| Name | p38 |
|---|---|
| Synonyms | AIMP 2; p38; AIMP2; JTV 1; JTV1; JTV1 gene; JTV1 protein; Multisynthetase complex auxiliary component p38… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17257889 | Nakagawa H, Matsumiya T, Sakaki H, Imaizumi T, Kubota K, Kusumi A, Kobayashi W, Kimura H: Expression of vascular endothelial growth factor by photodynamic therapy with mono-L-aspartyl chlorin e6 (NPe6) in oral squamous cell carcinoma. Oral Oncol. 2007 Jul;43(6):544-50. Epub 2007 Jan 25. The expression mRNAs for VEGF, c-jun and c-fos induced by Npe6-mediated PDT were inhibited by SB203580, p38 MAPK inhibitors, and the expression of VEGF mRNA was inhibited by cycloheximide (CHX), a protein synthesis inhibitor. |
32(0,1,1,2) | Details |
| 17147231 | Liang PY, Zeng YY, Wang T, Xing FY, Zhao JX, Jiang X, Di JF: [The effect of p38 on the cycloheximide-induced HL-60 cell death through mitochondria pathway]. Zhonghua Xue Ye Xue Za Zhi. 2006 Jun;27(6):398-402. |
12(0,0,2,2) | Details |
| 19648110 | King EM, Holden NS, Gong W, Rider CF, Newton R: Inhibition of NF-kappaB-dependent transcription by MKP-1: transcriptional repression by glucocorticoids occurring via p38 MAPK. J Biol Chem. 2009 Sep 25;284(39):26803-15. Epub 2009 Jul 31. |
9(0,0,0,9) | Details |
| 17329956 | Matsumoto E, Hatanaka M, Bohgaki M, Maeda S: PKC pathway and ERK/MAPK pathway are required for induction of cyclin D1 and p21Waf1 during 12-o-tetradecanoylphorbol 13--induced differentiation of myeloleukemia cells. Kobe J Med Sci. 2006;52(6):181-94. Induction of p21Waf1 expression in TPA-treated HL60 cells was inhibited with PKC inhibitor bisindolylmaleimide I and Go6976, MEK inhibitor PD98059, and p38 mitogen-actibated protein kinase (MAPK) inhibitor SB202190. |
1(0,0,0,1) | Details |
| 16835229 | Fukui N, Ikeda Y, Ohnuki T, Hikita A, Tanaka S, Yamane S, Suzuki R, Sandell LJ, Ochi T: Pro-inflammatory cytokine tumor necrosis factor-alpha induces bone morphogenetic protein-2 in chondrocytes via mRNA stabilization and transcriptional up-regulation. J Biol Chem. 2006 Sep 15;281(37):27229-41. Epub 2006 Jul 11. The results of nuclear run-off assay and cycloheximide treatment consistently indicated that ATDC5 cells acquire the capacity to synthesize BMP-2 mRNA in the nuclei during the differentiation process. Further experiments revealed that TNF-alpha modulates mRNA stability via p38 signal transduction pathway, whereas the cytokine also augmented the expression of BMP-2 through transcriptional up-regulation via the transcriptional factor NF-kappaB. |
1(0,0,0,1) | Details |
| 17429344 | Lee HT, Kim M, Jan M, Penn RB, Emala CW: Renal tubule necrosis and apoptosis modulation by A1 receptor expression. Kidney Int. 2007 Jun;71(12):1249-61. Epub 2007 Apr 11. Receptor-overexpressing cells were protected against peroxide-induced necrosis and tumor necrosis factor-alpha/cycloheximide-induced apoptosis. Overexpression of the receptor resulted in a significantly higher baseline expression of both total and phosphorylated heat-shock protein (HSP) 27; the latter due to A1 receptor enhancement of p38 and AP2 mitogen-activated protein kinase activities. |
1(0,0,0,1) | Details |
| 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. |
1(0,0,0,1) | Details |
| 15585589 | Chen YH, Hung PF, Kao YH: IGF-I downregulates resistin gene expression and protein secretion. . Am J Physiol Endocrinol Metab. 2005 May;288(5):E1019-27. Epub 2004 Dec 7. These data demonstrate that IGF-I downregulates Rstn gene expression via IGF-IR-dependent and MEK1-, p38 MAPK-, and phosphoinositide 3-kinase-independent pathways and likely modifies the distribution of Rstn protein between the intracellular and extracellular compartments via a p38 MAPK-dependent pathway. Treatment with cycloheximide, but not with actinomycin D, prevented IGF-I-suppressed Rstn mRNA expression, suggesting that IGF-I destabilizes Rstn mRNA and that IGF-I's effect requires new protein, but not mRNA, synthesis. |
1(0,0,0,1) | Details |
| 17264307 | Ratthe C, Pelletier M, Chiasson S, Girard D: Molecular mechanisms involved in interleukin-4-induced human neutrophils: expression and regulation of suppressor of cytokine signaling. J Leukoc Biol. 2007 May;81(5):1287-96. Epub 2007 Jan 30. The effect of IL-4 on SOCS3 protein expression was increased markedly when the proteasome inhibitor MG132 was added to the cultures, but this was inhibited by cycloheximide, suggesting that SOCS3 is de novo-synthesized in response to IL-4. We also demonstrated that IL-4 induced phosphorylation of Syk, p38, Erk-1/2, JNK, Jak-1, Jak-2, STAT6, and STAT1 and that treatment of cells with the inhibitors SB203580, PD98059, or AG490 reversed the ability of IL-4 to delay neutrophil apoptosis. |
1(0,0,0,1) | Details |
| 15519494 | Yoshida M, Niwa M, Ishisaki A, Hirade K, Ito H, Shimizu K, Kato K, Kozawa O: Methotrexate enhances -stimulated heat shock protein 27 induction in osteoblasts. Prostaglandins Leukot Essent Fatty Acids. 2004 Dec;71(6):351-62. We previously showed that stimulates the induction of heat shock protein 27 (HSP27) via protein kinase C (PKC)-dependent p38 mitogen-activated protein (MAP) kinase and p44/p42 MAP kinase in osteoblast-like MC3T3-E1 cells. |
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 |
| 16198345 | Lim WC, Park M, Bahn JJ, Inoue H, Lee YJ: Hypertonic induction of cyclooxygenase-2 occurs independently of NF-kappaB and is inhibited by the glucocorticoid receptor in A549 cells. FEBS Lett. 2005 Oct 10;579(24):5430-6. This induction was a transcriptional event that occurred in the absence of the protein synthesis inhibitor cycloheximide and was the result of enhanced promoter activity, as examined with the use of full-length COX-2 promoter-driven reporter plasmids. The p38 MAPK inhibitor, SB203580, or MEK1/2 inhibitor, U0126, inhibited hypertonic induction of COX-2 expression. |
1(0,0,0,1) | Details |
| 19684181 | McEwen ST, Balus SF, Durand MJ, Lombard JH: Angiotensin II maintains cerebral vascular relaxation via EGF receptor transactivation and ERK1/2. Am J Physiol Heart Circ Physiol. 2009 Oct;297(4):H1296-303. Epub 2009 Aug 14. The protective effect of ANG II infusion to restore vascular relaxation was eliminated by coinfusion of either the EGF receptor kinase inhibitor AG-1478 (20 microg/h), the ERK1/2 inhibitor PD-98059 (10 microg/h), or the protein synthesis inhibitor cycloheximide (5 microg/h). In ANG II-infused rats fed HS diet, and in rats fed LS diet, vasodilator responses to reduced PO (2) and iloprost were unaffected by the p38 MAP kinase inhibitor SB-203580 and the phosphatidylinositol 3-kinase inhibitor wortmannin. |
1(0,0,0,1) | Details |
| 16704410 | Harrison EM, McNally SJ, Devey L, Garden OJ, Ross JA, Wigmore SJ: Insulin induces heme oxygenase-1 through the phosphatidylinositol 3-kinase/Akt pathway and the Nrf2 transcription factor in renal cells. FEBS J. 2006 Jun;273(11):2345-56. The induction of heme oxygenase-1 in renal adenocarcinoma cells was blocked by actinomycin D and cycloheximide and was abolished by the phosphatidylinositol 3-kinase inhibitor, LY294002, but not by the inactive analog LY303511. |
0(0,0,0,0) | Details |
| 18767967 | Scott DW, Longpre JM, Loo G: Upregulation of GADD153 by involvement of MAPK. . DNA Cell Biol. 2008 Nov;27(11):607-14. -induced upregulation of GADD153 mRNA was attenuated by actinomycin D, but apparently not by cycloheximide. |
0(0,0,0,0) | Details |
| 17373649 | Li JP, Yang JL: Cyclin B1 proteolysis via p38 MAPK signaling participates in G2 checkpoint elicited by arsenite. J Cell Physiol. 2007 Aug;212(2):481-8. |
6(0,0,0,6) | Details |
| 16978838 | Hu JH, Chen T, Zhuang ZH, Kong L, Yu MC, Liu Y, Zang JW, Ge BX: Feedback control of MKP-1 expression by p38. . Cell Signal. 2007 Feb;19(2):393-400. Epub 2006 Jul 25. The mRNA level of MKP-1 is not affected by inhibition of p38, but the expression of MKP-1 is inhibited by treatment of cycloheximide. |
6(0,0,0,6) | Details |
| 15557226 | Rahaus M, Desloges N, Wolff MH: Replication of varicella-zoster virus is influenced by the levels of JNK/SAPK and p38/MAPK activation. J Gen Virol. 2004 Dec;85(Pt 12):3529-40. Blocking gene expression by treating cells with actinomycin D or cycloheximide prior to infection resulted in activation of neither JNK/SAPK nor p38/MAPK. |
5(0,0,0,5) | Details |
| 17615150 | Lamirand A, Mercier G, Ramauge M, Pierre M, Courtin F: Hypoxia stabilizes type 2 deiodinase activity in rat astrocytes. . Endocrinology. 2007 Oct;148(10):4745-53. Epub 2007 Jul 5. Specific inhibitors of ERK, p38 MAPK, or phosphatidylinositol 3-kinase pathways were without any effect on hypoxia-increased D2 activity, eliminating their role in the effects of hypoxia. Cycloheximide did not block the effect of hypoxia on D2 activity and D2 half-life was enhanced under hypoxia demonstrating a posttranslational action of hypoxia. |
1(0,0,0,1) | Details |
| 17889962 | Busse M, Schwarzburger M, Berger F, Hacker C, Munz B: Strong induction of the Tis11B gene in myogenic differentiation. Eur J Cell Biol. 2008 Jan;87(1):31-8. Epub 2007 Sep 24. Pretreatment of the cells with the translation inhibitor cycloheximide demonstrated that Tis11B was a primary response gene in this process. Since specific inhibitors of p38 MAP kinase completely blocked Tis11B induction, we conclude that expression of the Tis11B gene is regulated at least in part by this signaling pathway which plays a central role in myogenesis. |
1(0,0,0,1) | Details |
| 15956580 | Hargett D, McLean T, Bachenheimer SL: Herpes simplex virus ICP27 activation of stress kinases JNK and p38. . J Virol. 2005 Jul;79(13):8348-60. Cycloheximide reversal or treatment of wild-type virus-infected cells as well as infection with the ICP4 mutant vi13 indicated that only the immediate-early class of viral proteins were required for SAPK activation. |
5(0,0,0,5) | Details |
| 16434099 | Gonzalez TV, Farrant SA, Mantis NJ: Ricin induces IL-8 secretion from human monocyte/macrophages by activating the p38 MAP kinase pathway. Mol Immunol. 2006 Apr;43(11):1920-3. Epub 2006 Jan 24. |
4(0,0,0,4) | Details |
| 18442799 | Ogura H, Tsukumo Y, Sugimoto H, Igarashi M, Nagai K, Kataoka T: ERK and p38 MAP kinase are involved in downregulation of cell surface TNF receptor 1 induced by acetoxycycloheximide. Int Immunopharmacol. 2008 Jun;8(6):922-6. Epub 2008 Mar 18. The protein synthesis inhibitor cycloheximide (CHX) and its structural derivative acetoxycycloheximide (Ac-CHX) have been recently shown to block the TNF-alpha-induced activation of NF-kappaB via ectodomain shedding of TNF receptor 1 (TNF-R1) in human lung carcinoma A549 cells. |
4(0,0,0,4) | Details |
| 16313754 | Wang XY, Li WQ, Lu J, Li N, Li JS: [Mechanism of reduction of albumin expression induced by lipopolysaccharide in rat hepatocytes]. Chin Med J. 2005 Oct 20;118(20):1695-702. The present study was designed to identify if the reduction of albumin expression is directly induced by LPS and modulated by activated extracellular signal-regulated protein kinase (ERK) and p38 mitogen-activated protein kinase (MAPK) in rat hepatocytes. In another group, hepatocytes were pretreated with 100, 40 or 20 micromol/L of cycloheximide (CHX, an inhibitor of protein synthesis) for 30 minutes followed by 1 microg/ml LPS for 24 hours. |
4(0,0,0,4) | Details |
| 17240354 | Sato F, Imaizumi T, Sashinami H, Yoshida H, Kusumi T, Mori F, Wakabayashi K, Nakane A, Satoh K, Kijima H: Upregulation of vascular endothelial growth factor by heat-killed Listeria monocytogenes in macrophages. Biochem Biophys Res Commun. 2007 Mar 9;354(2):608-12. Epub 2007 Jan 16. Pretreatment of cells with cycloheximide, a protein synthesis inhibitor, inhibited the induction of VEGF mRNA by HKLM. Induction of VEGF by HKLM was partially inhibited by treatment of cells with SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor, or a neutralizing antibody against tumor necrosis factor-alpha (TNF-alpha). |
3(0,0,0,3) | Details |
| 16236272 | Ho AK, McNeil L, Terriff D, Price DM, Chik CL: Role of protein turnover in the activation of p38 mitogen-activated protein kinase in rat pinealocytes. Biochem Pharmacol. 2005 Dec 5;70(12):1840-50. Epub 2005 Oct 19. The stimulatory effect of NE on phosphorylated MKK3/6 and p38MAPK, but not phosphorylated p42/44MAPK, was blocked by treatment with actinomycin or cycloheximide, indicating a requirement of transcription and translation in activation of the p38MAPK but not the p42/44MAPK pathway. |
1(0,0,0,1) | Details |
| 17078024 | Ejarque-Ortiz A, Medina MG, Tusell JM, Perez-Gonzalez AP, Serratosa J, Saura J: Upregulation of CCAAT/enhancer binding protein beta in activated astrocytes and microglia. Glia. 2007 Jan 15;55(2):178-88. It is elicited by low concentrations of LPS (almost maximal effect at 1 ng/mL) and it is reversed by the protein synthesis inhibitor cycloheximide. The LPS-induced increase in microglial C/EBPbeta is prevented by coadministration of the MAP kinase inhibitors SB203580 (p38 inhibitor) + SP600125 (JNK inhibitor) or SB203580 + U0126 (ERK inhibitor). |
1(0,0,0,1) | Details |
| 17893873 | Galan-Moya EM, Hernandez-Losa J, Aceves Luquero CI, de la Cruz-Morcillo MA, Ramirez-Castillejo C, Callejas-Valera JL, Arriaga A, Aranburo AF, Ramon y Cajal S, Silvio Gutkind J, Sanchez-Prieto R: c-Abl activates p38 MAPK independently of its kinase activity: Implications in cisplatin-based therapy. Int J Cancer. 2008 Jan 15;122(2):289-97. |
4(0,0,0,4) | Details |
| 16308312 | Yeh CT, Yen GC: Involvement of p38 MAPK and Nrf2 in phenolic acid-induced P-form phenol sulfotransferase expression in human hepatoma HepG2 cells. Carcinogenesis. 2006 May;27(5):1008-17. Epub 2005 Nov 23. Actinomycin D and cycloheximide inhibited -responsive PST-P mRNA expression, indicating that is a requirement for transcription and de novo protein synthesis. |
4(0,0,0,4) | Details |
| 16109301 | Abate A, Yang G, Wong RJ, Schroder H, Stevenson DK, Dennery PA: decreases hemin-mediated heme oxygenase-1 induction. Free Radic Biol Med. 2005 Sep 15;39(6):711-8. Epub 2005 Feb 26. Furthermore, through the use of specific inhibitors, APG's effect was found to be unrelated to its PKC, CK 2, PI 3 K, p38, or ERK inhibitory activities. |
1(0,0,0,1) | Details |
| 18417179 | Asare N, Landvik NE, Lagadic-Gossmann D, Rissel M, Tekpli X, Ask K, Lag M, Holme JA: 1-Nitropyrene (1-NP) induces apoptosis and apparently a non-apoptotic programmed cell death (paraptosis) in Hepa1c1c7 cells. Toxicol Appl Pharmacol. 2008 Jul 15;230(2):175-86. Epub 2008 Feb 29. In contrast, cycloheximide markedly reduced both the number of apoptotic and PI-positive cells as well as the cytoplasmic vacuolization, suggesting that 1-NP induced paraptotic cell death. All the MAPKs; ERK1/2, p38 and JNK, appear to be involved in the death process since marked activation was observed upon 1-NP exposure, and their inhibitors partly reduced the induced cell death. |
1(0,0,0,1) | Details |
| 16734383 | Dunford JE, Rogers MJ, Ebetino FH, Phipps RJ, Coxon FP: Inhibition of protein prenylation by bisphosphonates causes sustained activation of Rac, Cdc42, and Rho GTPases. J Bone Miner Res. 2006 May;21(5):684-94. The Rac-GTP that increased after N-BP treatment was newly translated, cytoplasmic unprenylated protein, because it was not labeled with [(14) C] and the increase in Rac-GTP was prevented by cycloheximide. In macrophages, this also leads to sustained, Rac-mediated activation of p38. |
4(0,0,0,4) | Details |
| 17113042 | Hsu YL, Chang JK, Tsai CH, Chien TT, Kuo PL: induces human osteoblast differentiation through bone morphogenetic protein-2/p38 mitogen-activated protein kinase pathway. Biochem Pharmacol. 2007 Feb 15;73(4):504-14. Epub 2006 Oct 26. Induction of differentiation by is associated with increased activation of SMAD1/5/8 and p38 mitogen-activated protein kinases. |
3(0,0,0,3) | Details |
| 19583809 | Keating N, Mroz MS, Scharl MM, Marsh C, Ferguson G, Hofmann AF, Keely SJ: Physiological concentrations of bile acids down-regulate agonist induced secretion in colonic epithelial cells. J Cell Mol Med. 2009 Aug;13(8B):2293-303. Epub 2009 Jul 6. The EGFr inhibitor, AG1478, and the protein synthesis inhibitor, cycloheximide, reversed the antisecretory effects of DCA, while the MAPK inhibitors, PD98059 and SB203580, did not. DCA (50 microM) rapidly stimulated phosphorylation of the epidermal growth factor receptor (EGFr) and both ERK and p38 MAPKs (mitogen-activated protein kinases). |
1(0,0,0,1) | Details |
| 16874031 | Finn PF, Mesires NT, Vine M, Dice JF: Effects of small molecules on chaperone-mediated autophagy. Autophagy. 2005 Oct-Dec;1(3):141-5. Epub 2005 Oct 11. CMA is also partially inhibited when the p38 mitogen activated protein kinase is blocked. We demonstrate that CMA, like MA, is inhibited by protein synthesis inhibitors anisomycin and cycloheximide. |
1(0,0,0,1) | Details |
| 18086809 | Stone MK, Kolling GL, Lindner MH, Obrig TG: p38 mitogen-activated protein kinase mediates lipopolysaccharide and tumor necrosis factor alpha induction of shiga toxin 2 sensitivity in human umbilical vein endothelial cells. Infect Immun. 2008 Mar;76(3):1115-21. Epub 2007 Dec 17. Cell viability assays indicated that the p38 mitogen-activated protein kinase (MAPK) inhibitors SB202190 and SB203580 and the general protein synthesis inhibitor cycloheximide inhibited both the LPS and TNF-alpha sensitization of HUVEC to Stx2, while all other inhibitors tested did not inhibit this sensitization. |
3(0,0,0,3) | Details |
| 16581040 | Xiong W, Kojic LZ, Zhang L, Prasad SS, Douglas R, Wang Y, Cynader MS: Anisomycin activates p38 MAP kinase to induce LTD in mouse primary visual cortex. Brain Res. 2006 Apr 26;1085(1):68-76. Epub 2006 Apr 11. In contrast, two other protein synthesis inhibitors, emetine and cycloheximide, have no effect either on baseline synaptic transmission or on LTD. |
3(0,0,0,3) | Details |
| 15944291 | Wojciechowski W, Li H, Marshall S, Dell'Agnola C, Espinoza-Delgado I: Enhanced expression of CD20 in human tumor B cells is controlled through ERK-dependent mechanisms. J Immunol. 2005 Jun 15;174(12):7859-68. The effect of bryostatin-1 on CD20 expression in non-Hodgkin's lymphoma cells was mediated through the MAPK kinase/ERK signal transduction pathway and involved protein kinase C, but was independent of p38 MAPK and was insensitive to dexamethasone. |
1(0,0,0,1) | Details |
| 15640153 | Pillinger MH, Marjanovic N, Kim SY, Scher JU, Izmirly P, Tolani S, Dinsell V, Lee YC, Blaser MJ, Abramson SB: Matrix metalloproteinase secretion by gastric epithelial cells is regulated by E prostaglandins and MAPKs. J Biol Chem. 2005 Mar 18;280(11):9973-9. Epub 2005 Jan 7. MMP-1 secretion required activation of the MAPK Erk and subsequent protein synthesis but was down-regulated by the alternate MAPK, p38. |
1(0,0,0,1) | Details |
| 15519673 | Hosoi T, Wada S, Suzuki S, Okuma Y, Akira S, Matsuda T, Nomura Y: Bacterial endotoxin induces IL-20 expression in the glial cells. Brain Res Mol Brain Res. 2004 Nov 4;130(1-2):23-9. Pretreatment with protein synthesis inhibitor puromycin or cycloheximide failed to inhibit the expression of IL-20, suggesting that the expression was not dependent on de novo protein synthesis. Furthermore, a p38 MAP kinase inhibitor, SB203580, inhibited LPS-induced expression of IL-20 mRNA. |
3(0,0,0,3) | Details |
| 17050539 | Tew SR, Hardingham TE: Regulation of SOX9 mRNA in human articular chondrocytes involving p38 MAPK activation and mRNA stabilization. J Biol Chem. 2006 Dec 22;281(51):39471-9. Epub 2006 Oct 18. Disruption of actin stress fibers using any of these redifferentiation stimuli also supported the superinduction of SOX9 by cycloheximide. |
3(0,0,0,3) | Details |
| 19950198 | Sakowicz-Burkiewicz M, Kocbuch K, Grden M, Szutowicz A, Pawelczyk T: Regulation of receptors expression in rat B lymphocytes by insulin. J Cell Biochem. 2010 Feb 1;109(2):396-405. The insulin effect on A (2B)-AR expression was blocked by p38 MAP kinase inhibitor (SB 203580). Pretreatment of B cells with cycloheximide completely blocked the insulin action on A (1)-AR and A (2A)-AR mRNA, but not on A (2B)-AR expression. |
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 |
| 16543731 | Heo JS, Han HJ: PKC and MAPKs pathways mediate EGF-induced stimulation of 2-deoxyglucose uptake in mouse embryonic stem cells. Cell Physiol Biochem. 2006;17(3-4):145-58. Epub 2006 Mar 14. SB 203580 [p38 mitogen activated protein kinase (MAPK) inhibitor] or PD 98059 (p44/42 MAPKs inhibitor) blocked EGF-induced increase of 2-DG uptake. Actinomycin D and cycloheximide completely blocked the effect of EGF on 2-DG uptake. |
3(0,0,0,3) | Details |
| 16467189 | El Sayah M, Medeiros R, Fernandes ES, Campos MM, Calixto JB: Mechanisms underlying lipopolysaccharide-induced kinin B1 receptor up-regulation in the pig iris sphincter in vitro. Mol Pharmacol. 2006 May;69(5):1701-8. Epub 2006 Feb 7. The up-regulation of B1 receptors by lipopolysaccharide stimulation was decreased by the inhibitors of protein synthesis, cycloheximide and actinomycin D, and by dexamethasone and the nuclear factor-kappaB (NF-kappaB) inhibitor pyrrolidinedithiocarbamate (PDTC). In addition, lipopolysaccharide-induced up-regulation of B1 receptors in the pig iris sphincter was significantly reduced by the p38 inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl) (SB203580) and to a lesser extent by the extracellular signal-regulated kinases 1 and 2 (ERK1/2) blocker 2'-amino-3'-methoxyflavone (PD98059). |
2(0,0,0,2) | Details |
| 15743925 | Phagoo SB, Reddi K, Silvallana BJ, Leeb-Lundberg LM, Warburton D: Infection-induced kinin B1 receptors in human pulmonary fibroblasts: role of intact pathogens and p38 mitogen-activated protein kinase-dependent signaling. J Pharmacol Exp Ther. 2005 Jun;313(3):1231-8. Epub 2005 Mar 2. The protein synthesis inhibitor cycloheximide and transcriptional inhibitor actinomycin D abrogated the B (1) response to B. cen. indicating de novo B (1) R synthesis. |
2(0,0,0,2) | Details |
| 16141313 | Tian Q, Li J, Xie X, Sun M, Sang H, Zhou C, An T, Hu L, Ye RD, Wang MW: Stereospecific induction of nuclear factor-kappaB activation by isochamaejasmin. Mol Pharmacol. 2005 Dec;68(6):1534-42. Epub 2005 Sep 1. Isochamaejasmin also induced time-dependent phosphorylation of the mitogen-activated protein kinases extracellular signal-regulated kinase 1/2 and p38, and a novel protein kinase C (PKCdelta). It is noteworthy that the two stereoisomers and the methyl derivative did not induce detectable activation of NF-kappaB and were more cytotoxic than isochamaejasmin, which could partially rescue cycloheximide-induced apoptosis. |
1(0,0,0,1) | Details |
| 16159906 | Liu HS, Chen YH, Hung PF, Kao YH: Inhibitory effect of green tea (-)- on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway. Am J Physiol Endocrinol Metab. 2006 Feb;290(2):E273-81. Epub 2005 Sep 13. Treatment with cycloheximide did not prevent -suppressed Rstn mRNA levels, which suggests that the effect of does not require new protein synthesis. |
0(0,0,0,0) | Details |
| 19439980 | Triggiani M, Granata F, Petraroli A, Loffredo S, Frattini A, Staiano RI, Monaco G, Marone G: Inhibition of secretory phospholipase A2-induced cytokine production in human lung macrophages by budesonide. Int Arch Allergy Immunol. 2009;150(2):144-55. Epub 2009 May 11. Activation of mitogen-activated kinases ERK 1/2 and p38 was assessed by Western blot. |
2(0,0,0,2) | Details |
| 16817231 | Siri S, Chen MJ, Chen TT: Biological activity of rainbow trout Ea4-peptide of the pro-insulin-like growth factor (pro-IGF)-I on promoting attachment of breast cancer cells (MDA-MB-231) via alpha2- and beta1-integrin. J Cell Biochem. 2006 Dec 15;99(6):1524-35. Expression of fibronectin 1 gene induced by rtEa4-peptide in MDA-MB-231 cells was abolished by inhibitors of PI3K, PKC, Mek1/2, JNK1/2, and p38 MAPK signaling transduction molecules. Blocking new protein synthesis by cycloheximide significantly reduced the attachment of MDA-MB-231 cells to rtEa4-peptide coated wells by 50%. |
2(0,0,0,2) | Details |
| 19376214 | Ridley W, Matsuoka M: -induced cyclooxygenase-2 expression and production in A549 human pulmonary epithelial cells. Toxicol Lett. 2009 Aug 10;188(3):180-5. Epub 2009 Apr 17. NaF-induced accumulation of COX-2 transcript was abolished by actinomycin D, but not cycloheximide. Phosphorylated forms of mitogen-activated protein kinases (MAPKs)-including extracellular signal-regulated protein kinase (ERK), c-Jun NH (2)-terminal kinase, and p38-increased after NaF exposure, while treatment with the MAPK/ERK kinase inhibitor U0126 and the p38 inhibitor SB203580 markedly suppressed COX-2 expression. |
2(0,0,0,2) | Details |
| 18223264 | Molloy ES, Morgan MP, Doherty GA, McDonnell B, O'Byrne J, Fitzgerald DJ, McCarthy GM: Mechanism of basic crystal-stimulated matrix metalloproteinase-13 expression by osteoarthritic synovial fibroblasts: inhibition by Ann Rheum Dis. 2008 Dec;67(12):1773-9. Epub 2008 Jan 26. BCP crystal-stimulated MMP-13 mRNA expression was blocked by inhibition of the extracellular regulated kinase (ERK1/2) and p38 mitogen activated protein kinase (MAPK) pathways and inhibition of the activation of nuclear factor kappaB. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | Details |
| 15647476 | Verma P, Chierzi S, Codd AM, Campbell DS, Meyer RL, Holt CE, Fawcett JW: Axonal protein synthesis and degradation are necessary for efficient growth cone regeneration. J Neurosci. 2005 Jan 12;25(2):331-42. Application of protein synthesis inhibitors (cycloheximide and anisomycin) to cut axons, including axons whose cell bodies were removed, or proteasome inhibitors (lactacystin and N-acetyl-Nor---Al) all result in a reduction in the proportion of transected axons able to reform growth cones. Similar inhibition of growth cone formation was observed on addition of target of rapamycin (TOR), p38 MAPK (mitogen-activated protein kinase), and caspase-3 inhibitors. |
2(0,0,0,2) | Details |
| 16951370 | Rahman MS, Yamasaki A, Yang J, Shan L, Halayko AJ, Gounni AS: IL-17A induces eotaxin-1/CC chemokine ligand 11 expression in human airway smooth muscle cells: role of MAPK (Erk1/2, JNK, and p38) pathways. J Immunol. 2006 Sep 15;177(6):4064-71. Moreover, IL-17A significantly induced eotaxin-1/CCL11 release and mRNA expression, an effect that was abrogated with cycloheximide and actinomycin D treatment. |
2(0,0,0,2) | Details |
| 16339571 | Han B, Mura M, Andrade CF, Okutani D, Lodyga M, dos Santos CC, Keshavjee S, Matthay M, Liu M: TNFalpha-induced long pentraxin PTX3 expression in human lung epithelial cells via JNK. J Immunol. 2005 Dec 15;175(12):8303-11. Pretreatment with either actinomycin D or cycloheximide abolished TNF-alpha-induced PTX3 expression, indicating the requirement for both transcriptional and translational regulation. |
0(0,0,0,0) | Details |
| 17067562 | Frias MA, Rebsamen MC, Gerber-Wicht C, Lang U: activates Stat3 in neonatal rat ventricular cardiomyocytes: A role in cardiac hypertrophy. Cardiovasc Res. 2007 Jan 1;73(1):57-65. Epub 2006 Sep 27. Nuclear Stat3 phosphorylation induced by is also suppressed by the translation and transcription inhibitors, cycloheximide and actinomycin D, respectively. |
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 |
| 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. |
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 |
| 19188658 | Kulasekaran P, Scavone CA, Rogers DS, Arenberg DA, Thannickal VJ, Horowitz JC: Endothelin-1 and transforming growth factor-beta1 independently induce fibroblast resistance to apoptosis via AKT activation. Am J Respir Cell Mol Biol. 2009 Oct;41(4):484-93. Epub 2009 Feb 2. Activation of the PI3K/AKT pathway by ET-1 inhibits fibroblast apoptosis, and this inhibition is reversed by blockade of p38 MAPK or PI3K. |
2(0,0,0,2) | Details |
| 17477937 | Lim W, Jung J, Surh Y, Inoue H, Lee Y: Hypertonic and induces COX-2 via different signaling pathways in mouse cortical collecting duct M-1 cells. Life Sci. 2007 May 8;80(22):2085-92. Epub 2007 Apr 1. The treatment also increased COX-2 mRNA accumulation in a cycloheximide-independent manner, suggesting that ongoing protein synthesis is not required for COX-2 induction. The COX-2-inductive effect of hypertonicity was inhibited by SB203580, indicating that the effect is mediated by p38 MAPK. |
2(0,0,0,2) | Details |
| 17308068 | Bachmann M, Dragoi C, Poleganov MA, Pfeilschifter J, Muhl H: Interleukin-18 directly activates T-bet expression and function via p38 mitogen-activated protein kinase and nuclear factor-kappaB in acute myeloid leukemia-derived predendritic KG-1 cells. Mol Cancer Ther. 2007 Feb;6(2):723-31. Blockage of translation by cycloheximide, usage of neutralizing antibodies, and the inability of IFNgamma to mediate significant p38 mitogen-activated protein kinase activation in KG-1 cells clearly revealed that activation of T-bet was not via autocrine IFNgamma. |
2(0,0,0,2) | Details |
| 17941091 | Chiu YC, Huang TH, Fu WM, Yang RS, Tang CH: Ultrasound stimulates MMP-13 expression through p38 and JNK pathway in osteoblasts. J Cell Physiol. 2008 May;215(2):356-65. Cycloheximide (an inhibitor of protein translocation) and actinomycin D (an inhibitor of gene transcription) did not inhibit the MMP-13, c-Fos, and c-Jun mRNA expression, suggesting that such expression does not require de novo protein synthesis and not change their stabilities. p38 inhibitor, SB203580 or JNK inhibitor, SP600125 but not ERK inhibitor, PD98059 attenuated the US-induced MMP-13, c-Fos, and c-Jun expression; these results were further substantiated by transfecting with the dominant negative mutants of p38 or JNK. |
2(0,0,0,2) | 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. |
2(0,0,0,2) | Details |
| 17331500 | Bian ZM, Elner SG, Elner VM: Regulation of VEGF mRNA expression and protein secretion by TGF-beta2 in human retinal pigment epithelial cells. Exp Eye Res. 2007 May;84(5):812-22. Epub 2007 Jan 9. Moreover, TGF-beta2-induced RPE VEGF secretion was significantly reduced by inhibitors of mitogen-activated protein (MAP) kinase (MEK) (U0126), p38 (SB202190), c-Jun NH2-terminal kinase (JNK), Sp600125, protein tyrosine kinase (PTK) and phosphatidylinositol 3-kinase (PI3K) (Ly294002). Stimulation of VEGF expression by TGF-beta2 was blocked by cycloheximide, suggesting that de novo protein synthesis is required. |
2(0,0,0,2) | Details |
| 18162528 | Shankar K, Liu X, Singhal R, Chen JR, Nagarajan S, Badger TM, Ronis MJ: Chronic consumption leads to disruption of homeostasis associated with induction of renal -24-hydroxylase (CYP24A1). Endocrinology. 2008 Apr;149(4):1748-56. Epub 2007 Dec 27. In addition, inhibition of MAPK signaling pathways with the MAPK kinase inhibitor U0126 or the p38 inhibitor SB203580 inhibited EtOH induction of CYP24A1. CYP24A1 mRNA induction in RPTCs was also inhibited by the protein synthesis inhibitor cycloheximide. |
1(0,0,0,1) | Details |
| 17182689 | Mangino G, Percario ZA, Fiorucci G, Vaccari G, Manrique S, Romeo G, Federico M, Geyer M, Affabris E: In vitro treatment of human monocytes/macrophages with myristoylated recombinant Nef of human immunodeficiency virus type 1 leads to the activation of mitogen-activated protein kinases, IkappaB kinases, and interferon regulatory factor 3 and to the release of beta interferon. J Virol. 2007 Mar;81(6):2777-91. Epub 2006 Dec 20. Previously, we reported that Nef treatment of primary human monocyte-derived macrophages (MDMs) induces a cycloheximide-independent activation of NF-kappaB and the synthesis and secretion of a set of chemokines/cytokines that activate STAT1 and STAT3. Here, we show that Nef treatment is capable of hijacking cellular signaling pathways, inducing a very rapid regulatory response in MDMs that is characterized by the rapid and transient phosphorylation of the alpha and beta subunits of the IkappaB kinase complex and of JNK, ERK1/2, and p38 mitogen-activated protein kinase family members. |
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| 17177854 | Neu R, Adams S, Munz B: Differential expression of entactin-1/nidogen-1 and entactin-2/nidogen-2 in myogenic differentiation. Differentiation. 2006 Dec;74(9-10):573-82. Furthermore, treatment with the translation inhibitor cycloheximide could show that entactin-2 is a primary response gene. As p38 MAP kinase is an important regulator of myogenic differentiation, we also analyzed the possibility that entactin-2 might be a target of this pathway. |
1(0,0,0,1) | Details |
| 18422969 | Necela BM, Su W, Thompson EA: Toll-like receptor 4 mediates cross-talk between peroxisome proliferator-activated receptor gamma and nuclear factor-kappaB in macrophages. Immunology. 2008 Nov;125(3):344-58. Epub 2008 Apr 18. Inhibition of PPARgamma expression was not blocked by cycloheximide, indicating that de novo protein synthesis is not required for LPS-mediated suppression of PPARgamma. |
0(0,0,0,0) | Details |
| 16034134 | Grehan JF, Levay-Young BK, Fogelson JL, Francois-Bongarcon V, Benson BA, Dalmasso AP: IL-4 and IL-13 induce protection of porcine endothelial cells from killing by human complement and from apoptosis through activation of a phosphatidylinositide 3-kinase/Akt pathway. J Immunol. 2005 Aug 1;175(3):1903-10. We found that porcine EC incubated with IL-4 or IL-13, but not with IL-10 or IL-11, became protected from killing by complement and apoptosis induced by TNF-alpha plus cycloheximide. |
0(0,0,0,0) | Details |
| 18184892 | Young SR, Bianchi R, Wong RK: Signaling mechanisms underlying group I mGluR-induced persistent AHP suppression in CA3 hippocampal neurons. J Neurophysiol. 2008 Mar;99(3):1105-18. Epub 2008 Jan 9. Preincubation of slices in inhibitors of protein synthesis (cycloheximide or anisomycin) prevented the persistent suppression of AHPs by Similarly, preincubation of slices in an inhibitor of p38 MAP kinase (SB 203580) prevented persistent AHP suppression. |
2(0,0,0,2) | Details |
| 19041363 | Asare N, Lag M, Lagadic-Gossmann D, Rissel M, Schwarze P, Holme JA: 3-Nitrofluoranthene (3-NF) but not 3-aminofluoranthene (3-AF) elicits apoptosis as well as programmed necrosis in Hepa1c1c7 cells. Toxicology. 2009 Jan 31;255(3):140-50. Epub 2008 Nov 7. Cycloheximide completely attenuated 3-NF-induced cell death. Increase in the number as well as size of lysosomes, myelinosomes, and activation of autophagy were also observed. 3-NF induced phosphorylation of ERK1/2, JNK and p38 MAPKs. |
2(0,0,0,2) | Details |
| 16495213 | Carraro-Lacroix LR, Ramirez MA, Zorn TM, Reboucas NA, Malnic G: Increased NHE1 expression is associated with serum deprivation-induced differentiation in immortalized rat proximal tubule cells. Am J Physiol Renal Physiol. 2006 Jul;291(1):F129-39. Epub 2006 Feb 21. The altered activity of NHE1 was consistent with an increase of both transcription and translation of the antiporter, as the utilization of actinomycin D and cycloheximide significantly inhibited the upregulation of NHE1 induced by serum withdrawal. |
0(0,0,0,0) | Details |
| 17532486 | Lin HY, Shen SC, Lin CW, Yang LY, Chen YC: Baicalein inhibition of peroxide-induced apoptosis via ROS-dependent heme oxygenase 1 gene expression. Biochim Biophys Acta. 2007 Jul;1773(7):1073-86. Epub 2007 Apr 22. In the present study, baicalein (BE) but not its glycoside, baicalin (BI), induced heme oxygenase-1 (HO-1) gene expression at both the mRNA and protein levels, and the BE-induced HO-1 protein was blocked by adding cycloheximide (CHX) or actinomycin D (Act D). |
0(0,0,0,0) | Details |
| 19396617 | Carraro-Lacroix LR, Girardi AC, Malnic G: Long-term regulation of vacuolar H (+)-ATPase by angiotensin II in proximal tubule cells. Pflugers Arch. 2009 Sep;458(5):969-79. Epub 2009 Apr 26. Inhibition of phosphatidylinositol-3-kinase (PI3K) by wortmannin and of p38 mitogen-activated protein kinase (MAPK) by SB 203580 also blocked this effect. |
2(0,0,0,2) | Details |
| 19286921 | Croons V, Martinet W, Herman AG, Timmermans JP, De Meyer GR: The protein synthesis inhibitor anisomycin induces macrophage apoptosis in rabbit atherosclerotic plaques through p38 mitogen-activated protein kinase. J Pharmacol Exp Ther. 2009 Jun;329(3):856-64. Epub 2009 Mar 13. We showed recently that the protein synthesis inhibitor cycloheximide, in contrast to puromycin, selectively depleted macrophages in rabbit atherosclerotic plaques without affecting smooth muscle cells (SMCs). |
2(0,0,0,2) | Details |
| 17209135 | Kuang PP, Zhang XH, Rich CB, Foster JA, Subramanian M, Goldstein RH: Activation of elastin transcription by transforming growth factor-beta in human lung fibroblasts. Am J Physiol Lung Cell Mol Physiol. 2007 Apr;292(4):L944-52. Epub 2007 Jan 5. The induction of elastin hnRNA and mRNA expression by TGF-beta was abolished by pretreatments with TGF-beta receptor I inhibitor, global transcription inhibitor actinomycin D, and partially blocked by addition of protein synthesis inhibitor cycloheximide, but was not affected by the p44/42 MAPK inhibitor U0126. |
0(0,0,0,0) | Details |
| 16740979 | Chen YH, Lee MJ, Chang HH, Hung PF, Kao YH: 17 beta- stimulates resistin gene expression in 3T3-L1 adipocytes via the estrogen receptor, extracellularly regulated kinase, and CCAAT/enhancer binding protein-alpha pathways. Endocrinology. 2006 Sep;147(9):4496-504. Epub 2006 Jun 1. Treatment with either actinomycin D or cycloheximide prevented E2-stimulated resistin mRNA expression, suggesting that the effect of E2 requires new mRNA and protein synthesis. |
0(0,0,0,0) | 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. In contrast to CHX, E-73 drastically induced activation of extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and p38 MAP kinase. |
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 |
| 17659437 | Reidy MR, Ellis J, Schmitz EA, Kraus DM, Bulla GA: Apoptosis of dedifferentiated hepatoma cells is independent of NF-kappaB activation in response to LPS. Biosci Rep. 2007 Oct;27(4-5):235-46. Dedifferentiated hepatoma cells, in contrast to most other cell types including hepatoma cells, undergo apoptosis when treated with lipopolysaccharide (LPS) plus the protein synthesis inhibitor cycloheximide (CHx). |
0(0,0,0,0) | Details |
| 17495535 | Lee SH, Lee SJ, Kim JH, Park BJ: Chemical carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine, is a specific activator of oncogenic Ras. Cell Cycle. 2007 May 15;6(10):1257-64. Epub 2007 May 6. Activation of Erk by MNNG could not suppressed by cycloheximide and ALLN. |
0(0,0,0,0) | Details |
| 17706224 | Zhang W, Zhang Y, Edvinsson L, Xu CB: Up-regulation of thromboxane A2 receptor expression by lipid soluble smoking particles through post-transcriptional mechanisms. Atherosclerosis. 2008 Feb;196(2):608-16. Epub 2007 Aug 13. This up-regulation was not affected by a general transcriptional inhibitor actinomycin D, but was almost completely abolished by cycloheximide, a general translational inhibitor. |
0(0,0,0,0) | Details |
| 15671029 | Vertino AM, Bula CM, Chen JR, Almeida M, Han L, Bellido T, Kousteni S, Norman AW, Manolagas SC: Nongenotropic, anti-apoptotic signaling of 1alpha,25 (OH) 2- and analogs through the ligand binding domain of the receptor in osteoblasts and osteocytes. J Biol Chem. 2005 Apr 8;280(14):14130-7. Epub 2005 Jan 25. Finally, actinomycin D or cycloheximide prevented the anti-apoptotic effect of 1alpha,25 (OH) 2D3, indicating that transcriptional events are also required. |
0(0,0,0,0) | Details |
| 16452486 | Seymour KJ, Roberts LE, Fini MA, Parmley LA, Oustitch TL, Wright RM: Stress activation of mammary epithelial cell xanthine oxidoreductase is mediated by p38 MAPK and CCAAT/enhancer-binding protein-beta. J Biol Chem. 2006 Mar 31;281(13):8545-58. Epub 2006 Feb 1. We demonstrate here that XOR was induced in HC11 cells by low dose cycloheximide and that expression was blocked by inhibitors of p38 MAPK. |
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| 18339016 | Fujisawa T, Ide K, Holtzman MJ, Suda T, Suzuki K, Kuroishi S, Chida K, Nakamura H: Involvement of the p38 MAPK pathway in IL-13-induced mucous cell metaplasia in mouse tracheal epithelial cells. Respirology. 2008 Mar;13(2):191-202. Cycloheximide also diminished activation of p38 MAPK and induction of MUC5AC mRNA expression by IL-13. |
85(1,1,1,5) | Details |
| 17197193 | Fritzenwanger M, Meusel K, Foerster M, Kuethe F, Krack A, Figulla HR: Cardiotrophin-1 induces interleukin-6 synthesis in human umbilical vein endothelial cells. Cytokine. 2006 Nov;36(3-4):101-6. Epub 2007 Jan 2. For the pathway determination following inhibitors were used: (signal transducer and activation of transcription (STAT) 3 phosphorylation), wortmannin (phosphatiylinositol 3-kinase (PI3K)), SB203580 (p38 mitogen-activated protein kinase (MAPK)), AG490 (Janus kinase (JAK) 2), PD98059 (mitogen-activated protein kinase kinase (MEK) 1/2), parthenolide (nuclear factor kappaB) and cycloheximide (protein biosynthesis). |
82(1,1,1,2) | Details |
| 16464966 | Balzary RW, Cocks TM: Lipopolysaccharide induces epithelium- and (2)-dependent relaxation of mouse isolated trachea through activation of cyclooxygenase (COX)-1 and COX-2. J Pharmacol Exp Ther. 2006 May;317(2):806-12. Epub 2006 Feb 7. The LPS antagonist polymixin B; the nonselective COX inhibitor indomethacin; the selective COX-1 and COX-2 inhibitors 5-(4-chlorophenyl)-1-(4-methoxyphenyl)-3-(trifluoromethyl)-1H-pyrazole (SC560) and 4-[5-(4-chlorophenyl)-1-(trifluoromethyl)-1H-pyrazol-1-yl]-benzenesulfonam ide (SC236), respectively; the transcription inhibitor actinomycin D; the translation inhibitor cycloheximide; the p38 mitogen-activated protein kinase (p38 MAPK) inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)-1H-imadazole (SB203580); and a combination of the mixed DP/EP1/EP2 receptor antagonist 6-isopropoxy-9-xanthone-2-carboxylic acid (AH6809) and the EP4 receptor antagonist 4'-[3-butyl-5-oxo-1-(2-trifluoromethyl-phenyl)-1-5-dihydro-[1,2,4] triazol- 4-ylmethyl]-biphenyl-2- (3-methyl-thiophene-2-carbonyl)-amide (L-161982) all abolished relaxation to LPS, giving instead slowly developing, small contractions over 60 min. |
32(0,1,1,2) | Details |
| 15531589 | Gerhard R, Tatge H, Genth H, Thum T, Borlak J, Fritz G, Just I: Clostridium difficile toxin A induces expression of the stress-induced early gene product RhoB. J Biol Chem. 2005 Jan 14;280(2):1499-505. Epub 2004 Nov 5. The up-regulation of RhoB was approximately 15-fold and was based on the de novo synthesis of the GTPase because cycloheximide completely inhibited the toxin A effect. The p38 MAPK inhibitor SB202190 reduced the expression of RhoB, indicating a participation of the p38 MAPK in this stress response. |
1(0,0,0,1) | Details |
| 19384564 | Smith AJ, Smith RA, Stone TW: 5-Hydroxyanthranilic acid, a metabolite, generates oxidative stress and neuronal death via p38 activation in cultured cerebellar granule neurones. Neurotox Res. 2009 May;15(4):303-10. Epub 2009 Mar 4. |
1(0,0,0,1) | Details |
| 17501665 | Lambert C, Oury C, Dejardin E, Chariot A, Piette J, Malaise M, Merville MP, Franchimont N: Further insights in the mechanisms of interleukin-1beta stimulation of osteoprotegerin in osteoblast-like cells. J Bone Miner Res. 2007 Sep;22(9):1350-61. Post-transcriptional effects were examined by using cycloheximide and actinomycin D. |
0(0,0,0,0) | 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. -induced HO-1 protein expression was inhibited by actinomycin D and cycloheximide, suggesting that de novo transcription and translation are required in this process. |
0(0,0,0,0) | Details |
| 19657054 | Tew SR, Peffers MJ, McKay TR, Lowe ET, Khan WS, Hardingham TE, Clegg PD: Hyperosmolarity regulates SOX9 mRNA posttranscriptionally in human articular chondrocytes. Am J Physiol Cell Physiol. 2009 Oct;297(4):C898-906. Epub 2009 Aug 5. We previously showed that activation of p38 MAPK by cycloheximide in human chondrocytes leads to stabilization of SOX9 mRNA (Tew SR and Hardingham TE. |
83(1,1,1,3) | Details |
| 19233135 | Kato T, Ikemoto M, Hato F, Kitagawa S: Granule swelling and cleavage of mitogen-activated protein kinases in human neutrophils undergoing apoptosis. Biochem Biophys Res Commun. 2009 Apr 10;381(3):434-8. Epub 2009 Feb 20. Extracellular signal-regulated kinase and p38 have been shown to be cleaved in human neutrophils undergoing apoptosis induced by tumor necrosis factor-alpha and cycloheximide. |
81(1,1,1,1) | Details |
| 15805247 | Cinar B, De Benedetti A, Freeman MR: Post-transcriptional regulation of the androgen receptor by Mammalian target of rapamycin. Cancer Res. 2005 Apr 1;65(7):2547-53. The signal to attenuate AR was mediated by the mammalian target of rapamycin, as shown by genetic and pharmacologic methods, and was independent of ErbB2/HER-2, extracellular signal-regulated kinase 1/2, and p38 mitogen-activated protein kinase pathways. |
1(0,0,0,1) | Details |
| 19289468 | Kurada BR, Li LC, Mulherkar N, Subramanian M, Prasad KV, Prabhakar BS: MADD, a splice variant of IG20, is indispensable for MAPK activation and protection against apoptosis upon tumor necrosis factor-alpha treatment. J Biol Chem. 2009 May 15;284(20):13533-41. Epub 2009 Mar 16. We investigated the physiological role of endogenous MAPK-activating death domain-containing protein (MADD), a splice variant of the IG20 gene, that can interact with TNFR1 in tumor necrosis factor-alpha (TNFalpha)-induced activation of NF-kappaB, MAPK, ERK1/2, JNK, and p38. Abrogation of MADD expression rendered cells highly susceptible to TNFalpha-induced apoptosis in the absence of cycloheximide. |
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| 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. |
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| 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 |
| 18337456 | Robinson VL, Shalhav O, Otto K, Kawai T, Gorospe M, Rinker-Schaeffer CW: Mitogen-activated protein kinase kinase 4/c-Jun NH2-terminal kinase kinase 1 protein expression is subject to translational regulation in prostate cancer cell lines. Mol Cancer Res. 2008 Mar;6(3):501-8. Mitogen-activated protein kinase kinase 4/c-Jun NH (2)-terminal kinase kinase 1 (MKK4/JNKK1; hereafter referred to as MKK4) is a dual-specificity kinase with a critical role in regulating the activity of c-Jun NH (2)-terminal kinase and p38 kinases. |
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| 16684952 | Cohen M, Marchand-Adam S, Lecon-Malas V, Marchal-Somme J, Boutten A, Durand G, Crestani B, Dehoux M: HGF synthesis in human lung fibroblasts is regulated by oncostatin M. . Am J Physiol Lung Cell Mol Physiol. 2006 Jun;290(6):L1097-103. OSM-induced HGF secretion was inhibited by PD-98059 (a specific pharmacological inhibitor of ERK1/2), SB-203580 (a p38 MAPK inhibitor), and SP-600125 (a JNK inhibitor) by 70, 82, and 100%, respectively, whereas basal HGF secretion was only inhibited by SP-600125 by 30%. HGF was released in its cleaved mature form, and its secretion was completely inhibited in the presence of cycloheximide, indicating a de novo protein synthesis. |
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| 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. |
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| 18708082 | Luo SF, Lin CC, Chen HC, Lin WN, Lee IT, Lee CW, Hsiao LD, Yang CM: Involvement of MAPKs, NF-kappaB and p300 co-activator in IL-1beta-induced cytosolic phospholipase A2 expression in canine tracheal smooth muscle cells. Toxicol Appl Pharmacol. 2008 Nov 1;232(3):396-407. Epub 2008 Jul 29. IL-1beta-induced cPLA2 expression and production was inhibited by actinomycin D and cycloheximide, indicating the involvement of transcriptional and translational events in these responses. |
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| 15714461 | Shi YH, Wang YX, Bingle L, Gong LH, Heng WJ, Li Y, Fang WG: In vitro study of HIF-1 activation and VEGF release by bFGF in the T47D breast cancer cell line under normoxic conditions: involvement of PI-3K/Akt and MEK1/ERK pathways. J Pathol. 2005 Mar;205(4):530-6. In addition, the translation inhibitor cycloheximide confirmed that bFGF-induced HIF-1alpha protein expression was due to de novo protein synthesis. |
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| 17194804 | Lee SY, Cherla RP, Tesh VL: Simultaneous induction of apoptotic and survival signaling pathways in macrophage-like THP-1 cells by Shiga toxin 1. Infect Immun. 2007 Mar;75(3):1291-302. Epub 2006 Dec 28. Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. |
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| 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 involvement of the p38 and JNK pathways in the selective effects of anisomycin and cycloheximide on MMP/TIMP expression was supported by use of pharmacological inhibitors. |
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