High-resolution structural analysis of branched actin networks at the sites of clathrin-mediated endocytosis sheds light on the role of actin in endocytosis and mechanisms controlling actin assembly.
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http://dx.doi.org/10.1016/j.cub.2011.06.029 | DOI Listing |
Front Immunol
January 2025
IrsiCaixa, Badalona, Spain.
Introduction: HIV-1 exploits dendritic cells (DCs) to spread throughout the body via specific recognition of gangliosides present on the viral envelope by the CD169/Siglec-1 membrane receptor. This interaction triggers the internalization of HIV-1 within a structure known as the sac-like compartment. While the mechanism underlying sac-like compartment formation remains elusive, prior research indicates that the process is clathrin-independent and cell membrane cholesterol-dependent and involves transient disruption of cortical actin.
View Article and Find Full Text PDFJ Cell Sci
January 2025
Department of Cellular & Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Here, we apply SuperResNET network analysis of dSTORM single-molecule localization microscopy (SMLM) to determine how the clathrin endocytosis inhibitors pitstop 2, dynasore and Latrunculin A alter the morphology of clathrin-coated pits. SuperResNET analysis of HeLa and Cos7 cells identifies: small oligomers (Class I); pits and vesicles (Class II); and larger clusters corresponding to fused pits or clathrin plaques (Class III). Pitstop 2 and dynasore induce distinct homogeneous populations of Class II structures in HeLa cells suggesting that they arrest endocytosis at different stages.
View Article and Find Full Text PDFLife (Basel)
January 2025
The Laboratory of Personalized Chemo-Radiation Therapy, Institute of Future Biophysics, Moscow 141700, Russia.
Cancer-related deaths primarily occur due to metastasis, a process involving the migration and invasion of cancer cells. In most solid tumors, metastasis occurs through collective cell migration (CCM), guided by "cellular leaders". These leader cells generate forces through actomyosin-mediated protrusion and contractility.
View Article and Find Full Text PDFNat Commun
January 2025
Hoxworth Center, College of Medicine, University of Cincinnati, Cincinnati, OH, USA.
Many micro-particles including pathogens strongly adhere to hosts. It remains elusive how macrophages detach these surface-bound particles during phagocytosis. We show that, rather than binding directly to these particles, macrophages form unique β integrin-mediated adhesion structures at the cell-substrate interfaces, specifically encircling the surface-bound particles.
View Article and Find Full Text PDFCell Signal
January 2025
Division of Bioengineering, Graduate School of Engineering Science, The University of Osaka, Japan; R(3) Institute for Newly-Emerging Science Design, The University of Osaka, Japan; Global Center for Medical Engineering and Informatics, The University of Osaka, Japan. Electronic address:
Aging proceeds with the accumulation of senescent cells in multiple organs. These cells exhibit increased size compared to young cells, which promotes further senescence and age-related diseases. Currently, the molecular mechanism behind the maintenance of such huge cell architecture undergoing senescence remains poorly understood.
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