G-CSF improves murine G6PC3-deficient neutrophil function by modulating apoptosis and energy homeostasis

Severe congenital neutropenia resulting from G6PC3 deficiency with increased neutrophil CXCR4 expression and myelokathexis

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Lack of glucose recycling between endoplasmic reticulum and cytoplasm underlies cellular dysfunction in glucose-6-phosphatase- -deficient neutrophils in a congenital neutropenia syndrome

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PI-3-K and AKT: Onto the mitochondria☆

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Regulation of neutrophil apoptosis by modulation of PKB/Akt activation

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A Syndrome with Congenital Neutropenia and Mutations inG6PC3

(2009) Kaan Boztug et al.   NEW ENGLAND JOURNAL OF MEDICINE

Neutrophil stress and apoptosis underlie myeloid dysfunction in glycogen storage disease type Ib

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