Impaired neutrophil activity and increased susceptibility to bacterial infection in mice lacking glucose-6-phosphatase–β

Eitemau Tebyg

• Lack of glucose recycling between endoplasmic reticulum and cytoplasm underlies cellular dysfunction in glucose-6-phosphatase-β–deficient neutrophils in a congenital neutropenia syndrome
  gan: Jun, Hyun Sik, et al.
  Cyhoeddwyd: (2010)
• Glucose-6-phosphate transporter gene therapy corrects metabolic and myeloid abnormalities in glycogen storage disease type Ib mice
  gan: Yiu, Wai Han, et al.
  Cyhoeddwyd: (2006)
• Glucose-6-phosphatase-β, implicated in a congenital neutropenia syndrome, is essential for macrophage energy homeostasis and functionality
  gan: Jun, Hyun Sik, et al.
  Cyhoeddwyd: (2012)
• Functional analysis of mutations in a severe congenital neutropenia syndrome caused by glucose-6-phosphatase-β deficiency
  gan: Lin, Su Ru, et al.
  Cyhoeddwyd: (2014)
• Minimal hepatic glucose-6-phosphatase-α activity required to sustain survival and prevent hepatocellular adenoma formation in murine glycogen storage disease type Ia
  gan: Lee, Young Mok, et al.
  Cyhoeddwyd: (2015)