ArticleThe Journal of cell biology1998
Mechanical fluctuations of the membrane-skeleton are dependent on F-actin ATPase in human erythrocytes.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 130 citations in OpenAlex.
- Mechanical adaptivity of red blood cell flickering to extrinsic membrane stiffening by the solid-like biosurfactant β-Aescin.Biophysical journal · 2025Article
- The multifaceted role of aquaporins in physiological cell migration.American journal of physiology. Cell physiology · 2023Review
- Differential Gene Expression in Host Ubiquitination Processes in Childhood Malarial Anemia.Frontiers in genetics · 2021Article
- Differential dielectroscopic data on the relation of erythrocyte membrane skeleton to erythrocyte deformability and flicker.European biophysics journal : EBJ · 2021Article
- Fast and synchronized fluctuations of cortical actin negatively correlate with nucleoli liquid-liquid phase separation in T cells.European biophysics journal : EBJ · 2020Article
- Quantitative absorption imaging of red blood cells to determine physical and mechanical properties.RSC advances · 2020Article
- Heat damage of cytoskeleton in erythrocytes increases membrane roughness and cell rigidity.Journal of biological physics · 2019Article
- Optical Tracking of Nanometer-Scale Cellular Membrane Deformation Associated with Single Vesicle Release.ACS sensors · 2019Article
- Measurements on ATP induced cellular fluctuations using real-time dual view transport of intensity phase microscopy.Biomedical optics express · 2019Article
- Three-Dimensional Shapes and Cell Deformability of Rat Red Blood Cells during and after Asphyxial Cardiac Arrest.Emergency medicine international · 2019Article
- Identification of Oxidative Stress in Red Blood Cells with Nanoscale Chemical Resolution by Infrared Nanospectroscopy.International journal of molecular sciences · 2018Article
- Myosin IIA interacts with the spectrin-actin membrane skeleton to control red blood cell membrane curvature and deformability.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Erythrocyte Aging, Protection via Vesiculation: An Analysis Methodology via Oscillatory Flow.Frontiers in physiology · 2018Article
- Squeezing for Life - Properties of Red Blood Cell Deformability.Frontiers in physiology · 2018Review
- Mechanical diagnosis of human erythrocytes by ultra-high speed manipulation unraveled critical time window for global cytoskeletal remodeling.Scientific reports · 2017Article
- Protection of the biconcave profile of human erythrocytes against osmotic damage by ultraviolet-A irradiation through membrane-cytoskeleton enhancement.Cell death discovery · 2017Article
- Yap/Taz transcriptional activity is essential for vascular regression via Ctgf expression and actin polymerization.PloS one · 2017Article
- Electrical Oscillations in Two-Dimensional Microtubular Structures.Scientific reports · 2016Article
- Measuring fast stochastic displacements of bio-membranes with dynamic optical displacement spectroscopy.Nature communications · 2015Article
- Direct Cytoskeleton Forces Cause Membrane Softening in Red Blood Cells.Biophysical journal · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell membrane fluctuations (CMF) of human erythrocytes, measured by point dark field microscopy, were shown to depend, to a large extent, on intracellular MgATP (Levin, S.V., and R. Korenstein. 1991. Biophys. J. 60:733-737). The present study extends that investigation and associates CMF with F-actin's ATPase activity. MgATP was found to reconstitute CMF in red blood cell (RBC) ghosts and RBC skeletons to their levels in intact RBCs, with an apparent Kd of 0.29 mM. However, neither non-hydrolyzable ATP analogues (AMP-PNP, ATPgammaS) nor hydrolyzable ones (ITP, GTP), were able to elevate CMF levels. The inhibition of ATPase activity associated with the RBC's skeleton, carried out either by the omission of the MgATP substrate or by the use of several inhibitors (vanadate, phalloidin, and DNase I), resulted in a strong decrease of CMF. We suggest that the actin's ATPase, located at the pointed end of the short actin filament, is responsible for the MgATP stimulation of CMF in RBCs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.