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@ARTICLE{Kerimoglu:139386,
      author       = {Kerimoglu, Cemil and Sakib, M Sadman and Jain, Gaurav and
                      Benito, Eva and Burkhardt, Susanne and Capece, Vincenzo and
                      Kaurani, Lalit and Halder, Rashi and Agís-Balboa, Roberto
                      Carlos and Stilling, Roman and Urbanke, Hendrik and Kranz,
                      Andrea and Stewart, A Francis and Fischer, Andre},
      title        = {{KMT}2{A} and {KMT}2{B} {M}ediate {M}emory {F}unction by
                      {A}ffecting {D}istinct {G}enomic {R}egions.},
      journal      = {Cell reports},
      volume       = {20},
      number       = {3},
      issn         = {2211-1247},
      address      = {[New York, NY]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-05708},
      pages        = {538-548},
      year         = {2017},
      abstract     = {Kmt2a and Kmt2b are H3K4 methyltransferases of the
                      Set1/Trithorax class. We have recently shown the importance
                      of Kmt2b for learning and memory. Here, we report that Kmt2a
                      is also important in memory formation. We compare the
                      decrease in H3K4 methylation and de-regulation of gene
                      expression in hippocampal neurons of mice with knockdown of
                      either Kmt2a or Kmt2b. Kmt2a and Kmt2b control largely
                      distinct genomic regions and different molecular pathways
                      linked to neuronal plasticity. Finally, we show that the
                      decrease in H3K4 methylation resulting from Kmt2a knockdown
                      partially recapitulates the pattern previously reported in
                      CK-p25 mice, a model for neurodegeneration and memory
                      impairment. Our findings point to the distinct functions of
                      even closely related histone-modifying enzymes and provide
                      essential insight for the development of more efficient and
                      specific epigenetic therapies against brain diseases.},
      keywords     = {Animals / Gene Expression Regulation, Enzymologic /
                      Hippocampus: enzymology / Histone-Lysine
                      N-Methyltransferase: biosynthesis / Histone-Lysine
                      N-Methyltransferase: genetics / Memory / Methylation / Mice
                      / Myeloid-Lymphoid Leukemia Protein: biosynthesis /
                      Myeloid-Lymphoid Leukemia Protein: genetics / Neurons:
                      enzymology / Myeloid-Lymphoid Leukemia Protein (NLM
                      Chemicals) / Histone-Lysine N-Methyltransferase (NLM
                      Chemicals) / Kmt2a protein, mouse (NLM Chemicals)},
      cin          = {AG Fischer / AG Bonn 2 / AG Sananbenesi / Göttingen
                      common},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1440012 /
                      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:28723559},
      doi          = {10.1016/j.celrep.2017.06.072},
      url          = {https://pub.dzne.de/record/139386},
}