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Cytoskeleton (Hoboken) ; 73(5): 258-68, 2016 May.
Article in English | MEDLINE | ID: mdl-27106882

ABSTRACT

B-lymphocytes are migrating cells that specialize in antigen presentation, antibody secretion, and endocytosis; these processes implicate the modulation of plasma membrane elasticity. Cell stiffness is a force generated by the interaction between the actin-cytoskeleton and the plasma membrane, which requires the participation of several proteins. These proteins include class I myosins, which are now considered to play a role in controlling membrane-cytoskeleton interactions. In this study, we identified the motor protein Myosin 1g (Myo1g) as a mediator of this phenomenon. The absence of Myo1g decreased the cell stiffness, affecting cell adhesion, cell spreading, phagocytosis, and endocytosis in B-lymphocytes. The results described here reveal a novel molecular mechanism by which Myo1g mediates and regulates cell stiffness in B-lymphocytes. © 2016 Wiley Periodicals, Inc.


Subject(s)
Actin Cytoskeleton/metabolism , B-Lymphocytes/metabolism , Cell Membrane/metabolism , Endocytosis/physiology , Minor Histocompatibility Antigens/metabolism , Myosins/metabolism , Phagocytosis/physiology , Actin Cytoskeleton/genetics , Animals , B-Lymphocytes/cytology , Cell Adhesion/physiology , Cell Membrane/genetics , Female , Mice , Mice, Knockout , Minor Histocompatibility Antigens/genetics , Myosins/genetics
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