Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Porras 2017 Stem Cells

From Bioblast
Revision as of 10:43, 24 June 2019 by Krumschnabel Gerhard (talk | contribs)
(diff) โ† Older revision | Latest revision (diff) | Newer revision โ†’ (diff)
Publications in the MiPMap
Porras DP, Abbaszadeh M, Bhattacharya D, D'Souza NC, Edjiu NR, Perry CG, Scimรจ A (2017) p107 determines a metabolic checkpoint required for adipocyte lineage fates. Stem Cells 35:1378-91.

ยป PMID: 28233396

Porras DP, Abbaszadeh M, Bhattacharya D, D'Souza NC, Edjiu NR, Perry CG, Scime A (2017) Stem Cells

Abstract: We show that the transcriptional corepressor p107 orchestrates a metabolic checkpoint that determines adipocyte lineage fates for non-committed progenitors. p107 accomplishes this when stem cell commitment would normally occur in growth arrested cells. p107-deficient embryonic progenitors are characterized by a metabolic state resembling aerobic glycolysis that is necessary for their pro-thermogenic fate. Indeed, during growth arrest they have a reduced capacity for NADH partitioning between the cytoplasm and mitochondria. Intriguingly, this occurred despite an increase in the capacity for mitochondrial oxidation of non-glucose substrates. The significance of metabolic reprogramming is underscored by the disruption of glycolytic capacities in p107-depleted progenitors that reverted their fates from pro-thermogenic to white adipocytes. Moreover, the manipulation of glycolytic capacity on nonspecified embryonic and adult progenitors forced their beige fat commitment. These innovative findings introduce a new approach to increase pro-thermogenic adipocytes based on simply promoting aerobic glycolysis to manipulate nonspecified progenitor fate decisions. Stem Cells 2017.

ยฉ 2017 AlphaMed Press. โ€ข Keywords: Aerobic glycolysis, Beige/brown adipocytes, Metabolism, Progenitor fate, p107 โ€ข Bioblast editor: Kandolf G โ€ข O2k-Network Lab: CA Toronto Perry CG


Labels: MiParea: Respiration, Genetic knockout;overexpression 


Organism: Mouse  Tissue;cell: Fat, Fibroblast  Preparation: Intact cells 


Coupling state: LEAK, OXPHOS  Pathway: F, N  HRR: Oxygraph-2k