ArticleThe Journal of clinical investigation1997
Truncation of the cytoplasmic domain of beta3 in a variant form of Glanzmann thrombasthenia abrogates signaling through the integrin alpha(IIb)beta3 complex.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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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.
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Who cites it
35 citing papers in PubMed, 113 citations in OpenAlex.
- Platelet FcγRIIA is dispensable for hemostasis and arterial thrombosis in the absence of FcγRIIA-specific extracellular stimuli.Research and practice in thrombosis and haemostasis · 2026Article
- Profiling the Genetic and Molecular Characteristics of Glanzmann Thrombasthenia: Can It Guide Current and Future Therapies?Journal of blood medicine · 2021Review
- ITGB3-mediated uptake of small extracellular vesicles facilitates intercellular communication in breast cancer cells.Nature communications · 2020Article
- Topological Adaptation of Transmembrane Domains to the Force-Modulated Lipid Bilayer Is a Basis of Sensing Mechanical Force.Current biology : CB · 2020Article
- Discoidin-domain receptor coordinates cell-matrix adhesion and collective polarity in migratory cardiopharyngeal progenitors.Nature communications · 2019Article
- Clinical and molecular insights into Glanzmann's thrombasthenia in China.Clinical genetics · 2018Article
- An intracytoplasmic β3 Leu718 deletion in a patient with a novel platelet phenotype.Blood advances · 2017Article
- The integrin adhesome: from genes and proteins to human disease.Nature reviews. Molecular cell biology · 2014Review
- Talin and kindlin: the one-two punch in integrin activation.Frontiers of medicine · 2014Review
- Glanzmann thrombasthenia: state of the art and future directions.Seminars in thrombosis and hemostasis · 2013Review
- Reconstruction of integrin activation.Blood · 2012Review
- Integrin αIIb-mediated PI3K/Akt activation in platelets.PloS one · 2012Article
- Do cell junction protein mutations cause an airway phenotype in mice or humans?American journal of respiratory cell and molecular biology · 2011Review
- Article
- Dominant inheritance of a novel integrin beta3 mutation associated with a hereditary macrothrombocytopenia and platelet dysfunction in two Italian families.Haematologica · 2009Article
- Article
- Eptifibatide-induced thrombocytopenia and thrombosis in humans require FcgammaRIIa and the integrin beta3 cytoplasmic domain.The Journal of clinical investigation · 2009Article
- Review
- Article
- Mechanisms and consequences of agonist-induced talin recruitment to platelet integrin alphaIIbbeta3.The Journal of cell biology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Glanzmann thrombasthenia is an inherited bleeding disorder characterized by absence or dysfunction of the platelet integrin alpha(IIb)beta3. Patient RM is a thrombasthenic variant whose platelets fail to aggregate in response to physiological agonists, despite the fact that they express abundant levels of alpha(IIb)beta3 on their surface. Binding of soluble fibrinogen or fibrinogen mimetic antibodies to RM platelets did not occur, except in the presence of ligand-induced binding site (LIBS) antibodies that transformed the RM integrin complex into an active conformation from outside the cell. Sequence analysis of PCR-amplified genomic DNA and platelet mRNA revealed a C2268T nucleotide substitution in the gene encoding the integrin beta3 subunit that resulted in an Arg724Ter mutation, producing a truncated protein containing only the first eight of the 47 amino acids normally present in the cytoplasmic domain. Functional analysis of both RM platelets and CHO cells stably expressing this truncated integrin revealed that the alpha(IIb)beta3Arg724Ter complex is able to mediate binding to immobilized fibrinogen, though downstream events, including cytoskeletally-mediated cell spreading and tyrosine phosphorylation of focal adhesion kinase, pp125FAK, fail to occur. These studies establish the importance of the membrane-distal portion of the integrin beta3 cytoplasmic domain in bidirectional transmembrane signaling in human platelets, and the role of integrin signaling in maintaining normal hemostasis in vivo.
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