ArticleScientific reports2021
Yippee like 4 (Ypel4) is essential for normal mouse red blood cell membrane integrity.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- The YPEL genePlant signaling & behavior · 2026Article
- Whole Blood Transcriptomic Analysis of Sickle Cell Trait.European journal of haematology · 2026Article
- Yippee-like protein Moh1 links gene expression to metabolism and selective stress resistance inMicrobial cell (Graz, Austria) · 2026Article
- miRNA-1 regulation is necessary for mechanical overload-induced muscle hypertrophy in male mice.Physiological reports · 2025Article
- Enhancing terminal erythroid differentiation in human embryonic stem cells through TRIB3 overexpression.Heliyon · 2024Article
- Identification of common biomarkers in diabetic kidney disease and cognitive dysfunction using machine learning algorithms.Scientific reports · 2024Article
- Dynamic proximity interaction profiling suggests that YPEL2 is involved in cellular stress surveillance.Protein science : a publication of the Protein Society · 2024Article
- Impacts of vitrification on the transcriptome of human ovarian tissue in patients with gynecological cancer.Frontiers in genetics · 2023Article
- Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The YPEL family genes are highly conserved across a diverse range of eukaryotic organisms and thus potentially involved in essential cellular processes. Ypel4, one of five YPEL family gene orthologs in mouse and human, is highly and specifically expressed in late terminal erythroid differentiation (TED). In this study, we investigated the role of Ypel4 in murine erythropoiesis, providing for the first time an in-depth description of a Ypel4-null phenotype in vivo. We demonstrated that the Ypel4-null mice displayed a secondary polycythemia with macro- and reticulocytosis. While lack of Ypel4 did not affect steady-state TED in the bone marrow or spleen, the anemia-recovering capacity of Ypel4-null cells was diminished. Furthermore, Ypel4-null red blood cells (RBC) were cleared from the circulation at an increased rate, demonstrating an intrinsic defect of RBCs. Scanning electron micrographs revealed an ovalocytic morphology of Ypel4-null RBCs and functional testing confirmed reduced deformability. Even though Band 3 protein levels were shown to be reduced in Ypel4-null RBC membranes, we could not find support for a physical interaction between YPEL4 and the Band 3 protein. In conclusion, our findings provide crucial insights into the role of Ypel4 in preserving normal red cell membrane integrity.
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