Neutrophil spontaneous death is mediated by down-regulation of autocrine signaling through GPCR, PI3Kγ, ROS, and actin

Proceedings of the National Academy of Sciences of the United States of America

Volumn 107, Issue 7, 2010, Pages 2950-2955

  Xu, Yuanfu ^a   Loison, Fabien ^b,c   Luo, Hongbo R ^b,c  

^a INSTITUTE OF HEMATOLOGY AND BLOOD DISEASES HOSPITAL   (China)

^b HARVARD MEDICAL SCHOOL   (United States)

^c BOSTON CHILDREN S HOSPITAL   (United States)

Author keywords

Akt; Apoptosis; Reactive oxygen species

Indexed keywords

ACTIN; CHEMOKINE; G PROTEIN COUPLED RECEPTOR; PHOSPHATIDYLINOSITOL 3 KINASE; PHOSPHATIDYLINOSITOL 3 KINASE GAMMA; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE; PROTEIN KINASE B; REACTIVE OXYGEN METABOLITE;

ACTIN POLYMERIZATION; APOPTOSIS; ARTICLE; AUTOCRINE EFFECT; CELL DEATH; CELL TYPE; DOWN REGULATION; ENZYME ACTIVITY; ENZYME INACTIVATION; FEEDBACK SYSTEM; HOMEOSTASIS; INFLAMMATION; NEUTROPHIL; POSITIVE FEEDBACK; PRIORITY JOURNAL;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ACTINS; APOPTOSIS; AUTORADIOGRAPHY; BLOTTING, WESTERN; DOWN-REGULATION; ENZYME-LINKED IMMUNOSORBENT ASSAY; FLOW CYTOMETRY; HUMANS; ISOENZYMES; NEUTROPHILS; PHOSPHATIDYLINOSITOL PHOSPHATES; REACTIVE OXYGEN SPECIES; RECEPTORS, G-PROTEIN-COUPLED;

EID: 77649262734     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0912717107     Document Type: Article

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