Myo1g is an active player in maintaining cell stiffness in B-lymphocytes
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...
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Veröffentlicht in: | Cytoskeleton (Hoboken, N.J.) N.J.), 2016-05, Vol.73 (5), p.258-268 |
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Sprache: | eng |
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Zusammenfassung: | 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. |
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ISSN: | 1949-3584 1949-3592 |
DOI: | 10.1002/cm.21299 |