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@ARTICLE{Duggimpudi:858402,
      author       = {Duggimpudi, Sujitha and Kloetgen, Andreas and Maney,
                      Sathish Kumar and Münch, Philipp C. and Hezaveh, Kebria and
                      Shaykhalishahi, Hamed and Hoyer, Wolfgang and McHardy, Alice
                      C. and Lang, Philipp A. and Borkhardt, Arndt and Hoell,
                      Jessica I.},
      title        = {{T}ranscriptome-wide analysis uncovers the targets of the
                      {RNA}-binding protein {MSI}2 and effects of {MSI}2's
                      {RNA}-binding activity on {IL}-6 signaling},
      journal      = {The journal of biological chemistry},
      volume       = {293},
      number       = {40},
      issn         = {1083-351X},
      address      = {Bethesda, Md.},
      publisher    = {Soc.72889},
      reportid     = {FZJ-2018-07288},
      pages        = {15359 - 15369},
      year         = {2018},
      abstract     = {The RNA-binding protein Musashi 2 (MSI2) has emerged as an
                      important regulator in cancer initiation, progression, and
                      drug resistance. Translocations and deregulation of the MSI2
                      gene are diagnostic of certain cancers, including chronic
                      myeloid leukemia (CML) with translocation t(7;17), acute
                      myeloid leukemia (AML) with translocation t(10;17), and some
                      cases of B-precursor acute lymphoblastic leukemia (pB-ALL).
                      To better understand the function of MSI2 in leukemia, the
                      mRNA targets that are bound and regulated by MSI2 and their
                      MSI2-binding motifs need to be identified. To this end,
                      using photoactivatable ribonucleoside cross-linking and
                      immunoprecipitation (PAR-CLIP) and the Multiple EM for Motif
                      Elicitation (MEME) analysis tool, here we identified
                      MSI2’s mRNA targets and the consensus RNA-recognition
                      element (RRE) motif recognized by MSI2 (UUAG). Of note, MSI2
                      knockdown altered the expression of several genes with roles
                      in eukaryotic initiation factor 2 (eIF2), hepatocyte growth
                      factor (HGF), and epidermal growth factor (EGF) signaling
                      pathways. We also show that MSI2 regulates classic
                      interleukin-6 (IL-6) signaling by promoting the degradation
                      of the mRNA of IL-6 signal transducer (IL6ST or GP130),
                      which, in turn, affected the phosphorylation statuses of
                      signal transducer and activator of transcription 3 (STAT3)
                      and the mitogen-activated protein kinase ERK. In summary, we
                      have identified multiple MSI2-regulated mRNAs and provided
                      evidence that MSI2 controls IL6ST activity that control
                      oncogenic signaling networks. Our findings may help inform
                      strategies for unraveling the role of MSI2 in leukemia to
                      pave the way for the development of targeted therapies.},
      cin          = {ICS-6},
      ddc          = {540},
      cid          = {I:(DE-Juel1)ICS-6-20110106},
      pnm          = {553 - Physical Basis of Diseases (POF3-553)},
      pid          = {G:(DE-HGF)POF3-553},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30126842},
      UT           = {WOS:000446549200003},
      doi          = {10.1074/jbc.RA118.002243},
      url          = {https://juser.fz-juelich.de/record/858402},
}