Histone Demethylases

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  Subject Areas on Research

  • A rationally-designed chimeric KDM1A/KDM1B histone demethylase tower domain deletion mutant retaining enzymatic activity. 
  • Cell-type-dependent histone demethylase specificity promotes meiotic chromosome condensation in Arabidopsis. 
  • Clipping of arginine-methylated histone tails by JMJD5 and JMJD7. 
  • Comparative analysis of small molecules and histone substrate analogues as LSD1 lysine demethylase inhibitors. 
  • Creation of versatile cloning platforms for transgene expression and dCas9-based epigenome editing. 
  • Demethylation of H3K27 Is Essential for the Induction of Direct Cardiac Reprogramming by miR Combo. 
  • Facile synthesis of substituted trans-2-arylcyclopropylamine inhibitors of the human histone demethylase LSD1 and monoamine oxidases A and B. 
  • Histone demethylases in neuronal differentiation, plasticity, and disease. 
  • JMJD5 couples with CDK9 to release the paused RNA polymerase II. 
  • KDM1 class flavin-dependent protein lysine demethylases. 
  • KMT2D maintains neoplastic cell proliferation and global histone H3 lysine 4 monomethylation. 
  • Loss of tumor suppressor KDM6A amplifies PRC2-regulated transcriptional repression in bladder cancer and can be targeted through inhibition of EZH2. 
  • Lysine-Specific Demethylase 1A (KDM1A/LSD1): Product Recognition and Kinetic Analysis of Full-Length Histones. 
  • Lysine-specific histone demethylase 1 inhibitors control breast cancer proliferation in ERα-dependent and -independent manners. 
  • Opposing LSD1 complexes function in developmental gene activation and repression programmes. 
  • Regional glutamine deficiency in tumours promotes dedifferentiation through inhibition of histone demethylation. 
  • The histone demethylase Kdm6b regulates a mature gene expression program in differentiating cerebellar granule neurons. 
  • Thermodynamic characterization of the binding interaction between the histone demethylase LSD1/KDM1 and CoREST. 
  • Use of pH and kinetic isotope effects to establish chemistry as rate-limiting in oxidation of a peptide substrate by LSD1. 
  • trans-2-Phenylcyclopropylamine is a mechanism-based inactivator of the histone demethylase LSD1.