| Name | Protein S |
|---|---|
| Synonyms | PROS; PSA; PROS 1; PROS 2; PROS1; PROS2; PROSP; PS 26… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17200126 | Adams KW, Cooper GM: Rapid turnover of mcl-1 couples translation to cell survival and apoptosis. J Biol Chem. 2007 Mar 2;282(9):6192-200. Epub 2007 Jan 2. Induction of apoptosis by cycloheximide was detected within 2-4 h and blocked by proteasome inhibitors, indicating that degradation of short-lived protein (s) was required. |
82(1,1,1,2) | Details |
| 18223147 | Chung HS, Koo AJ, Gao X, Jayanty S, Thines B, Jones AD, Howe GA: Regulation and function of Arabidopsis JASMONATE ZIM-domain genes in response to wounding and herbivory. Plant Physiol. 2008 Mar;146(3):952-64. Epub 2008 Jan 25. Experiments performed with the protein synthesis inhibitor cycloheximide provided evidence that JAZs, MYC2, and genes encoding several JA biosynthetic enzymes are primary response genes whose expression is derepressed upon COI1-dependent turnover of a labile repressor protein (s). |
31(0,1,1,1) | Details |
| 16888780 | Wieckowski E, Atarashi Y, Stanson J, Sato TA, Whiteside TL: FAP-1-mediated activation of NF-kappaB induces resistance of head and neck cancer to Fas-induced apoptosis. J Cell Biochem. 2007 Jan 1;100(1):16-28. In the presence of cycloheximide, the selected SCCHN sublines become susceptible to CH-11 Ab, and showed cleavage of caspase-8, suggesting that apoptosis resistance was mediated by an inhibitory protein (s) acting upstream of caspase-8. |
31(0,1,1,1) | Details |
| 17014691 | Fernandes PA, Cecon E, Markus RP, Ferreira ZS: Effect of TNF-alpha on the synthetic pathway in the rat pineal gland: basis for a 'feedback' of the immune response on circadian timing. J Pineal Res. 2006 Nov;41(4):344-50. In fact, a protein (s) transcribed, later on, as shown by cycloheximide, was responsible for the reversal of the inhibition of Aa-nat transcription. |
31(0,1,1,1) | Details |
| 17599377 | Khan S, Liu S, Stoner M, Safe S: Cobaltous chloride and hypoxia inhibit aryl hydrocarbon receptor-mediated responses in breast cancer cells. Toxicol Appl Pharmacol. 2007 Aug 15;223(1):28-38. Epub 2007 May 25. These results suggest that hypoxia rapidly induces protein (s) that inhibit Ah-responsiveness and these may be similar to constitutively expressed inhibitors of Ah-responsiveness (under normoxia) that are also inhibited by cycloheximide. |
31(0,1,1,1) | Details |
| 16252307 | Meloni BP, Van Dyk D, Cole R, Knuckey NW: Proteome analysis of cortical neuronal cultures following cycloheximide, heat stress and MK801 preconditioning. Proteomics. 2005 Dec;5(18):4743-53. Of 150 differentially expressed protein spots selected for identification the protein or tentative protein (s) were identified in 84 cases, representing 50 different proteins. |
2(0,0,0,2) | Details |
| 16236128 | Ding A, Yu H, Yang J, Shi S, Ehrt S: Induction of macrophage-derived SLPI by Mycobacterium tuberculosis depends on TLR2 but not MyD88. Immunology. 2005 Nov;116(3):381-9. This induction signifies the presence of a TLR2-dependent but MyD88-independent M. tuberculosis signalling pathway, suggesting involvement of adaptor protein (s) other than MyD88 in M. tuberculosis-mediated induction of SLPI. HK-Mtb-induced SLPI mRNA expression was sensitive neither to a protein synthesis inhibitor, cycloheximide, nor to an actin polymerization blocker, cytochalasin D. |
1(0,0,0,1) | 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. The activation of Stat3 occurs mainly through EP4 and involves ERK1/2 as well as newly synthesized protein (s). Nuclear Stat3 phosphorylation induced by is also suppressed by the translation and transcription inhibitors, cycloheximide and actinomycin D, respectively. |
1(0,0,0,1) | Details |
| 19843871 | Qi D, Cai K, Wang O, Li Z, Chen J, Deng B, Qian L, Le Y: Fatty acids induce amylin expression and secretion by pancreatic {beta}-cells. Am J Physiol Endocrinol Metab. 2009 Oct 20. Ca (2+) and PKC signaling pathways and de novo synthesized protein (s) were involved in FA-induced amylin expression. Pretreatment of MIN6 cells with Ca (2+) chelator (EGTA, BAPTA/AM), protein kinase C (PKC) inhibitor Go6976, or protein synthesis inhibitor cycloheximide significantly inhibited FA-induced amylin mRNA expression. |
1(0,0,0,1) | Details |
| 15561559 | Dewitte-Orr SJ, Zorzitto JR, Sutton LP, Bols NC: Preferential induction of apoptosis in the rainbow trout macrophage cell line, RTS11, by actinomycin D, cycloheximide and double stranded RNA. Fish Shellfish Immunol. 2005 Apr;18(4):279-95. The sensitizing of RTS11 to poly IC killing by AMD or CHX could be explained by a decrease in the level of a short-lived anti-apoptotic protein (s) and/or by the triggering of a ribotoxic stress. The rainbow trout macrophage cell line RTS11 was found to be considerably more sensitive than rainbow trout fibroblast (RTG-2) and Chinook salmon epithelial (CHSE-214) cell lines to killing by macromolecular synthesis inhibitors, actinomycin D (AMD) and cycloheximide (CHX), a synthetic double stranded RNA (dsRNA), polyinosinic:polycytidylic acid (poly IC), and combinations of poly IC with AMD or CHX. |
1(0,0,0,1) | Details |
| 18187254 | Li L, Wong CK: Effects of dexamethasone and dibutyryl cAMP on stanniocalcin-1 mRNA expression in rat primary Sertoli and Leydig cells. Mol Cell Endocrinol. 2008 Feb 13;283(1-2):96-103. Epub 2007 Dec 3. In addition, both DEX and dbcAMP mediated effects were found to be abolished by cycloheximide co-treatment. We suggested that the de novo synthesis of other protein (s) and mRNA may be involved in the regulation of the steady-state levels of STC1 mRNA in the treatments. |
1(0,0,0,1) | Details |
| 16133866 | Drexler HC, Euler M: Synergistic apoptosis induction by proteasome and histone deacetylase inhibitors is dependent on protein synthesis. Apoptosis. 2005 Aug;10(4):743-58. These results demonstrated that transcriptional activation by HDIs combined with proteasome inhibitor mediated posttranslational stabilization of protein (s) results in significantly enhanced CML apoptosis which was striktly dependent on uninterrupted protein synthesis. The most striking anti-apoptotic effect though was obtained by the translational inhibitor cycloheximide, which abolished caspase 8 processing, blocked Bid cleavage and maintained the mitochondrial transmembrane potential. |
1(0,0,0,1) | Details |
| 16904349 | Kovar J, Neubauerova J, Cimburova M, Truksa J, Balusikova K, Horak J: Stimulation of non-transferrin iron uptake by iron deprivation in K562 cells. Blood Cells Mol Dis. 2006 Sep-Oct;37(2):95-9. Epub 2006 Aug 9. The preincubation of K562 cells in iron-free medium together with the inhibitor of protein synthesis cycloheximide completely abrogated the stimulation of the iron uptake. It seems that the expression of an unknown or seemingly unrelated protein (s) is involved. |
1(0,0,0,1) | Details |
| 17397878 | Sekizawa K, Suzuki T, Kishi K: Cytogenetic study of the induction mechanism of chromosome-type aberrations by 1-beta-D-arabinofuranosylcytosine. Mutat Res. 2007 Jun 1;619(1-2):1-8. Epub 2007 Feb 25. Second, we demonstrate that the induction of DSBs or chromosome-type aberrations by AraC in human lymphocytes is inhibited by cycloheximide (CHM), an inhibitor of protein synthesis. Thus, we suggest that AraC-induced endonucleolytic protein (s) in lymphocytes mediate the formation of chromosome-type aberrations. |
1(0,0,0,1) | Details |
| 19115040 | Albrecht EA, Sarma JV, Ward PA: Activation by C5a of endothelial cell caspase 8 and cFLIP. Inflamm Res. 2009 Jan;58(1):30-7. CONCLUSIONS: These data suggest caspase 8 activation induced by C5a leads to cell death if protein synthesis of antiapoptotic protein (s) is blocked. |
1(0,0,0,1) | Details |
| 18433744 | Ishikawa F, Nose K, Shibanuma M: Downregulation of hepatocyte nuclear factor-4alpha and its role in regulation of gene expression by TGF-beta in mammary epithelial cells. Exp Cell Res. 2008 Jun 10;314(10):2131-40. Epub 2008 Mar 29. The repression was interfered by dominant negative forms of activin receptor-like kinase 5 (ALK5) and Smad3, and sensitive to cycloheximide, suggesting the involvement of additional protein (s) as well as ALK5 and Smad3 in the repression. |
0(0,0,0,0) | Details |
| 16824201 | Dimitrova DS: Nuclear transcription is essential for specification of mammalian replication origins. Genes Cells. 2006 Jul;11(7):829-44. Random initiation was not a consequence of inability to produce an essential protein (s), since initiation was site-specific within cells exposed to the translation inhibitor cycloheximide during the same interval of G1 phase. |
0(0,0,0,0) | Details |