| Name | protein as |
|---|---|
| Synonyms | A1 activator; PSAP; Protein C; CSAct; Cerebroside sulfatase activator; Cerebroside sulfate activator; Co beta glucosidase; Component C… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 17324936 | Saeki M, Irie Y, Ni L, Itsuki Y, Terao Y, Kawabata S, Kamisaki Y: Calcineurin potentiates the activation of procaspase-3 by accelerating its proteolytic maturation. J Biol Chem. 2007 Apr 20;282(16):11786-94. Epub 2007 Feb 26. Analysis by tandem mass spectrometry identified the protein as a regulatory subunit of calcineurin (calcineurin B). Overexpression of calcineurin B in HEK293 cells potentiated processing of caspase-3 and apoptosis triggered by tumor necrosis factor-alpha and cycloheximide treatment. |
1(0,0,0,1) | Details |
| 16988256 | Dennis VA, Jefferson A, Singh SR, Ganapamo F, Philipp MT: Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3. Infect Immun. 2006 Oct;74(10):5780-9. We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. Neither endogenous IL-10 nor the translation inhibitor cycloheximide blocked SOCS1/SOCS3 induction by B. burgdorferi and its lipoproteins, indicating that the expression of other genes is not required. |
1(0,0,0,1) | Details |
| 15561096 | Rivedal E, Leithe E: Connexin43 synthesis, phosphorylation, and degradation in regulation of transient inhibition of gap junction intercellular communication by the phorbol ester TPA in rat liver epithelial cells. Exp Cell Res. 2005 Jan 15;302(2):143-52. The data presented suggest that restoration of GJIC during continuous TPA exposure in normal and transformed rat liver epithelial cells is dependent on synthesis of Cx43 protein, as well as the transport of already synthesized Cx43 from intracellular pools to the plasma membrane. We show that coincubation of TPA with the protein synthesis inhibitor cycloheximide or the transcription inhibitor actinomycin D results in synergistic enhancement of the level of activated ERK1/2. |
1(0,0,0,1) | Details |
| 15814588 | Kuang PP, Goldstein RH: Regulation of elastin gene transcription by proteasome dysfunction. Am J Physiol Cell Physiol. 2005 Sep;289(3):C766-73. Epub 2005 Apr 6. We previously found that the downregulation of elastin gene transcription by IL-1beta is mediated via activation of NF-kappaB and CCAAT/enhancer binding protein (C/EBP) beta, both targets of the ubiquitin-proteasome pathway. Addition of cycloheximide blocked these increases and the downregulation of elastin mRNA by MG-132. |
1(0,0,0,1) | Details |
| 16245312 | Jinnin M, Ihn H, Asano Y, Yamane K, Trojanowska M, Tamaki K: Platelet derived growth factor induced tenascin-C transcription is phosphoinositide 3-kinase/Akt-dependent and mediated by Ets family transcription factors. J Cell Physiol. 2006 Mar;206(3):718-27. PDGF induced the expression of TN-C protein as well as mRNA in a dose-dependent manner. Actinomycin D, an RNA synthesis inhibitor, significantly blocked the PDGF-mediated upregulation of TN-C mRNA expression, whereas cycloheximide, a protein synthesis inhibitor, did not. |
1(0,0,0,1) | Details |
| 16359394 | Shen H, Moon J, Huq E: PIF1 is regulated by light-mediated degradation through the ubiquitin-26S proteasome pathway to optimize photomorphogenesis of seedlings in Arabidopsis. Plant J. 2005 Dec;44(6):1023-35. Further, de novo protein synthesis is not required for degradation of PIF1, as the presence of cycloheximide does not prevent degradation of PIF1 in the light. In this study we use the luciferase (LUC) activity of the LUC-PIF1 fusion protein as an indicator of the stability of PIF1 in various light conditions. |
1(0,0,0,1) | Details |
| 15604115 | Yeagley D, Quinn PG: 3',5'-cyclic adenosine monophosphate response element-binding protein and CCAAT enhancer-binding protein are dispensable for insulin inhibition of phosphoenolpyruvate carboxykinase transcription and for its synergistic induction by protein kinase A and glucocorticoids. Mol Endocrinol. 2005 Apr;19(4):913-24. Epub 2004 Dec 16. Recent reports suggested that CCAAT enhancer binding protein (C/EBP) binding to the PEPCK cAMP response element (CRE) plays a role in Dex induction and that insulin-induces inhibitory forms of C/EBPbeta to inhibit transcription. Cycloheximide did not block insulin inhibition, indicating that alternate translation of C/EBPbeta is not required. |
1(0,0,0,1) | Details |
| 17711404 | Chan SC, Lin SC, Li P: Regulation of Cidea protein stability by the ubiquitin-mediated proteasomal degradation pathway. Biochem J. 2007 Dec 1;408(2):259-66. In the present study we show that Cidea is a short-lived protein as measured by cycloheximide-based protein chase experiments in different cell lines or in differentiated brown adipocytes. |
6(0,0,1,1) | Details |
| 17947515 | Ahasan MM, Sweet C: Murine cytomegalovirus open reading frame m29.1 augments virus replication both in vitro and in vivo. J Gen Virol. 2007 Nov;88(Pt 11):2941-51. This delayed death until 31 days post-infection (p.i.) compared with wt (23 days p.i.) but at death virus yields were similar to wt. m29 gene transcription was initiated at early times post-infection, while production of a transcript from ORF m29.1 in the presence of cycloheximide indicated that it was an immediate-early gene. However, it is likely that each ORF expresses its own protein, as antiserum derived in rabbits to the m29.1 protein expressed in bacteria from the m29.1 ORF detected only one protein in Western blot analysis of the size predicted for the m29.1 protein. |
1(0,0,0,1) | Details |
| 18343803 | Oliver BG, Silver PM, White TC: Polyene susceptibility is dependent on nitrogen source in the opportunistic pathogen Candida albicans. J Antimicrob Chemother. 2008 Jun;61(6):1302-8. Epub 2008 Mar 13. This study evaluates the effect of protein as a nitrogen source on drug susceptibilities. Similar results were observed for cycloheximide, but not for fluconazole or caspofungin, and were observed for many C. albicans clinical isolates. |
1(0,0,0,1) | Details |
| 15780883 | Liu WJ, Chang YS, Wang CH, Kou GH, Lo CF: Microarray and RT-PCR screening for white spot syndrome virus immediate-early genes in cycloheximide-treated shrimp. Virology. 2005 Apr 10;334(2):327-41. In a promoter activity assay in Sf9 insect cells using EGFP (enhanced green fluorescence protein) as a reporter, ie1 showed very strong promoter activity, producing higher EGFP signals than the insect Orgyia pseudotsugata multicapsid nuclear polyhedrosis virus (OpMNPV) ie2 promoter. |
1(0,0,0,1) | Details |
| 20036734 | Yoon MJ, Kim EH, Lim JH, Kwon TK, Choi KS: and proteasomal dysfunction contribute to -induced paraptosis of malignant breast cancer cells. Free Radic Biol Med. 2010 Mar 1;48(5):713-26. Epub 2009 Dec 28. Inhibition of protein synthesis by cycloheximide blocked -induced vacuolation and subsequent cell death, indicating that protein synthesis is required for this process. The levels of AIP-1/Alix protein, a known inhibitor protein of paraptosis, were progressively downregulated in -treated malignant breast cancer cells, and AIP-1/Alix overexpression attenuated -induced death in these cells. |
1(0,0,0,1) | Details |
| 17245642 | Chen SP, Wu JL, Su YC, Hong JR: Anti-Bcl-2 family members, zfBcl-x (L) and zfMcl-1a, prevent cytochrome c release from cells undergoing betanodavirus-induced secondary necrotic cell death. Apoptosis. 2007 Jun;12(6):1043-60. To identify the mediator (s) of this necrotic process, a protein synthesis inhibitor (cycloheximide; CHX; 0.33 microg/ml) was used to block cytochrome c release as well as PS exposure and mitochondrial membrane permeability transition pore (MMP) loss. CHX (0.33 microg/ml) completely blocked viral protein B2 expression, and partly blocked protein A, protein alpha, and a pro-apoptotic death protein (Bad) expression. |
1(0,0,0,1) | Details |
| 16684888 | Lennartsson A, Vidovic K, Pass MB, Cowland JB, Gullberg U: -induced expression of bactericidal/permeability-increasing protein (BPI) in human myeloid cells correlates to binding of C/EBPbeta and C/EBPepsilon to the BPI promoter. J Leukoc Biol. 2006 Jul;80(1):196-203. Epub 2006 May 9. The induction is dependent on de novo protein synthesis, as judged by sensitivity to cycloheximide. Previous investigations have indicated a potential role of CCAAT/enhancer-binding protein (C/EBP) transcription factors in the regulation of BPI expression. |
1(0,0,0,1) | Details |
| 16087277 | Zupanska A, Dziembowska M, Ellert-Miklaszewska A, Gaweda-Walerych K, Kaminska B: Cyclosporine a induces growth arrest or programmed cell death of human glioma cells. Neurochem Int. 2005 Nov;47(6):430-41. In studied glioma cells, an accumulation of p21Cip1/Waf1 protein, a cell cycle inhibitor, was observed following CsA treatment, even in the absence of functional p53 tumour suppressor. |
1(0,0,0,1) | Details |
| 16887909 | Sinitskaya N, Salingre A, Klosen P, Revel FG, Pevet P, Simonneaux V: Differential expression of activator protein-1 proteins in the pineal gland of Syrian hamster and rat may explain species diversity in arylalkylamine N-acetyltransferase gene expression. Endocrinology. 2006 Nov;147(11):5052-60. Epub 2006 Aug 3. The present work investigated the contribution of phosphorylated cAMP-responsive element-binding protein, c-FOS, c-JUN, and JUN-B in the regulation of Aa-nat transcription in Syrian hamsters compared with rats. Indeed, early-night administration of a protein synthesis inhibitor (cycloheximide) markedly decreased AA-NAT mRNA levels in Syrian hamster. |
1(0,0,0,1) | Details |
| 16757808 | Araki W, Saito S, Takahashi-Sasaki N, Shiraishi H, Komano H, Murayama KS: Characterization of APH-1 mutants with a disrupted transmembrane GxxxG motif. J Mol Neurosci. 2006;29(1):35-43. These results collectively indicate that the three forms of APH-1 can replace each other in PS complexes and that the transmembrane GxxxG region is essential for the stability of the APH-1 protein as well as the assembly of PS complexes. Also, cycloheximide treatment of stable transfectants revealed that the mutant proteins are much less stable than the wild type. |
1(0,0,0,1) | Details |
| 18292516 | Roy KC, Maricic I, Khurana A, Smith TR, Halder RC, Kumar V: Involvement of secretory and endosomal compartments in presentation of an exogenous self-glycolipid to type II NKT cells. J Immunol. 2008 Mar 1;180(5):2942-50. Although plate-bound CD1d is inefficient in presenting lyso- at neutral pH, it is efficiently presented at acidic pH and in the presence of saposin C. Presentation of lyso- is inhibited in the presence of primaquine, concanamycin A, monensin, cycloheximide, and an inhibitor of microsomal triglyceride transfer protein but remains unchanged following treatment with brefeldin A. |
1(0,0,0,1) | Details |
| 18064628 | Espina B, Liang M, Russell RG, Hulley PA: Regulation of bim in glucocorticoid-mediated osteoblast apoptosis. J Cell Physiol. 2008 May;215(2):488-96. We found dose- and time-dependent upregulation of Bim protein, a pro-apoptotic Bcl-2 family member, with highest levels at 24-48 h for 1 microM Dex. Bim mRNA was upregulated in response to 1 microM Dex; both cycloheximide and the GC receptor antagonist, RU486, prevented Dex-induction of Bim protein, indicating transcriptional regulation involving the GC receptor. |
1(0,0,0,1) | Details |
| 18523582 | Saint-Georges Y, Garcia M, Delaveau T, Jourdren L, Le Crom S, Lemoine S, Tanty V, Devaux F, Jacq C: Yeast mitochondrial biogenesis: a role for the PUF RNA-binding protein Puf3p in mRNA localization. PLoS One. 2008 Jun 4;3(6):e2293. Unexpectedly, cycloheximide, supposed to solidify translational complexes, turned out to destabilize a class of mRNA-mitochondria interactions. We identified Puf3p, a Pumilio family RNA-binding protein, as the first trans-acting factor controlling the MLR phenomenon. |
1(0,0,0,1) | Details |