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@ARTICLE{Cox:136084,
      author       = {Cox, Brian J and Vollmer, Marion and Tamplin, Owen and Lu,
                      Mei and Biechele, Steffen and Gertsenstein, Marina and van
                      Campenhout, Claude and Floss, Thomas and Kühn, Ralf and
                      Wurst, Wolfgang and Lickert, Heiko and Rossant, Janet},
      title        = {{P}henotypic annotation of the mouse {X} chromosome.},
      journal      = {Genome research},
      volume       = {20},
      number       = {8},
      issn         = {1088-9051},
      address      = {Cold Spring Harbor, NY},
      publisher    = {Laboratory Press},
      reportid     = {DZNE-2020-02406},
      pages        = {1154-1164},
      year         = {2010},
      abstract     = {Mutational screens are an effective means used in the
                      functional annotation of a genome. We present a method for a
                      mutational screen of the mouse X chromosome using gene trap
                      technologies. This method has the potential to screen all of
                      the genes on the X chromosome without establishing mutant
                      animals, as all gene-trapped embryonic stem (ES) cell lines
                      are hemizygous null for mutations on the X chromosome. Based
                      on this method, embryonic morphological phenotypes and
                      expression patterns for 58 genes were assessed,
                      approximately $10\%$ of all human and mouse syntenic genes
                      on the X chromosome. Of these, 17 are novel embryonic lethal
                      mutations and nine are mutant mouse models of genes
                      associated with genetic disease in humans, including BCOR
                      and PORCN. The rate of lethal mutations is similar to
                      previous mutagenic screens of the autosomes. Interestingly,
                      some genes associated with X-linked mental retardation
                      (XLMR) in humans show lethal phenotypes in mice, suggesting
                      that null mutations cannot be responsible for all cases of
                      XLMR. The entire data set is available via the publicly
                      accessible website (http://xlinkedgenes.ibme.utoronto.ca/).},
      keywords     = {Acyltransferases / Animals / Base Sequence / Chromosomes,
                      Human, X: genetics / DNA Mutational Analysis: methods /
                      Genes, Lethal / Genes, X-Linked / Genetic Diseases,
                      X-Linked: genetics / Genetic Predisposition to Disease /
                      Genetic Testing: methods / Humans / Membrane Proteins:
                      genetics / Mental Retardation, X-Linked: genetics / Mice /
                      Molecular Sequence Annotation / Molecular Sequence Data /
                      Phenotype / Proto-Oncogene Proteins: genetics / Repressor
                      Proteins: genetics / X Chromosome: genetics / BCOR protein,
                      human (NLM Chemicals) / Membrane Proteins (NLM Chemicals) /
                      Proto-Oncogene Proteins (NLM Chemicals) / Repressor Proteins
                      (NLM Chemicals) / Acyltransferases (NLM Chemicals) / PORCN
                      protein, human (NLM Chemicals)},
      cin          = {AG Wurst},
      ddc          = {540},
      cid          = {I:(DE-2719)1140001},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:20548051},
      pmc          = {pmc:PMC2909578},
      doi          = {10.1101/gr.105106.110},
      url          = {https://pub.dzne.de/record/136084},
}