Metabolic regulation of hematopoietic stem cells in the hypoxic niche.
By T. Suda, K. Takubo, G. Semenza. Cell Stem Cell, 2011
807 citations recorded by the source corpus.
Subfields: Cancer Research, Genetics, Hematology
View Paper: https://www.semanticscholar.org/paper/373fb2b54fdf0c35f3d548aa7bad6aeb923f70b4
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In Cancer Research
- G. Semenza
- Richard J. Johnson
- T. Suda
- K. Takubo
- C. V. Dang
- M. C. Simon
- D. Hanahan
- Navdeep S. Chandel
In Genetics
In Hematology
Citations in the corpus
- Metabolic Plasticity in Stem Cell Homeostasis and Differentiation (2012, neutral): “This reprogramming recapitulates features of embryonic archetypes (Takahashi and Yamanaka, 2006), including prioritized anabolic processes for generation of cell constituents (Folmes et al., 2011a).”
- The Mitochondrial Basis of Aging (2016, background): “…HSCs are generally thought to, instead, rely on glycolytic metabolism as the major source of their ATP, presumably in keeping with the low oxygen environment of the HSC niche, and as a mechanism to minimize the long-term deleterious effects of mitochondrial ROS production (Suda et al., 2011).”
- HIF-1 mediates metabolic responses to intratumoral hypoxia and oncogenic mutations. (2013, neutral): “ROS levels vary widely in cancer cells, with high ROS levels often associated with cell proliferation (43), whereas low ROS levels have been associated with resistance to chemotherapy (44) and the stem cell phenotype (45, 46).”
- Modulation of Myelopoiesis Progenitors Is an Integral Component of Trained Immunity (2018, background): “, 2014), whereas the activation of OXPHOS is associated with their functional impairment, loss of self-renewal potential, and induction of DNA damage (Suda et al., 2011; Takizawa et al., 2017; Takubo et al., 2013; Walter et al., 2015).”
- Hypoxia-Inducible Factors in Physiology and Medicine (2012, background): “This may be particularly important in stem cells, in which avoidance of DNA damage is critical (Suda et al., 2011).”
- Regulation of glycolysis by Pdk functions as a metabolic checkpoint for cell cycle quiescence in hematopoietic stem cells. (2013, background): “Although stem cells probably exhibit metabolic characteristics allowing them to meet diverse energy demands, it is not known whether their metabolic phenotype differs from that of transiently amplifying progenitors and terminally differentiated cells and, if so, how metabolic phenotypes directly def”