Glucose-6-phosphatase-β, implicated in a congenital neutropenia syndrome, is essential for macrophage energy homeostasis and functionality

Podobne zapisy

• Lack of glucose recycling between endoplasmic reticulum and cytoplasm underlies cellular dysfunction in glucose-6-phosphatase-β–deficient neutrophils in a congenital neutropenia syndrome
  od: Jun, Hyun Sik, i wsp.
  Wydane: (2010)
• G-CSF improves murine G6PC3-deficient neutrophil function by modulating apoptosis and energy homeostasis
  od: Jun, Hyun Sik, i wsp.
  Wydane: (2011)
• Molecular mechanisms of neutrophil dysfunction in glycogen storage disease type Ib
  od: Jun, Hyun Sik, i wsp.
  Wydane: (2014)
• Severe congenital neutropenia resulting from G6PC3 deficiency with increased neutrophil CXCR4 expression and myelokathexis
  od: McDermott, David H., i wsp.
  Wydane: (2010)
• Functional analysis of mutations in a severe congenital neutropenia syndrome caused by glucose-6-phosphatase-β deficiency
  od: Lin, Su Ru, i wsp.
  Wydane: (2014)