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@ARTICLE{Sharma:153373,
      author       = {Sharma, Amit and Liu, Hongde and Tobar-Tosse, Fabian and
                      Chand Dakal, Tikam and Ludwig, Michael and Holz, Frank G and
                      Loeffler, Karin U and Wüllner, Ullrich and Herwig-Carl,
                      Martina C},
      title        = {{U}biquitin {C}arboxyl-{T}erminal {H}ydrolases ({UCH}s):
                      {P}otential {M}ediators for {C}ancer and
                      {N}eurodegeneration.},
      journal      = {International journal of molecular sciences},
      volume       = {21},
      number       = {11},
      issn         = {1422-0067},
      address      = {Basel},
      publisher    = {Molecular Diversity Preservation International},
      reportid     = {DZNE-2020-01370},
      pages        = {3910 -},
      year         = {2020},
      abstract     = {Emerging evidence suggests an inverse association between
                      cancer and neurodegenerative diseases (NDD). Although
                      phenotypically different, both diseases display a
                      significant imbalance in the ubiquitination/deubiquitination
                      processes. Therefore, we particularly investigated the
                      expression of ubiquitin C-terminal hydrolases (UCHs: UCH-L1,
                      UCH-L3, UCH-L5 and BAP1), a subfamily of deubiquitinating
                      enzymes (DUBs), using publically available datasets (GTEx,
                      TCGA) and observed altered expression of UCH-L1, UCH-L3,
                      UCH-L5 in 17 cancer types. Interestingly, UCH-L1 (known to
                      be enriched in neurons and interacting with the Parkinson's
                      disease-associated protein α-synuclein) appeared to be a
                      prognostic indicator of unfavorable outcome in endometrial
                      and urothelial cancer, while increased expression of UCH-L3
                      and UCH-L5 was associated with poor survival in liver and
                      thyroid cancer, respectively. In normal tissues, UCH-L1 was
                      found to be strongly expressed in the cerebral cortex and
                      hypothalamus, while UCH-L3 expression was somewhat higher in
                      the testis. The occurrence of mutation rates in UCHs also
                      suggests that BAP1 and UCH-L5 may play a more dominant role
                      in cancers than UCH-L1 and UCH-L3. We also characterized the
                      functional context and configuration of the repeat elements
                      in the promoter of DUBs genes and found that UCHs are highly
                      discriminatory for catabolic function and are mainly
                      enriched with LINE/CR1 repeats. Regarding the thesis of an
                      inverse association between cancer and NDD, we observed that
                      among all DUBs, UCHs are the one most involved in both
                      entities. Considering a putative therapeutic potential based
                      on presumed common mechanisms, it will be useful to
                      determine whether other DUBs can compensate for the loss of
                      UCH activity under physiological conditions. However,
                      experimental evidence is required to substantiate this
                      argument.},
      keywords     = {Brain: metabolism / Databases, Genetic / Gene Expression
                      Profiling / Gene Expression Regulation / Humans / Neoplasms:
                      enzymology / Neurodegenerative Diseases: enzymology /
                      Phenotype / Prognosis / Protein Domains / Tumor Suppressor
                      Proteins: metabolism / Ubiquitin Thiolesterase: genetics /
                      Ubiquitin Thiolesterase: metabolism / Ubiquitination},
      cin          = {AG Wüllner ; AG Wüllner 2},
      ddc          = {540},
      cid          = {I:(DE-2719)1011302},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32486284},
      pmc          = {pmc:PMC7312489},
      doi          = {10.3390/ijms21113910},
      url          = {https://pub.dzne.de/record/153373},
}