% 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{Ferrarese:182750,
      author       = {R. Ferrarese and A. Izzo and G. Andrieux$^*$ and S. Lagies
                      and J. P. Bartmuss and A. P. Masilamani and A. Wasilenko and
                      D. Osti and S. Faletti and R. Schulzki and S. Yuan and E.
                      Kling and V. Ribecco and D. H. Heiland and S. Tholen and M.
                      Prinz and G. Pelicci and B. Kammerer and M. Börries$^*$ and
                      M. S. Carro},
      title        = {{ZBTB}18 inhibits {SREBP}-dependent lipid synthesis by
                      halting {CTBP}s and {LSD}1 activity in glioblastoma.},
      journal      = {Life science alliance},
      volume       = {6},
      number       = {1},
      issn         = {2575-1077},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DKFZ-2022-02892},
      pages        = {e202201400 -},
      year         = {2023},
      note         = {Print 2023},
      abstract     = {Enhanced fatty acid synthesis is a hallmark of tumors,
                      including glioblastoma. SREBF1/2 regulate the expression of
                      enzymes involved in fatty acid and cholesterol synthesis.
                      Yet, little is known about the precise mechanism regulating
                      SREBP gene expression in glioblastoma. Here, we show that a
                      novel interaction between the co-activator/co-repressor CTBP
                      and the tumor suppressor ZBTB18 regulates the expression of
                      SREBP genes. In line with our findings, metabolic assays and
                      glucose tracing analysis confirm the reduction in several
                      phospholipid species upon ZBTB18 expression. Our study
                      identifies CTBP1/2 and LSD1 as co-activators of SREBP genes
                      and indicates that the functional activity of the CTBP-LSD1
                      complex is altered by ZBTB18. ZBTB18 binding to the SREBP
                      gene promoters is associated with reduced LSD1 demethylase
                      activity of H3K4me2 and H3K9me2 marks. Concomitantly, the
                      interaction between LSD1, CTBP, and ZNF217 is increased,
                      suggesting that ZBTB18 promotes LSD1 scaffolding function.
                      Our results outline a new epigenetic mechanism enrolled by
                      ZBTB18 and its co-factors to regulate fatty acid synthesis
                      that could be targeted to treat glioblastoma patients.},
      cin          = {FR01},
      ddc          = {570},
      cid          = {I:(DE-He78)FR01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36414381},
      doi          = {10.26508/lsa.202201400},
      url          = {https://inrepo02.dkfz.de/record/182750},
}