Y. (2017). 2, 3, 7, 8‐Tetrachlorodibenzo‐p‐dioxin promotes endothelial cell apoptosis through activation of EP3/p38MAPK/Bcl‐2 pathway. Journal of Cellular and Molecular Medicine, 21(12), 3540-3551.

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Inhibition of Signaling Pathways in TNF-α and IL-1β Stimulation

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The following chemical inhibitors were used to inhibit signalling pathways while cells were stimulated with TNF-α or IL-1β for 3 days, and purchased from Cayman Chemical: SB203580 (13067, 10 μM) to inhibit p38 MAPK, SP600125 (10010466, 20 μM) to inhibit JNK, U0126 (70970, 5 μM) to inhibit ERK1/2. The stock solutions of the inhibitors were dissolved in dimethylsulfoxide (DMSO, Sigma) at 10 mM. DMSO (1:500 dilution, or 28 mM) was used as a control.

Wan Wong S., Tamatam C.R., Cho I.S., Toth P.T., Bargi R., Belvitch P., Lee J.C., Rehman J., Reddy S.P, & Shin J.W. (2021). Inhibition of aberrant tissue remodelling by mesenchymal stromal cells singly coated with soft gels presenting defined chemomechanical cues. Nature biomedical engineering, 6(1), 54-66.

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Investigating Cellular Signaling Pathways

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DON was obtained from Sigma-Aldrich (St. Louis, MO, USA). Cell culture medium and supplements were purchased from Life Technologies (Grand Island, NY, USA). Anti-phospho-p38 (4511), anti-p38 (8690), anti-phospho-JNK (4668), anti-JNK (9252), anti-phospho-ERK (4370), anti-ERK (4695) and anti-β-actin (4970) antibodies were purchased from Cell Signaling Technology (Beverly, MA, USA). SB203580 was obtained from Promega (Madison, WI, USA). U0126 and SP600125 were acquired from Cayman Chemicals (Ann Arbor, MI, USA).

Zhang H., Deng X., Zhou C., Wu W, & Zhang H. (2020). Deoxynivalenol Induces Inflammation in IPEC-J2 Cells by Activating P38 Mapk And Erk1/2. Toxins, 12(3), 180.

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Culturing Human Lung Carcinoma A549 Cells

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Human lung carcinoma type 2 epithelium-like A549 cells, purchased from Riken BioResource Center Cell Bank (Tsukuba, Ibaraki, Japan), were grown in Dulbecco’s modified Eagle’s medium (DMEM; Sigma-Aldrich Life Sciences, MO, USA) with 10% heat-inactivated fetal bovine serum (FBS; GE Healthcare Japanhealth, Tokyo, Japan), 100 U/ml penicillin, 100 mg/ml streptomycin in 10 cm dishes at 37 °C in a humidified atmosphere of 5% CO2. A549 cell line has been characterized as an in vitro model of alveolar type 2 pneumocytes of the human lung because of capacity of secreting lung surfactant-associated glycoproteins [8 (link)].
Reagents were purchased commercially as follows: human IL-1β (Humanzyme, Chicago, IL, USA); human TNF-α (Prospec, Rehovot, Israel), human IFN-γ (Peprotech, NJ, USA); dexamethasone, Fas ligand (super Fas Ligand) (Enzo, PA, USA); RIPA buffer (Thermo Fischer Scientific, Tokyo, Japan); lipopolysaccharide (LPS: E. coli O111:B4, Sigma-Aldrich Life Sciences); rapamycin, parthenolide, SP600125, SB203580, U0123, LY294002, and QVD-OPh (Cayman Chemical, MI, USA).
Antibodies were as follows: anti-iNOS (R&D systems, MN, USA); anti-HO-1 (Enzo); anti-beta actin (MBL, Nagoya, Japan); anti-JNK (Abcam Japan, Tokyo, Japan); anti-cox-2 (BD Japan, Tokyo, Japan); anti-ICAM-1 (Santa Cruz Biotechnology, TX, USA). All of the other antibodies were purchased from CST Japan, Tokyo, Japan.

Kuwajima K., Chang K., Furuta A., Bougaki M., Uchida K., Sawamura S, & Yamada Y. (2019). Synergistic cytoprotection by co-treatment with dexamethasone and rapamycin against proinflammatory cytokine-induced alveolar epithelial cell injury. Journal of Intensive Care, 7, 12.

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