ArticlePloS one2010
Ezrin is highly expressed in early thymocytes, but dispensable for T cell development in mice.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Congenital enteropathy caused by ezrin deficiency.Human genetics · 2025Article
- Inherited human ezrin deficiency impairs adaptive immunity.The Journal of allergy and clinical immunology · 2023Article
- A Murine Model of X-Linked Moesin-Associated Immunodeficiency (X-MAID) Reveals Defects in T Cell Homeostasis and Migration.Frontiers in immunology · 2021Article
- Sequential binding of ezrin and moesin to L-selectin regulates monocyte protrusive behaviour during transendothelial migration.Journal of cell science · 2018Article
- Ezrin tunes the magnitude of humoral immunity.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Expression of ezrin in human embryonic, fetal, and normal adult tissues.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2011Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundEzrin/radixin/moesin (ERM) proteins are highly homologous proteins that function to link cargo molecules to the actin cytoskeleton. Ezrin and moesin are both expressed in mature lymphocytes, where they play overlapping roles in cell signaling and polarity, but their role in lymphoid development has not been explored. METHODOLOGY/PRINCIPAL
findingsWe characterized ERM protein expression in lymphoid tissues and analyzed the requirement for ezrin expression in lymphoid development. In wildtype mice, we found that most cells in the spleen and thymus express both ezrin and moesin, but little radixin. ERM protein expression in the thymus was differentially regulated, such that ezrin expression was highest in immature thymocytes and diminished during T cell development. In contrast, moesin expression was low in early thymocytes and upregulated during T cell development. Mice bearing a germline deletion of ezrin exhibited profound defects in the size and cellularity of the spleen and thymus, abnormal thymic architecture, diminished hematopoiesis, and increased proportions of granulocytic precursors. Further analysis using fetal liver chimeras and thymic transplants showed that ezrin expression is dispensable in hematopoietic and stromal lineages, and that most of the defects in lymphoid development in ezrin(-/-) mice likely arise as a consequence of nutritional stress. CONCLUSIONS/SIGNIFICANCE: We conclude that despite high expression in lymphoid precursor cells, ezrin is dispensable for lymphoid development, most likely due to redundancy with moesin.
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