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Histone deacetylase 10

HDAC10, HD10
The protein encoded by this gene belongs to the histone deacetylase family, members of which deacetylate lysine residues on the N-terminal part of the core histones. Histone deacetylation modulates chromatin structure, and plays an important role in transcriptional regulation, cell cycle progression, and developmental events. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Aug 2011] (from NCBI)
Top mentioned proteins: Histone, HDAC, HD11, HDAC6, HDAC3
Papers on HDAC10
Identification of HDAC6-Selective Inhibitors of Low Cancer Cell Cytotoxicity.
Kozikowski et al., Chicago, United States. In Chemmedchem, Jan 2016
In the present work, we show that structural modification of these isoxazole-based inhibitors leads to high potency and selectivity for HDAC6 over HDAC1-3 and HDAC10, while unexpectedly abolishing their ability to block cell growth.
Growth attenuation is associated with histone deacetylase 10-induced autophagy in the liver.
Gat-Yablonski et al., Tel Aviv-Yafo, Israel. In J Nutr Biochem, Jan 2016
At the same time, we found that the level of HDAC10 was significantly increased.
Olig1 Acetylation and Nuclear Export Mediate Oligodendrocyte Development.
Macklin et al., Shanghai, China. In J Neurosci, Jan 2016
Olig1 acetylation and deacetylation are regulated by the acetyltransferase CREB-binding protein and the histone deacetylases HDAC1, HDAC3, and HDAC10.
Inhibition of Histone Deacetylases Permits Lipopolysaccharide-Mediated Secretion of Bioactive IL-1β via a Caspase-1-Independent Mechanism.
Bode et al., Heidelberg, Germany. In J Immunol, Jan 2016
Genetic studies excluded HDAC6 and HDAC10 as relevant HDAC targets in this pathway, whereas pharmacological inhibitor studies implicated the involvement of HDAC11.
Isotype-Specific Inhibition of Histone Deacetylases: Identification of Optimal Targets for Radiosensitization.
Kim et al., Seoul, South Korea. In Cancer Res Treat, Dec 2015
Results: Among 11 HDAC isotypes tested, specific inhibition of 7 isotypes (HDAC1, HDAC3, HDAC4, HDAC6, HDAC7, HDAC10, and HDAC11) enhanced radiation lethality in SQ20B cells.
Histone Deacetylase 10 Regulates the Cell Cycle G2/M Phase Transition via a Novel Let-7-HMGA2-Cyclin A2 Pathway.
Seto et al., Tampa, United States. In Mol Cell Biol, Oct 2015
Here, we report that HDAC10 regulates the cell cycle via modulation of cyclin A2 expression, and cyclin A2 overexpression rescues HDAC10 knockdown-induced G2/M transition arrest.
Potent and Selective Inhibitors of Histone Deacetylase-3 Containing Chiral Oxazoline Capping Groups and a N-(2-Aminophenyl)-benzamide Binding Unit.
Thomas et al., London, United Kingdom. In J Med Chem, Oct 2015
Weak inhibition of all other HDAC isoforms (HDAC4, 5, 6, 7, and 9: IC50 > 100 000 nM; HDAC8: IC50 = 25 000 nM; HDAC10: IC50 > 4000 nM; HDAC11: IC50 > 2000 nM) confirmed the Class I selectivity of 15k.
Review article: selective histone deacetylase isoforms as potential therapeutic targets in inflammatory bowel diseases.
Silver et al., London, United Kingdom. In Aliment Pharmacol Ther, 2015
HDAC2, HDAC3, HDAC6, HDAC9 and HDAC10 isoforms seem to be specifically involved in chronic intestinal inflammation, justifying the use of selective inhibitors as new therapeutic strategies in IBD.
The genomic and transcriptomic landscape of anaplastic thyroid cancer: implications for therapy.
Jones et al., Vancouver, Canada. In Bmc Cancer, 2014
RESULTS: The most prevalent mutations were those of TP53 and BRAF; repeated alterations of the epigenetic machinery such as frame-shift deletions of HDAC10 and EP300, loss of SMARCA2 and fusions of MECP2, BCL11A and SS18 were observed.
Epigenetic therapy of cancer with histone deacetylase inhibitors.
Saldanha et al., Bengaluru, India. In J Cancer Res Ther, 2014
HDAC enzymes are grouped into four different classes namely Class I (HDAC1, HDAC2, HDAC3, and HDAC8), Class II (HDAC4, HDAC5, HDAC6, HDAC7, HDAC9, and HDAC10), Class III HDAC and Class IV (HDAC11).
ABVD in older patients with early-stage Hodgkin lymphoma treated within the German Hodgkin Study Group HD10 and HD11 trials.
Borchmann et al., Köln, Germany. In J Clin Oncol, 2013
PATIENTS AND METHODS: We analyzed the feasibility and efficacy of four cycles of ABVD in older patients age 60 to 75 years with early-stage HL who were treated within the German Hodgkin Study Group (GHSG) HD10 and HD11 trials; results were compared with those of younger patients treated within these trials.
Quality control of involved-field radiotherapy for patients with early stage Hodgkin's lymphoma based on a central prospective review. Comparison of the results between two study generations of the German Hodgkin Study Group.
Eich et al., Münster, Germany. In Strahlenther Onkol, 2012
PURPOSE: Based on experience in trials HD10 and HD11 (1998-2003), the radiotherapy reference center of the German Hodgkin Study Group (GHSG) continued their central prospective radiation oncological review in trials HD13 and HD14.
Histone deacetylases 9 and 10 are required for homologous recombination.
Parvin et al., Columbus, United States. In J Biol Chem, 2011
Histone deacetylases 9 and 10 are required for homologous recombination.
Chemoproteomics profiling of HDAC inhibitors reveals selective targeting of HDAC complexes.
Drewes et al., Heidelberg, Germany. In Nat Biotechnol, 2011
We also identified the anti-inflammatory drug bufexamac as a class IIb (HDAC6, HDAC10) HDAC inhibitor.
Inhibition of histone deacetylase 10 induces thioredoxin-interacting protein and causes accumulation of reactive oxygen species in SNU-620 human gastric cancer cells.
Kim et al., Seoul, South Korea. In Mol Cells, 2010
HDAC10 is involved in transcriptional downregulation of TXNIP, leading to altered reactive oxygen species signaling in human gastric cancer cells.
Histone deacetylase 10 relieves repression on the melanogenic program by maintaining the deacetylation status of repressors.
Yang et al., T'ai-chung-shih, Taiwan. In J Biol Chem, 2010
Results not only show that HDAC10 regulates melanogenesis but also demonstrate that the transcriptional activities of Pax3 and KAP1 are intimately linked to their acetylation status.
HDAC10 promoter polymorphism associated with development of HCC among chronic HBV patients.
Shin et al., Seoul, South Korea. In Biochem Biophys Res Commun, 2007
Results suggest that the "T" allele of HDAC10-589C>T affect on the increased transcription activity, and might accelerate HCC development through increased expression of HDAC10.
Outcome of patients experiencing progression or relapse after primary treatment with two cycles of chemotherapy and radiotherapy for early-stage favorable Hodgkin's lymphoma.
Josting et al., Köln, Germany. In J Clin Oncol, 2007
PATIENTS AND METHODS: Of 1,129 patients with early-stage favorable HL enrolled onto the HD7/HD10/HD13 trials of the German Hodgkin Study Group, 42 patients were identified with treatment failure, of whom eight had primary progressive disease, seven had early relapse (< or = 12 months), and 27 had late relapse (> 12 months).
[A teleradiotherapeutic network for lymphoma patients within the competence network malignant lymphomas].
Müller et al., Köln, Germany. In Rontgenpraxis, 2006
Since January 2001 more than 700 patients (trials HD10-HD15 of the German Hodgkin Study Group, GHSG) could be assessed after digital transfer via internet, on mobile data carriers or an ISDN-connection in the radiotherapy reference center Cologne.
Reduced expression of class II histone deacetylase genes is associated with poor prognosis in lung cancer patients.
Takahashi et al., Nagoya, Japan. In Int J Cancer, 2004
Reduced expression of histone deacetylase 10 is associated lung cancer
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