1 Ocak 2019 Dergi makalesi Açık Erişim

Cheng, Chia-Wei; Biton, Moshe; Haber, Adam L.; Gunduz, Nuray; Eng, George; Gaynor, Liam T.; Tripathi, Surya; Calibasi-Koca, Gizem; Rickelt, Steffen; Butty, Vincent L.; Moreno-Serrano, Marta; Iqbal, Ameena M.; Bauer-Rowe, Khristian E.; Imada, Shinya; Ulutas, Mehmet Sefa; Mylonas, Constantine; Whary, Mark T.; Levine, Stuart S.; Basbinar, Yasemin; Hynes, Richard O.; Hynes, Richard O.

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  "@context": "https://schema.org/", 
  "@id": 72519, 
  "@type": "ScholarlyArticle", 
  "creator": [
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Cheng, Chia-Wei"
    }, 
    {
      "@type": "Person", 
      "name": "Biton, Moshe"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Broad Inst Harvard & MIT, Klarman Cell Observ, Cambridge, MA 02142 USA", 
      "name": "Haber, Adam L."
    }, 
    {
      "@type": "Person", 
      "name": "Gunduz, Nuray"
    }, 
    {
      "@type": "Person", 
      "name": "Eng, George"
    }, 
    {
      "@type": "Person", 
      "affiliation": "Dana Farber Canc Inst, 450 Brookline Ave, Boston, MA 02215 USA", 
      "name": "Gaynor, Liam T."
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Tripathi, Surya"
    }, 
    {
      "@type": "Person", 
      "name": "Calibasi-Koca, Gizem"
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Rickelt, Steffen"
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Dept Biol, BioMicro Ctr, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Butty, Vincent L."
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Moreno-Serrano, Marta"
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Iqbal, Ameena M."
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Koch Inst Integrat Canc Res, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Bauer-Rowe, Khristian E."
    }, 
    {
      "@type": "Person", 
      "name": "Imada, Shinya"
    }, 
    {
      "@type": "Person", 
      "name": "Ulutas, Mehmet Sefa"
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Dept Biol, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Mylonas, Constantine"
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Dept Biol Engn, Div Comparat Med, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Whary, Mark T."
    }, 
    {
      "@type": "Person", 
      "affiliation": "MIT, Dept Biol, BioMicro Ctr, 77 Massachusetts Ave, Cambridge, MA 02139 USA", 
      "name": "Levine, Stuart S."
    }, 
    {
      "@type": "Person", 
      "affiliation": "Dokuz Eylul Univ, Inst Oncol, Dept Translat Oncol, Izmir, Turkey", 
      "name": "Basbinar, Yasemin"
    }, 
    {
      "@type": "Person", 
      "name": "Hynes, Richard O."
    }, 
    {
      "@type": "Person", 
      "name": "Hynes, Richard O."
    }
  ], 
  "datePublished": "2019-01-01", 
  "description": "Little is known about how metabolites couple tissuespecific stem cell function with physiology. Here we show that, in the mammalian small intestine, the expression of Hmgcs2 (3-hydroxy-3-methylglutarylCoA synthetase 2), the gene encoding the ratelimiting enzyme in the production of ketone bodies, including beta-hydroxybutyrate (beta OHB), distinguishes self-renewing Lgr5(+) stem cells (ISCs) from differentiated cell types. Hmgcs2 loss depletes beta OHB levels in Lgr5(+) ISCs and skews their differentiation toward secretory cell fates, which can be rescued by exogenous beta OHB and class I histone deacetylase (HDAC) inhibitor treatment. Mechanistically, beta OHB acts by inhibiting HDACs to reinforce Notch signaling, instructing ISC self-renewal and lineage decisions. Notably, although a high-fat ketogenic diet elevates ISC function and postinjury regeneration through beta OHB-mediated Notch signaling, a glucose-supplemented diet has the opposite effects. These findings reveal how control of beta OHB-activated signaling in ISCs by diet helps to fine-tune stem cell adaptation in homeostasis and injury.", 
  "headline": "Ketone Body Signaling Mediates Intestinal Stem Cell Homeostasis and Adaptation to Diet", 
  "identifier": 72519, 
  "image": "https://aperta.ulakbim.gov.tr/static/img/logo/aperta_logo_with_icon.svg", 
  "license": "http://www.opendefinition.org/licenses/cc-by", 
  "name": "Ketone Body Signaling Mediates Intestinal Stem Cell Homeostasis and Adaptation to Diet", 
  "url": "https://aperta.ulakbim.gov.tr/record/72519"
}