| Name | c Jun N terminal kinase (protein family or complex) |
|---|---|
| Synonyms | c Jun N terminal kinase; JNK; c Jun NH (2) terminal kinase; Jun N terminal kinase |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16794604 | Centeno C, Repici M, Chatton JY, Riederer BM, Bonny C, Nicod P, Price M, Clarke PG, Papa S, Franzoso G, Borsello T: Role of the JNK pathway in -mediated excitotoxicity of cortical neurons. Cell Death Differ. 2007 Feb;14(2):240-53. Epub 2006 Jun 23. Excitotoxic insults induce c-Jun N-terminal kinase (JNK) activation, which leads to neuronal death and contributes to many neurological conditions such as cerebral ischemia and neurodegenerative disorders. |
1(0,0,0,1) | Details |
| 15961565 | Xiao L, Qi A, Chen Y: Cultured embryonic hippocampal neurons deficient in glucocorticoid (GC) receptor: a novel model for studying nongenomic effects of GC in the neural system. Endocrinology. 2005 Sep;146(9):4036-41. Epub 2005 Jun 16. In this study, we found that the Erk1/2, c-Jun N-terminal kinase (JNK), and p38 MAPKs were activated in these neurons by BSA-conjugated within 15 min of treatment. This activation was not blocked by RU38486, spironolactone, or cycloheximide. |
1(0,0,0,1) | Details |
| 16123165 | Ishikawa T, Hwang K, Lazzarino D, Morris PL: Sertoli cell expression of steroidogenic acute regulatory protein-related lipid transfer 1 and 5 domain-containing proteins and sterol regulatory element binding protein-1 are interleukin-1beta regulated by activation of c-Jun N-terminal kinase and cyclooxygenase-2 and cytokine induction. Endocrinology. 2005 Dec;146(12):5100-11. Epub 2005 Aug 25. IL-1beta rapidly decreases levels of precursor and mature sterol regulatory element-binding protein-1, changes not altered by cycloheximide, suggesting coordinate regulation of StARD1 and -D5, but not StARD4, expression. |
1(0,0,0,1) | Details |
| 19716839 | Charlson AT, Zeliadt NA, Wattenberg EV: Extracellular signal regulated kinase 5 mediates signals triggered by the novel tumor promoter palytoxin. Toxicol Appl Pharmacol. 2009 Dec 1;241(2):143-53. Epub 2009 Aug 28. Cycloheximide, okadaic acid, and orthovanadate did not mimic the effect of palytoxin on ERK5. We previously showed that palytoxin activates three major members of the mitogen activated protein kinase (MAPK) family, extracellular signal regulated kinase 1 and 2 (ERK1/2), c-Jun N-terminal kinase (JNK), and p38. |
1(0,0,0,1) | Details |
| 15825190 | Suzuki M, Koike T: Early apoptotic and late necrotic components associated with altered Ca2+ homeostasis in a peptide-delivery model of -induced neuronal death. J Neurosci Res. 2005 May 15;80(4):549-61. Enhanced c-Jun phosphorylation showed c-Jun N-terminal kinase (JNK) activation. |
1(0,0,0,1) | Details |
| 17989348 | Papineni S, Chintharlapalli S, Safe S: Methyl 2-cyano-3,11-dioxo-18 beta-olean-1,12-dien-30-oate is a peroxisome proliferator-activated receptor-gamma agonist that induces receptor-independent apoptosis in LNCaP prostate cancer cells. Mol Pharmacol. 2008 Feb;73(2):553-65. Epub 2007 Nov 7. However, induction of these responses by beta-CDODA-Me was PPARgamma-independent and due to activation of phosphatidylinositol-3-kinase, mitogen-activated protein kinase, and jun N-terminal kinase pathways by this compound. In contrast, beta-CDODA-Me also decreased androgen receptor (AR) and prostate-specific antigen (PSA) mRNA and protein levels through kinase-independent pathways. beta-CDODA-Me repressed AR mRNA transcription, whereas decreased PSA mRNA levels were dependent on protein synthesis and were reversed by cycloheximide. |
1(0,0,0,1) | Details |
| 18056701 | Fei Q, McCormack AL, Di Monte DA, Ethell DW: Paraquat neurotoxicity is mediated by a Bak-dependent mechanism. . J Biol Chem. 2008 Feb 8;283(6):3357-64. Epub 2007 Dec 4. Oxidative stress, c-Jun N-terminal kinase activation, and alpha-synuclein aggregation are each induced by PQ, but details of the cell death mechanisms involved remain unclear. Changes in nuclear morphology and loss of viability were blocked by cycloheximide, caspase inhibitor, and Bcl-2 overexpression. |
1(0,0,0,1) | Details |
| 17498698 | Ohnishi M, Katsuki H, Fujimoto S, Takagi M, Kume T, Akaike A: Involvement of thrombin and mitogen-activated protein kinase pathways in hemorrhagic brain injury. Exp Neurol. 2007 Jul;206(1):43-52. Epub 2007 Apr 14. Intracerebroventricular injection of argatroban or cycloheximide, both of which prevent thrombin cytotoxicity in vitro, exhibited a significant neuroprotective effect against ICH-induced injury. ICH-induced neuron loss was also prevented by a MAP kinase kinase inhibitor (PD98059) and a c-Jun N-terminal kinase inhibitor (SP600125). |
1(0,0,0,1) | Details |
| 19920324 | Ji L, Chauhan A, Chauhan V: Upregulation of Cytoplasmic Gelsolin, an Amyloid-beta-Binding Protein, Under Oxidative Stress Conditions: Involvement of Protein Kinase C. J Alzheimers Dis. 2009 Nov 17. Pretreatment of cells with cycloheximide (an inhibitor of protein synthesis) resulted in significant inhibition of H However, both H |
1(0,0,0,1) | Details |
| 15525600 | Lin KH, Chen CY, Chen SL, Yen CC, Huang YH, Shih CH, Shen JJ, Yang RC, Wang CS: Regulation of fibronectin by thyroid hormone receptors. . J Mol Endocrinol. 2004 Oct;33(2):445-58. Blockade of protein synthesis by cycloheximide almost completely inhibited the concomitant induction of FN mRNA by T3, indicating that T3 indirectly regulates FN. In an effort to elucidate the we demonstrated the involvement of the signaling pathways involved in the activation of FN by T3, mitogen activated protein kinase/c-Jun N-terminal kinase/p38 MAPK (MAPK/JNK/p38) pathway. |
1(0,0,0,1) | Details |
| 19553664 | Sommerfeld A, Reinehr R, Haussinger D: Bile acid-induced epidermal growth factor receptor activation in quiescent rat hepatic stellate cells can trigger both proliferation and apoptosis. J Biol Chem. 2009 Aug 14;284(33):22173-83. Epub 2009 Jun 24. When, however, a JNK signal was induced by coadministration of cycloheximide or peroxide (H2O2), activated EGFR associated with CD95 and triggered EGFR-mediated CD95- phosphorylation and subsequent formation of the death-inducing signaling complex. |
0(0,0,0,0) | Details |
| 20339118 | Montezano AC, Burger D, Paravicini TM, Chignalia AZ, Yusuf H, Almasri M, He Y, Callera GE, He G, Krause KH, Lambeth D, Quinn MT, Touyz RM: Reduced Oxidase 5 (Nox5) Regulation by Angiotensin II and Endothelin-1 Is Mediated via /Calmodulin-Dependent, Rac-1-Independent Pathways in Human Endothelial Cells. Circ Res. 2010 Mar 25. Effects were inhibited by actinomycin D and cycloheximide and blunted by calmidazolium and low extracellular Ca (2+) ([Ca (2+)] e). |
0(0,0,0,0) | Details |
| 18491380 | Motoki T, Sugiura Y, Matsumoto Y, Tsuji T, Kubota S, Takigawa M, Gohda E: Induction of hepatocyte growth factor expression by in human fibroblasts through MAPK activation. J Cell Biochem. 2008 Jul 1;104(4):1465-76. The protein synthesis inhibitor cycloheximide completely inhibited upregulation of HGF mRNA induced by but superinduced HGF mRNA expression upregulated by 12-O-tetradecanoylphorbol 13-acetate (TPA). |
0(0,0,0,0) | Details |
| 18029162 | Sampieri CL, Nuttall RK, Young DA, Goldspink D, Clark IM, Edwards DR: Activation of p38 and JNK MAPK pathways abrogates requirement for new protein synthesis for phorbol ester mediated induction of select MMP and TIMP genes. Matrix Biol. 2008 Mar;27(2):128-38. Epub 2007 Oct 4. The requirement for ongoing translation was analysed using three protein synthesis inhibitors, anisomycin, cycloheximide and emetine. |
0(0,0,0,0) | Details |
| 18202854 | Sibayama-Imazu T, Fujisawa Y, Masuda Y, Aiuchi T, Nakajo S, Itabe H, Nakaya K: Induction of apoptosis in PA-1 ovarian cancer cells by is associated with an increase in the level of TR3/Nur77 and its accumulation in mitochondria and nuclei. J Cancer Res Clin Oncol. 2008 Jul;134(7):803-12. Epub 2008 Jan 17. Treatment of PA-1 cells with small interfering RNA (siRNA) directed against TR3, and with cycloheximide or SP600125 (an inhibitor of c-jun N-terminal kinase; JNK), separately, inhibited the VK (2)-induced synthesis of TR3 and apoptosis. |
81(1,1,1,1) | Details |
| 15670574 | Kadohara K, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: Acetoxycycloheximide (E-73) rapidly induces apoptosis mediated by the release of cytochrome c via activation of c-Jun N-terminal kinase. Biochem Pharmacol. 2005 Feb 15;69(4):551-60. Epub 2004 Dec 28. Cycloheximide (CHX) is an inhibitor of protein synthesis and commonly used to modulate death receptor-mediated apoptosis or to induce apoptosis in a number of normal and transformed cells. |
2(0,0,0,2) | Details |
| 18571430 | Gangadhar NM, Firestein SJ, Stockwell BR: A novel role for jun N-terminal kinase signaling in olfactory sensory neuronal death. Mol Cell Neurosci. 2008 Aug;38(4):518-25. Epub 2008 May 11. Here, we show that inhibition of transcription or translation, by actinomycin D or cycloheximide, respectively, suppresses pathways leading to death, prolonging the survival of OSNs in culture. |
2(0,0,0,2) | Details |
| 18719026 | Buzzelli MD, Nagarajan M, Radtka JF, Shumate ML, Navaratnarajah M, Lang CH, Cooney RN: Nuclear factor-kappaB mediates the inhibitory effects of tumor necrosis factor-alpha on growth hormone-inducible gene expression in liver. Endocrinology. 2008 Dec;149(12):6378-88. Epub 2008 Aug 21. Cycloheximide did not antagonize the inhibitory effects of TNF on GH-inducible IGF-I expression. CWSV-1 cells were transfected with GH-inducible Spi 2.1 or IGF-I promoter luciferase constructs, incubated with TNF signaling inhibitors (fumonisin B1 for sphingomyelinase and SP600125 for c-Jun N-terminal kinase), treated with or without TNF, and then stimulated with recombinant human GH. |
1(0,0,0,1) | Details |
| 16787641 | Ito Y, Oh-Hashi K, Kiuchi K, Hirata Y: p44/42 MAP kinase and c-Jun N-terminal kinase contribute to the up-regulation of caspase-3 in -induced apoptosis in PC12 cells. Brain Res. 2006 Jul 12;1099(1):1-7. Epub 2006 Jun 19. Up-regulation of caspase-3 protein was evident in -treated PC12 cells and was moderate in cisplatin-, rotenone- and A23187-treated cells but was not observed in serum deprivation-, anisomycin-, camptothecin-, cycloheximide- or staurosporine-treated cells in which all treatments induced extensive DNA fragmentation. |
1(0,0,0,1) | Details |
| 19094210 | Zayed N, Li X, Chabane N, Benderdour M, Martel-Pelletier J, Pelletier JP, Duval N, Fahmi H: Increased expression of lipocalin-type prostaglandin D2 synthase in osteoarthritic cartilage. Arthritis Res Ther. 2008;10(6):R146. Epub 2008 Dec 18. The upregulation of L-PGDS by IL-1beta was blocked by the translational inhibitor cycloheximide, indicating that this effect is indirect, requiring de novo protein synthesis. Specific inhibitors of the MAPK p38 (SB 203580) and c-jun N-terminal kinase (JNK) (SP600125) and of the NF-kappaB (SN-50) and Notch (DAPT) signalling pathways suppressed IL-1beta-induced upregulation of L-PGDS expression. |
1(0,0,0,1) | Details |
| 16506055 | Doronzo G, Russo I, Mattiello L, Riganti C, Anfossi G, Trovati M: Insulin activates hypoxia-inducible factor-1alpha in human and rat vascular smooth muscle cells via phosphatidylinositol-3 kinase and mitogen-activated protein kinase pathways: impairment in insulin resistance owing to defects in insulin signalling. Diabetologia. 2006 May;49(5):1049-63. Epub 2006 Feb 28. METHODS: Using aortic VSMC taken from humans and Zucker rats and cultured in normoxia, the following were evaluated: (1) dose-dependent (0.5, 1, 2 nmol/l) and time-dependent (2, 4, 6 h) effects exerted by insulin on HIF-1alpha content in both nucleus and cytosol, measured by Western blots; (2) insulin effects on HIF-1 DNA-binding activity on the VEGF gene, measured by electrophoretic mobility shift assay; and (3) involvement of the insulin signalling molecules in these insulin actions, by using the following inhibitors: LY294002 (PI3-K), PD98059 (extracellular signal regulated kinase [ERK]), SP600125 (Jun N terminal kinase [JNK]), SB203580 (p38 mitogen-activated protein kinase) and rapamycin (mammalian target of rapamycin), and by detecting the insulin signalling molecules by Western blots. The insulin-induced increase of HIF-1alpha is blunted by the translation inhibitor cycloheximide, LY294002, PD98059, SP600125 and rapamycin, but not by SB203580. |
1(0,0,0,1) | Details |
| 18439101 | Kato T, Noma H, Kitagawa M, Takahashi T, Oshitani N, Kitagawa S: Distinct role of c-Jun N-terminal kinase isoforms in human neutrophil apoptosis regulated by tumor necrosis factor-alpha and granulocyte-macrophage colony-stimulating factor. J Interferon Cytokine Res. 2008 Apr;28(4):235-43. TNF-alpha-induced JNK phosphorylation was sustained in the presence of cycloheximide, which was accompanied by accelerated neutrophil apoptosis. |
1(0,0,0,1) | Details |
| 19770273 | Steinmann J, Halldorsson S, Agerberth B, Gudmundsson GH: Phenylbutyrate induces antimicrobial peptide expression. Antimicrob Agents Chemother. 2009 Dec;53(12):5127-33. Epub 2009 Sep 21. Furthermore, we have demonstrated that inhibition of the mitogen-activated protein kinases MEK1/2 and c-Jun N-terminal kinase attenuate PBA-induced gene expression. |
1(0,0,0,1) | Details |
| 17070518 | Hosoi T, Matsunami N, Nagahama T, Okuma Y, Ozawa K, Takizawa T, Nomura Y: 2-Aminopurine inhibits leptin receptor signal transduction. Eur J Pharmacol. 2006 Dec 28;553(1-3):61-6. Epub 2006 Sep 28. In the present study, we investigated the effect of 2-aminopurine (2-AP), an inhibitor of double-strand RNA-activated protein kinase (PKR), on leptin signal transduction. 2-AP dose-dependently inhibited the leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) in HEK293 cells stably transfected with the Ob-Rb leptin receptor. The inhibitory effect of 2-AP was not mediated by newly synthesized protein because the inhibitory effect of 2-AP on leptin-induced STAT3 activation was not abrogated in the presence of the protein synthesis inhibitor cycloheximide. |
1(0,0,0,1) | Details |
| 19179479 | Armstrong SP, Caunt CJ, McArdle CA: Gonadotropin-releasing hormone and protein kinase C signaling to ERK: spatiotemporal regulation of ERK by docking domains and dual-specificity phosphatases. Mol Endocrinol. 2009 Apr;23(4):510-9. Epub 2009 Jan 29. Screening a short inhibitory RNA library targeting 16 DUSPs (nuclear-inducible DUSPs, cytoplasmic ERK MAPK phosphatases, c-Jun N-terminal kinase/p38 MAPK phosphatases, and atypical DUSPs) revealed GnRH effects to be influenced by DUSPs 5, 9, 10, 16, and 3 (i.e. by each DUSP class). Cycloheximide caused more sustained effects of GnRH and phorbol ester on ppERK, suggesting termination by nuclear-inducible DUSPs. |
1(0,0,0,1) | Details |
| 20157239 | Ji L, Chauhan A, Chauhan V: Upregulation of cytoplasmic gelsolin, an amyloid-beta-binding protein, under oxidative stress conditions: involvement of protein kinase C. J Alzheimers Dis. 2010 Jan;19(3):829-38. Pretreatment of cells with cycloheximide (an inhibitor of protein synthesis) resulted in significant inhibition of H (2) O (2) induced c-gelsolin expression, suggesting the possible de novo synthesis of c-gelsolin in cells. However, both H (2) O (2) and staurosporine activated the mitogen-activated protein kinases (MAPKs), i.e., c-Jun N-terminal kinase, P38, and extracellular signal-regulated kinase. |
1(0,0,0,1) | Details |
| 15965068 | Hou CC, Hung SL, Kao SH, Chen TH, Lee HM: induces heme-oxygenase expression in glomerular mesangial cells. Ann N Y Acad Sci. 2005 May;1042:235-45. Consistently, activated c-Jun N-terminal kinase (JNK) as demonstrated by kinase assays and by increasing phosphorylation of this kinase. -induced HO-1 protein expression was inhibited by actinomycin D and cycloheximide, suggesting that de novo transcription and translation are required in this process. |
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| 15913957 | Kakinuma H, Inomata H, Kitamura N: Enhanced JNK activation by NESK without kinase activity upon caspase-mediated cleavage during apoptosis. Cell Signal. 2005 Nov;17(11):1439-48. NESK belongs to the germinal center kinase (GCK) family and selectively activates the c-Jun N-terminal kinase (JNK) pathway when overexpressed in cultured cells. Treatment of NESK-transfected HeLa cells with TNF-alpha in the presence of cycloheximide or with staurosporine induced proteolytic cleavage of NESK. |
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| 16330215 | Fujimoto S, Katsuki H, Kume T, Akaike A: Thrombin-induced delayed injury involves multiple and distinct signaling pathways in the cerebral cortex and the striatum in organotypic slice cultures. Neurobiol Dis. 2006 Apr;22(1):130-42. Epub 2005 Dec 5. These effects were prevented by cycloheximide and actinomycin D but not by a caspase-3 inhibitor. In addition, inhibition of extracelluar signal-regulated kinase (ERK), Src kinase and protein kinase C prevented both neuronal injury in the cortex and shrinkage of the striatum, whereas inhibition of p38 mitogen-activated protein kinase and c-Jun N-terminal kinase prevented shrinkage of the striatum only. |
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