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Literature summary for 3.5.1.98 extracted from

  • Muralidhar, S.A.; Ramakrishnan, V.; Kalra, I.S.; Li, W.; Pace, B.S.
    Histone deacetylase 9 activates gamma-globin gene expression in primary erythroid cells (2011), J. Biol. Chem., 286, 2343-2353.
    View publication on PubMedView publication on EuropePMC

Organism

Organism UniProt Comment Textmining
Homo sapiens
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Source Tissue

Source Tissue Comment Organism Textmining
erythroid progenitor cell primary erythroid progenitor cell Homo sapiens
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K-562 cell K562 erythroleukemia cells treated with the HbF inducers hemin, trichostatin A, and sodium butanoate have significantly reduced mRNA levels of HDAC9 and its splice variant histone deacetylase-related protein Homo sapiens
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Expression

Organism Comment Expression
Homo sapiens K562 erythroleukemia cells treated with the HbF inducers hemin, trichostatin A, and sodium butanoate have significantly reduced mRNA levels of HDAC9 and its splice variant histone deacetylase-related protein down

General Information

General Information Comment Organism
physiological function HDAC9 gene knockdown produces dose-dependent gamma-globin gene silencing over an 80-320 nM range. Enforced expression of HDAC9 produces a dose-dependent 2.5fold increase in gammaglobin mRNA. HDAC9 binds in vivo in the upstream Ggamma-globin gene promoter region. Treatment of primary erythroid progenitors with HDAC9 siRNA results in 40 and 60% gamma-globin gene silencing in day 11 (early) and day 28 (late) progenitors, respectively. Enforced HDAC9 expression increases gamma-globin mRNA levels by 2.5fold with a simultaneous 7fold increase in fetal hemoglobin Homo sapiens