Person:
Beyaz, Semir

Profile Picture

Email Address

AA Acceptance Date

Birth Date

Research Projects

Organizational Units

Job Title

Last Name

Beyaz

First Name

Semir

Name

Beyaz, Semir

Filters

20162

Settings

Author's Publications: search.filters.isAuthorOfPublication.bb72b5e7-f61d-4185-b122-55e2c3b2525e

Search Results

Now showing 1 - 2 of 2
  • No Thumbnail Available
    Publication
    The histone demethylase UTX regulates the lineage-specific epigenetic program of invariant natural killer T cells
    (Springer Nature, 2016) Beyaz, Semir; Kim, Ji Hyung; Pinello, Luca; Xifaras, Michael E; Hu, Yu; Huang, Jialiang; Kerenyi, Marc A; Das, Partha Pratim; Barnitz, R Anthony; Herault, Aurelie; Dogum, Rizkullah; Haining, William; Yilmaz, Omer; Passegue, Emmanuelle; Yuan, Guo-Cheng; Orkin, Stuart; Winau, Florian
  • Thumbnail Image
    Publication
    High fat diet enhances stemness and tumorigenicity of intestinal progenitors
    (2016) Beyaz, Semir; Mana, Miyeko D.; Roper, Jatin; Kedrin, Dmitriy; Saadatpour, Assieh; Hong, Sue-Jean; Bauer-Rowe, Khristian E.; Xifaras, Michael E.; Akkad, Adam; Arias, Erika; Pinello, Luca; Katz, Yarden; Shinagare, Shweta; Abu-Remaileh, Monther; Mihaylova, Maria M.; Lamming, Dudley W.; Dogum, Rizkullah; Guo, Guoji; Bell, George W.; Selig, Martin; Nielsen, G. Petur; Gupta, Nitin; Ferrone, Cristina; Deshpande, Vikram; Yuan, Guo-Cheng; Orkin, Stuart; Sabatini, David M.; Yilmaz, Omer
    Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we find that high fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem-cells (ISCs) of the mammalian intestine. Mechanistically, HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-d) signature in intestinal stem and (non-ISC) progenitor cells, and pharmacologic activation of PPAR-d recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-d dependent manner. Interestingly, HFD- and agonist-activated PPAR-d signaling endow organoid-initiating capacity to progenitors, and enforced PPAR-d signaling permits these progenitors to form in vivo tumors upon loss of the tumor suppressor Apc. These findings highlight how diet-modulated PPAR-d activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumors.