FcγRIIb-mediated negative regulation of BCR signalling is associated with the recruitment of the MAPkinase-phosphatase, Pac-1, and the 3′-inositol phosphatase, PTEN

Cellular Signalling

Volumn 16, Issue 1, 2004, Pages 71-80

  Brown, Kirsty S ^a   Blair, Derek ^a   Reid, Steven D ^a   Nicholson, Emma K ^a   Harnett, Margaret M ^a  

^a UNIVERSITY OF GLASGOW   (United Kingdom)

Author keywords

Apoptosis; B lymphocytes; MAPkinase; Phosphatases; Proliferation; Signal transduction

Indexed keywords

3' INOSITOL PHOSPHATASE; FC RECEPTOR; IMMUNOGLOBULIN G; LYMPHOCYTE ANTIGEN RECEPTOR; MITOGEN ACTIVATED PROTEIN KINASE; MITOGEN ACTIVATED PROTEIN KINASE 1; PHOSPHATASE; RAS PROTEIN; UNCLASSIFIED DRUG; FCGR2B PROTEIN, MOUSE; ONCOPROTEIN; PAC1 PHOSPHATASE; PHOSPHATIDYLINOSITOL 3 KINASE; PHOSPHATIDYLINOSITOL 3,4,5 TRISPHOSPHATE 3 PHOSPHATASE; PROTEIN KINASE B; PROTEIN SERINE THREONINE KINASE; PROTEIN TYROSINE PHOSPHATASE; PTEN PROTEIN, MOUSE; TUMOR SUPPRESSOR PROTEIN;

ANIMAL CELL; ANIMAL TISSUE; ANTIBODY RESPONSE; ANTIGEN ANTIBODY COMPLEX; ARTICLE; CELL PROLIFERATION; CELL SURVIVAL; CONTROLLED STUDY; CORRELATION ANALYSIS; DEPHOSPHORYLATION; ENZYME ACTIVITY; ENZYME INDUCTION; ENZYME INHIBITION; MALE; MOUSE; NEGATIVE FEEDBACK; NONHUMAN; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; RECEPTOR AFFINITY; RECEPTOR BINDING; SIGNAL TRANSDUCTION; ANIMAL; APOPTOSIS; B LYMPHOCYTE; BAGG ALBINO MOUSE; CELL CULTURE; CELL DIVISION; DOWN REGULATION; DRUG EFFECT; ENZYMOLOGY; FEEDBACK SYSTEM; GENETICS; IMMUNOLOGY; METABOLISM; PHOSPHORYLATION;

1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; APOPTOSIS; B-LYMPHOCYTES; CELL DIVISION; CELL SURVIVAL; CELLS, CULTURED; DOWN-REGULATION; FEEDBACK, BIOCHEMICAL; MALE; MICE; MICE, INBRED BALB C; MITOGEN-ACTIVATED PROTEIN KINASES; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTEIN-TYROSINE-PHOSPHATASE; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; PTEN PHOSPHOHYDROLASE; RECEPTORS, ANTIGEN, B-CELL; RECEPTORS, IGG; SIGNAL TRANSDUCTION; TUMOR SUPPRESSOR PROTEINS;

EID: 0242352506     PISSN: 08986568     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0898-6568(03)00113-X     Document Type: Article

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