ArticleBlood2007
Tropomyosin modulates erythrocyte membrane stability.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Identification of a novel role for dematin in regulating red cell membrane function by modulating spectrin-actin interaction.The Journal of biological chemistry · 2012Trial
- Cell membrane-camouflaged inorganic nanoparticles for cancer therapy.Journal of nanobiotechnology · 2022Review
- Nanocarriers surface engineered with cell membranes for cancer targeted chemotherapy.Journal of nanobiotechnology · 2022Review
- Review
- Extracellular Vesicles from Red Blood Cells and Their Evolving Roles in Health, Coagulopathy and Therapy.International journal of molecular sciences · 2020Review
- From Experiments to Simulation: Shear-Induced Responses of Red Blood Cells to Different Oxygen Saturation Levels.Frontiers in physiology · 2019Article
- Stabilization of F-actin by tropomyosin isoforms regulates the morphology and mechanical behavior of red blood cells.Molecular biology of the cell · 2017Article
- Feisty filaments: actin dynamics in the red blood cell membrane skeleton.Current opinion in hematology · 2016Review
- Processing of Plasmodium falciparum Merozoite Surface Protein MSP1 Activates a Spectrin-Binding Function Enabling Parasite Egress from RBCs.Cell host & microbe · 2015Article
- Axon initial segment cytoskeleton comprises a multiprotein submembranous coat containing sparse actin filaments.The Journal of cell biology · 2014Article
- Hematopoietic protein-1 regulates the actin membrane skeleton and membrane stability in murine erythrocytes.PloS one · 2013Article
- Refined views of multi-protein complexes in the erythrocyte membrane.Blood cells, molecules & diseases · 2012Review
- Tropomodulins: pointed-end capping proteins that regulate actin filament architecture in diverse cell types.Cytoskeleton (Hoboken, N.J.) · 2012Review
- Native ultrastructure of the red cell cytoskeleton by cryo-electron tomography.Biophysical journal · 2011Article
- Phosphorylation-dependent perturbations of the 4.1R-associated multiprotein complex of the erythrocyte membrane.Biochemistry · 2011Article
- Erythrocyte adducin: a structural regulator of the red blood cell membrane.Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine · 2010Article
- Article
- Article
- Cytoskeletal tropomyosin Tm5NM1 is required for normal excitation-contraction coupling in skeletal muscle.Molecular biology of the cell · 2009Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The ternary complex of spectrin, actin, and 4.1R (human erythrocyte protein 4.1) defines the nodes of the erythrocyte membrane skeletal network and is inseparable from membrane stability under mechanical stress. These junctions also contain tropomyosin (TM) and the other actin-binding proteins, adducin, protein 4.9, tropomodulin, and a small proportion of capZ, the functions of which are poorly defined. Here, we have examined the consequences of selective elimination of TM from the membrane. We have shown that the mechanical stability of the membranes of resealed ghosts devoid of TM is grossly, but reversibly, impaired. That the decreased membrane stability of TM-depleted membranes is the result of destabilization of the ternary complex of the network junctions is demonstrated by the strongly facilitated entry into the junctions in situ of a beta-spectrin peptide, containing the actin- and 4.1R-binding sites, after extraction of the TM. The stabilizing effect of TM is highly specific, in that it is only the endogenous isotype, and not the slightly longer muscle TM that can bind to the depleted membranes and restore their mechanical stability. These findings have enabled us identify a function for TM in elevating the mechanical stability of erythrocyte membranes by stabilizing the spectrin-actin-4.1R junctional complex.
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What OpenQuestion holds
Registered trials
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.