| Name | IkappaBalpha |
|---|---|
| Synonyms | I kappa B alpha; Mad3; IKB alpha; IKBA; IKBalpha; IkappaBalpha; Inhibitor of kappa light chain gene enhancer in B cells alpha; MAD 3… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16405428 | Midwinter RG, Cheah FC, Moskovitz J, Vissers MC, Winterbourn CC: IkappaB is a sensitive target for oxidation by cell-permeable chloramines: inhibition of NF-kappaB activity by chloramine through oxidation. Biochem J. 2006 May 15;396(1):71-8. Reversion occurred in the presence of cycloheximide, but was prevented if thioredoxin reductase was inhibited, suggesting that it was due to endogenous sulphoxide reductase activity. In the present study, we have investigated the ability of HOCl, chloramine (Gly-Cl) and chloramine (Tau-Cl) to oxidize IkappaBalpha, the inhibitor of NF-kappaB (nuclear factor kappaB), and to prevent activation of the NF-kappaB pathway in Jurkat cells. |
7(0,0,0,7) | Details |
| 16690986 | Lee KY, Ho SC, Lin HC, Lin SM, Liu CY, Huang CD, Wang CH, Chung KF, Kuo HP: Neutrophil-derived elastase induces TGF-beta1 secretion in human airway smooth muscle via NF-kappaB pathway. Am J Respir Cell Mol Biol. 2006 Oct;35(4):407-14. Epub 2006 May 11. This induction was inhibited by actinomycin D (5 mM), cycloheximide (5 mM), and NF-kappaB inhibitors, including pyrrolidine dithiocarbamate (PDTC, 1 mM), (2.5 mM), and salyicylate (2.5 mM). Stimulation with NE was rapidly followed by association of IRAK with MyD88, phosphorylation of IkappaBalpha, and nuclear translocation of p65 with increased transactivation activity. |
1(0,0,0,1) | Details |
| 16551274 | Marasa BS, Rao JN, Zou T, Liu L, Keledjian KM, Zhang AH, Xiao L, Chen J, Turner DJ, Wang JY: Induced TRPC1 expression sensitizes intestinal epithelial cells to apoptosis by inhibiting NF-kappaB activation through Ca2+ influx. Biochem J. 2006 Jul 1;397(1):77-87. The expression of TRPC1 induced by stable transfection of IEC-6 cells with the wild-type TRPC1 gene (IEC-TRPC1 cells) increased Ca2+ influx after Ca2+ store depletion and repressed NF-kappaB transactivation, which was associated with an increase in susceptibility to apoptosis induced by exposure to TNFalpha (tumour necrosis factor-alpha) plus CHX (cycloheximide) (TNF-alpha/CHX), or STS (staurosporine). By contrast, the induction of endogenous NF-kappaB activity, by the depletion of cellular polyamines, promoted resistance to apoptosis, which was prevented by the ectopic expression of the IkappaBalpha super-repressor. |
1(0,0,0,1) | Details |
| 16728660 | von Wnuck Lipinski K, Keul P, Ferri N, Lucke S, Heusch G, Fischer JW, Levkau B: Integrin-mediated transcriptional activation of inhibitor of apoptosis proteins protects smooth muscle cells against apoptosis induced by degraded collagen. Circ Res. 2006 Jun 23;98(12):1490-7. Epub 2006 May 25. We show that exposure of SMC to collagen fragments resulted in a sustained activation of nuclear factor (NF)-kappaB via phosphorylation and degradation of IkappaBalpha. |
3(0,0,0,3) | Details |
| 15542827 | Deng J, Lu PD, Zhang Y, Scheuner D, Kaufman RJ, Sonenberg N, Harding HP, Ron D: Translational repression mediates activation of nuclear factor kappa B by phosphorylated translation initiation factor 2. Mol Cell Biol. 2004 Dec;24(23):10161-8. We have used a pharmacologically activable version of pancreatic ER kinase (PERK, an ER stress-responsive eIF2alpha kinase) to uncouple eIF2alpha phosphorylation from stress and found that phosphorylation of eIF2alpha is both necessary and sufficient to activate both NF-kappaB DNA binding and an NF-kappaB reporter gene. eIF2alpha phosphorylation-dependent NF-kappaB activation correlated with decreased levels of the inhibitor IkappaBalpha protein. |
2(0,0,0,2) | Details |
| 17316064 | Chaudhuri V, Potts BR, Karasek MA: Mechanisms of microvascular wound repair I. In Vitro Cell Dev Biol Anim. 2006 Nov-Dec;42(10):308-13. Inhibition of mitosis by mitomycin C did not reduce reendothelialization and both actinomycin D and cycloheximide inhibited repair by 80%. I-kappa B alpha, the inhibitory subunit of NF-kappa B (a transcription factor activated by oxidative stress), was upregulated following wounding. |
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. IkappaBalphaS/A and IkappaBalphaTrunc ameliorated the inhibitory effects of TNF on GH-inducible Spi 2.1 and IGF-I promoter activity. |
1(0,0,0,1) | Details |
| 17962448 | Goodkin ML, Epstein S, Asbell PA, Blaho JA: Nuclear translocation of NF-kappaB precedes apoptotic poly (ADP- polymerase cleavage during productive HSV-1 replication in corneal epithelial cells. Invest Ophthalmol Vis Sci. 2007 Nov;48(11):4980-8. HSV-1 stimulated the degradation of regulatory IkappaBalpha protein, resulting in nuclear translocation of NF-kappaB. |
1(0,0,0,1) | Details |
| 17435549 | Turner DJ, Alaish SM, Zou T, Rao JN, Wang JY, Strauch ED: Bile salts induce resistance to apoptosis through NF-kappaB-mediated XIAP expression. Ann Surg. 2007 Mar;245(3):415-25. Exposure of normal intestinal epithelial cells (IEC-6) to the conjugated bile salts taurodeoxycholate (TDCA) and (TCDCA) resulted in an increase in resistance to tumor necrosis factor (TNF)-alpha and cycloheximide (CHX)-induced apoptosis, and NF-kappaB activation. Specific inhibition of NF-kappaB by infection with an adenoviral vector that expresses the IkappaBalpha super-repressor (IkappaBSR) prevented the induction of XIAP expression and the bile salt-mediated resistance to apoptosis. |
1(0,0,0,1) | Details |
| 16354757 | Zhang HM, Keledjian KM, Rao JN, Zou T, Liu L, Marasa BS, Wang SR, Ru L, Strauch ED, Wang JY: Induced focal adhesion kinase expression suppresses apoptosis by activating NF-kappaB signaling in intestinal epithelial cells. Am J Physiol Cell Physiol. 2006 May;290(5):C1310-20. Epub 2005 Dec 14. Specific inhibition of NF-kappaB by the recombinant adenoviral vector containing the IkappaBalpha superrepressor prevented increased resistance to apoptosis in WT-FAK-transfected cells. |
1(0,0,0,1) | Details |
| 19787057 | Sung MH, Salvatore L, De Lorenzi R, Indrawan A, Pasparakis M, Hager GL, Bianchi ME, Agresti A: Sustained oscillations of NF-kappaB produce distinct genome scanning and gene expression profiles. PLoS One. 2009 Sep 29;4(9):e7163. Mathematical modeling suggests that NF-kappaB oscillations are selected over other non-oscillatory dynamics by fine-tuning the relative strengths of feedback loops like IkappaBalpha. |
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 |
| 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. 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. |
0(0,0,0,0) | Details |
| 17523868 | Morton ER, Blaho JA: Herpes simplex virus blocks Fas-mediated apoptosis independent of viral activation of NF-kappaB in human epithelial HEp-2 cells. J Interferon Cytokine Res. 2007 May;27(5):365-76. We found the following: (1) Treatment of HEp-2 cells with anti-Fas antibody or Fas ligand (FasL) alone did not induce apoptosis. (2) In addition, these inducers did not activate NF-kappaB in these cells. (3) The addition of cycloheximide (CHX) during these treatments caused a dramatic increase in programmed cell death. (4) HEp-2 cells infected with HSV for 6 h prior to anti-Fas plus CHX treatment were nonapoptotic, and (5) these cells possessed nuclear NFkappaB. (6) HSV blocked anti-Fas or FasL plus CHX-induced apoptosis in HEp-2 cells that stably expressed a dominant-negative form of IkappaBalpha. |
0(0,0,0,0) | 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. |
0(0,0,0,0) | Details |