ArticleThe Journal of clinical investigation1999
Protein 4.1R-deficient mice are viable but have erythroid membrane skeleton abnormalities.
Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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Who cites it
44 citing papers in PubMed, 123 citations in OpenAlex.
- PKR associates with 4.1R to promote anchorage-independent growth of hepatocellular carcinoma and lead to poor prognosis.Scientific reports · 2024Article
- Are EPB41 and alpha-synuclein diagnostic biomarkers of sport-related concussion? Findings from the NCAA and Department of Defense CARE Consortium.Journal of sport and health science · 2023Article
- Development of Mechanical Stability in Late-Stage Embryonic Erythroid Cells: Insights From Fluorescence Imaged Micro-Deformation Studies.Frontiers in physiology · 2021Article
- Epithelial-specific isoforms of protein 4.1R promote adherens junction assembly in maturing epithelia.The Journal of biological chemistry · 2020Article
- Protein 4.1R negatively regulates CD8Immunology · 2019Article
- Cytoskeletal Protein 4.1R Is a Positive Regulator of the FcεRI Signaling and Chemotaxis in Mast Cells.Frontiers in immunology · 2019Article
- Microfluidic assay of the deformability of primitive erythroblasts.Biomicrofluidics · 2017Article
- Circulating primitive erythroblasts establish a functional, protein 4.1R-dependent cytoskeletal network prior to enucleating.Scientific reports · 2017Article
- Proper cytoskeletal architecture beneath the plasma membrane of red blood cells requiresMolecular biology of the cell · 2017Article
- Innate B-1 B Cells Are Not Enriched in Red Blood Cell Autoimmune Mice: Importance of B Cell Receptor Transgenic Selection.Frontiers in immunology · 2017Article
- Protein 4.1R Influences Myogenin Protein Stability and Skeletal Muscle Differentiation.The Journal of biological chemistry · 2016Article
- Article
- Systematic Functional Dissection of Common Genetic Variation Affecting Red Blood Cell Traits.Cell · 2016Article
- Deletion of the intestinal plasma membrane calcium pump, isoform 1, Atp2b1, in mice is associated with decreased bone mineral density and impaired responsiveness to 1, 25-dihydroxyvitamin D3.Biochemical and biophysical research communications · 2015Article
- Article
- Cortical dynein and asymmetric membrane elongation coordinately position the spindle in anaphase.Cell · 2013Article
- ZFP36L2 is required for self-renewal of early burst-forming unit erythroid progenitors.Nature · 2013Article
- Strain-specific variations in cation content and transport in mouse erythrocytes.Physiological genomics · 2013Article
- Impaired intestinal calcium absorption in protein 4.1R-deficient mice due to altered expression of plasma membrane calcium ATPase 1b (PMCA1b).The Journal of biological chemistry · 2013Article
- Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
A diverse family of protein 4.1R isoforms is encoded by a complex gene on human chromosome 1. Although the prototypical 80-kDa 4.1R in mature erythrocytes is a key component of the erythroid membrane skeleton that regulates erythrocyte morphology and mechanical stability, little is known about 4.1R function in nucleated cells. Using gene knockout technology, we have generated mice with complete deficiency of all 4.1R protein isoforms. These 4.1R-null mice were viable, with moderate hemolytic anemia but no gross abnormalities. Erythrocytes from these mice exhibited abnormal morphology, lowered membrane stability, and reduced expression of other skeletal proteins including spectrin and ankyrin, suggesting that loss of 4. 1R compromises membrane skeleton assembly in erythroid progenitors. Platelet morphology and function were essentially normal, indicating that 4.1R deficiency may have less impact on other hematopoietic lineages. Nonerythroid 4.1R expression patterns, viewed using histochemical staining for lacZ reporter activity incorporated into the targeted gene, revealed focal expression in specific neurons in the brain and in select cells of other major organs, challenging the view that 4.1R expression is widespread among nonerythroid cells. The 4.1R knockout mice represent a valuable animal model for exploring 4.1R function in nonerythroid cells and for determining pathophysiological sequelae to 4.1R deficiency.
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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.