| Name | HDAC |
|---|---|
| Synonyms | HD7; HDAC 7; HDAC7; HD7B; HD9; HDAC; HDAC 9; HDAC7B… |
| Name | cycloheximide |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 15634758 | Bordin M, D'Atri F, Guillemot L, Citi S: Histone deacetylase inhibitors up-regulate the expression of tight junction proteins. Mol Cancer Res. 2004 Dec;2(12):692-701. Histone deacetylase (HDAC) inhibitors promote cell maturation, differentiation, and apoptosis through changes in gene expression. Up-regulation of cingulin is reversible and dose dependent and requires de novo protein synthesis and protein kinase activity, because it is inhibited by cycloheximide and by the protein kinase inhibitor H-7. |
4(0,0,0,4) | Details |
| 18504399 | Ishihara K, Kaneko M, Kitamura H, Takahashi A, Hong JJ, Seyama T, Iida K, Wada H, Hirasawa N, Ohuchi K: Mechanism for the decrease in the FIP1L1-PDGFRalpha protein level in EoL-1 cells by histone deacetylase inhibitors. Int Arch Allergy Immunol. 2008;146 Suppl 1:7-10. Epub 2008 May 27. BACKGROUND: Acetylation and deacetylation of proteins occur in cells in response to various stimuli, and are reversibly catalyzed by histone acetyltransferase and histone deacetylase (HDAC), respectively. Actinomycin D and cycloheximide were used to block RNA synthesis and protein synthesis, respectively, in the chasing experiment of the amount of FIP1L1-PDGFRalpha protein. |
4(0,0,0,4) | Details |
| 19094990 | Azzi A, Cosseau C, Grunau C: Schistosoma mansoni: developmental arrest of miracidia treated with histone deacetylase inhibitors. Exp Parasitol. 2009 Mar;121(3):288-91. Epub 2008 Dec 6. In the present study, we examined the effect of the histone deacetylase (HDAC) inhibitors trichostatin A (TSA), (VA) and - on the metamorphosis of larvae of the human blood-fluke Schistosoma mansoni from the free-swimming miracidia into the intramolluskal sporocyst. Other enzyme inhibitors such as cycloheximide or hydroxyurea had no effect on metamorphosis. |
3(0,0,0,3) | Details |
| 17596302 | Ye J, Gradoville L, Daigle D, Miller G: De novo protein synthesis is required for lytic cycle reactivation of Epstein-Barr virus, but not Kaposi's sarcoma-associated herpesvirus, in response to histone deacetylase inhibitors and protein kinase C agonists. J Virol. 2007 Sep;81(17):9279-91. Epub 2007 Jun 27. Using Northern blotting and quantitative reverse transcriptase PCR, we measured the kinetics of expression of the lytic cycle activator genes and determined whether abundance of mRNAs encoding these genes from either virus was reduced by treatment with cycloheximide (CHX), an inhibitor of protein synthesis. CHX blocked expression of mRNAs of EBV BZLF1 and BRLF1, the two EBV lytic cycle activator genes, when HH514-16 Burkitt lymphoma cells were treated with histone deacetylase (HDAC) inhibitors, or trichostatin A, or a DNA methyltransferase inhibitor, 5-Aza-2'- |
2(0,0,0,2) | Details |
| 18632985 | Wilson AJ, Byun DS, Nasser S, Murray LB, Ayyanar K, Arango D, Figueroa M, Melnick A, Kao GD, Augenlicht LH, Mariadason JM: HDAC4 promotes growth of colon cancer cells via repression of p21. Mol Biol Cell. 2008 Oct;19(10):4062-75. Epub 2008 Jul 16. The class II Histone deacetylase (HDAC), HDAC4, is expressed in a tissue-specific manner, and it represses differentiation of specific cell types. Conversely, overexpression of HDAC4 repressed p21 promoter activity. p21 was likely a direct target of HDAC4, because HDAC4 down-regulation increased p21 mRNA when protein synthesis was inhibited by cycloheximide. |
1(0,0,0,1) | Details |
| 15608694 | Inoue S, MacFarlane M, Harper N, Wheat LM, Dyer MJ, Cohen GM: Histone deacetylase inhibitors potentiate TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in lymphoid malignancies. Cell Death Differ. 2004 Dec;11 Suppl 2:S193-206. HDAC inhibitors sensitized resistant cells to TRAIL-induced apoptosis by facilitating formation of an active death-inducing signalling complex (DISC), leading to the rapid activation of caspase-8. |
2(0,0,0,2) | Details |
| 15899836 | Tran T, Shatnawi A, Zheng X, Kelley KM, Ratnam M: Enhancement of folate receptor alpha expression in tumor cells through the glucocorticoid receptor: a promising means to improved tumor detection and targeting. Cancer Res. 2005 May 15;65(10):4431-41. Histone deacetylase (HDAC) inhibitors potentiated dexamethasone induction of FR-alpha independent of changes in GR levels. |
2(0,0,0,2) | Details |
| 19117054 | Karmakar S, Foster EA, Smith CL: downregulation of the tumor suppressor gene BTG2 requires estrogen receptor-alpha and the REA corepressor. Int J Cancer. 2009 Apr 15;124(8):1841-51. Depletion of ERalpha by siRNA indicated that the receptor is required for E2 down regulation of BTG2 mRNA levels, and cycloheximide experiments indicated that the effect of E2 on BTG2 expression was independent of intermediary protein synthesis. Taken together, our results reveal a requirement of HDAC activity for basal BTG2 expression and the ERalpha-REA interaction for repression of the BTG2 gene. |
1(0,0,0,1) | Details |
| 15791453 | Murakami J, Asaumi J, Kawai N, Tsujigiwa H, Yanagi Y, Nagatsuka H, Inoue T, Kokeguchi S, Kawasaki S, Kuroda M, Tanaka N, Matsubara N, Kishi K: Effects of histone deacetylase inhibitor FR901228 on the expression level of telomerase reverse transcriptase in oral cancer. Cancer Chemother Pharmacol. 2005 Jul;56(1):22-8. Epub 2005 Mar 25. In the present study, the epigenetic effects of the histone deacetylase (HDAC) inhibitor FR901228 on hTERT transcription in oral cancer cell lines were analyzed by RT-PCR. Moreover, cotreatment of protein synthesis inhibitor cycloheximide (CHX) resulted in the induction of hTERT transcription by FR901228. |
2(0,0,0,2) | Details |
| 17828306 | You JS, Kang JK, Lee EK, Lee JC, Lee SH, Jeon YJ, Koh DH, Ahn SH, Seo DW, Lee HY, Cho EJ, Han JW: Histone deacetylase inhibitor apicidin downregulates DNA methyltransferase 1 expression and induces repressive histone modifications via recruitment of corepressor complex to promoter region in human cervix cancer cells. Oncogene. 2008 Feb 28;27(10):1376-86. Epub 2007 Sep 10. Here, we report that DNMT1 abnormally expressed in HeLa cells is downregulated by a histone deacetylase (HDAC) inhibitor apicidin, which is correlated with induction of repressive histone modifications on the promoter site. The downregulation of DNMT1 expression seems to require de novo protein synthesis, because the apicidin effect is antagonized by cycloheximide treatment. |
2(0,0,0,2) | Details |
| 16514187 | Endo T, Naito K, Kume S, Nishimura Y, Kashima K, Tojo H: Activities of maturation-promoting factor (MPF) and mitogen-activated protein kinase (MAPK) are not required for the global histone deacetylation observed after germinal vesicle breakdown (GVBD) in porcine oocytes. Reproduction. 2006 Mar;131(3):439-47. This deacetylation after AGVD was not affected by an MPF inhibitor, roscovitine, or an inhibitor of protein synthesis, cycloheximide, but was completely prevented by an inhibitor of histone deactylases (HDACs), trichostatine A. These results suggest that the MPF and MAPK activities were dispensable and the breakdown of the GV membrane was sufficient for the global histone deacetylation, which was catalyzed by HDAC activity. |
1(0,0,0,1) | Details |