PRDM16 Maintains Homeostasis of the Intestinal Epithelium by Controlling Region-Specific Metabolism

Rachel R. Stine, Alexander P. Sakers, Tara TeSlaa, Megan Kissig, Zachary E. Stine, Chan Wook Kwon, Lan Cheng, Hee Woong Lim, Klaus H. Kaestner, Joshua D. Rabinowitz, Patrick Seale

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

Metabolic program expression and dependency vary along the length of the small intestine. PRDM16 transcriptionally regulates fatty acid oxidation (FAO), which is highest in the upper small intestine. Loss of Prdm16 reduces FAO, leading to apoptosis and diminished epithelial differentiation of progenitor cells in the upper intestine.

Original languageEnglish (US)
Pages (from-to)830-845.e8
JournalCell stem cell
Volume25
Issue number6
DOIs
StatePublished - Dec 5 2019

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Genetics
  • Cell Biology

Keywords

  • apoptosis
  • differentiation
  • duodenum
  • fatty acid oxidation
  • intestinal stem cell
  • intestine
  • metabolism
  • PRDM16
  • transit amplifying cell

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  • Cite this

    Stine, R. R., Sakers, A. P., TeSlaa, T., Kissig, M., Stine, Z. E., Kwon, C. W., Cheng, L., Lim, H. W., Kaestner, K. H., Rabinowitz, J. D., & Seale, P. (2019). PRDM16 Maintains Homeostasis of the Intestinal Epithelium by Controlling Region-Specific Metabolism. Cell stem cell, 25(6), 830-845.e8. https://doi.org/10.1016/j.stem.2019.08.017