% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Kerimoglu:136804,
      author       = {Kerimoglu, Cemil and Agis-Balboa, Roberto C and Kranz,
                      Andrea and Stilling, Roman and Bahari-Javan, Sanaz and
                      Benito Garagorri, Eva and Halder, Rashi and Burkhardt,
                      Susanne and Stewart, Adrian Francis and Fischer, Andre},
      title        = {{H}istone-methyltransferase {MLL}2 ({KMT}2{B}) is required
                      for memory formation in mice.},
      journal      = {The journal of neuroscience},
      volume       = {33},
      number       = {8},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.57413},
      reportid     = {DZNE-2020-03126},
      pages        = {3452-3464},
      year         = {2013},
      abstract     = {The consolidation of long-term memories requires
                      differential gene expression. Recent research has suggested
                      that dynamic changes in chromatin structure play a role in
                      regulating the gene expression program linked to memory
                      formation. The contribution of histone methylation, an
                      important regulatory mechanism of chromatin plasticity that
                      is mediated by the counteracting activity of
                      histone-methyltransferases and histone-demethylases, is,
                      however, not well understood. Here we show that mice lacking
                      the histone-methyltransferase myeloid/lymphoid or
                      mixed-lineage leukemia 2 (mll2/kmt2b) gene in adult
                      forebrain excitatory neurons display impaired
                      hippocampus-dependent memory function. Consistent with the
                      role of KMT2B in gene-activation DNA microarray analysis
                      revealed that 152 genes were downregulated in the
                      hippocampal dentate gyrus region of mice lacking kmt2b.
                      Downregulated plasticity genes showed a specific deficit in
                      histone 3 lysine 4 di- and trimethylation, while histone 3
                      lysine 4 monomethylation was not affected. Our data
                      demonstrates that KMT2B mediates hippocampal histone 3
                      lysine 4 di- and trimethylation and is a critical player for
                      memory formation.},
      keywords     = {Animals / DNA-Binding Proteins: deficiency / DNA-Binding
                      Proteins: genetics / DNA-Binding Proteins: physiology /
                      Hippocampus: enzymology / Histone Methyltransferases /
                      Histone-Lysine N-Methyltransferase: deficiency /
                      Histone-Lysine N-Methyltransferase: genetics / Maze
                      Learning: physiology / Memory, Long-Term: physiology / Mice
                      / Mice, Inbred C57BL / Mice, Knockout / Mice, Transgenic /
                      Neoplasm Proteins: deficiency / Neoplasm Proteins: genetics
                      / Neoplasm Proteins: physiology / Neuronal Plasticity:
                      genetics / Neuronal Plasticity: physiology / DNA-Binding
                      Proteins (NLM Chemicals) / KMT2D protein, human (NLM
                      Chemicals) / Neoplasm Proteins (NLM Chemicals) / Histone
                      Methyltransferases (NLM Chemicals) / Histone-Lysine
                      N-Methyltransferase (NLM Chemicals)},
      cin          = {AG Fischer ; AG Fischer / RNAome database ; AG Sananbenesi
                      ; AG Sananbenesi / Göttingen common},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1410004 /
                      I:(DE-2719)6000014},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23426673},
      pmc          = {pmc:PMC6619533},
      doi          = {10.1523/JNEUROSCI.3356-12.2013},
      url          = {https://pub.dzne.de/record/136804},
}