ArticleMolecular and cellular biology2014
Absence of a red blood cell phenotype in mice with hematopoietic deficiency of SEC23B.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 51 citations in OpenAlex.
- LSD1 inhibition ameliorates congenital dyserythropoietic anemia type II.Science translational medicine · 2026Article
- p27Kip1 regulates γ-globin production.Blood · 2026Article
- A genome-wide screen identifies genes required for erythroid differentiation.Nature communications · 2025Article
- Hereditary disorders of ineffective erythropoiesis.Blood cells, molecules & diseases · 2025Review
- LMAN1 serves as a cargo receptor for thrombopoietin.JCI insight · 2024Article
- Genetics of hemostasis: from bedside to bench and back again.The Journal of clinical investigation · 2024Article
- Cargo selection in endoplasmic reticulum-to-Golgi transport and relevant diseases.The Journal of clinical investigation · 2023Review
- SEC23A rescues SEC23B-deficient congenital dyserythropoietic anemia type II.Science advances · 2021Article
- Vesicular formation regulated by ERK/MAPK pathway mediates human erythroblast enucleation.Blood advances · 2021Article
- Murine SEC24D can substitute functionally for SEC24C during embryonic development.Scientific reports · 2021Article
- Direct Generation of Immortalized Erythroid Progenitor Cell Lines from Peripheral Blood Mononuclear Cells.Cells · 2021Article
- ER-to-Golgi transport and SEC23-dependent COPII vesicles regulate T cell alloimmunity.The Journal of clinical investigation · 2021Article
- A new role of glutathione peroxidase 4 during human erythroblast enucleation.Blood advances · 2020Article
- Altered phenotype in LMAN1-deficient mice with low levels of residual LMAN1 expression.Blood advances · 2020Article
- The Endoplasmic Reticulum Cargo Receptor SURF4 Facilitates Efficient Erythropoietin Secretion.Molecular and cellular biology · 2020Article
- RAP-011 Rescues the Disease Phenotype in a Cellular Model of Congenital Dyserythropoietic Anemia Type II by Inhibiting the SMAD2-3 Pathway.International journal of molecular sciences · 2020Article
- Function of Arl4aa in the Initiation of Hematopoiesis in Zebrafish by Maintaining Golgi Complex Integrity in Hemogenic Endothelium.Stem cell reports · 2020Article
- Genetics and Genomics Approaches for Diagnosis and Research Into Hereditary Anemias.Frontiers in physiology · 2020Review
- Murine Surf4 is essential for early embryonic development.PloS one · 2020Article
- Coatopathies: Genetic Disorders of Protein Coats.Annual review of cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Congenital dyserythropoietic anemia type II (CDAII) is an autosomal recessive disease of ineffective erythropoiesis characterized by increased bi/multinucleated erythroid precursors in the bone marrow. CDAII results from mutations in SEC23B. The SEC23 protein is a core component of coat protein complex II-coated vesicles, which transport secretory proteins from the endoplasmic reticulum to the Golgi apparatus. Though the genetic defect underlying CDAII has been identified, the pathophysiology of this disease remains unknown. We previously reported that SEC23B-deficient mice die perinatally, exhibiting massive pancreatic degeneration, with this early mortality limiting evaluation of the adult hematopoietic compartment. We now report that mice with SEC23B deficiency restricted to the hematopoietic compartment survive normally and do not exhibit anemia or other CDAII characteristics. We also demonstrate that SEC23B-deficient hematopoietic stem cells (HSC) do not exhibit a disadvantage at reconstituting hematopoiesis when compared directly to wild-type HSC in a competitive repopulation assay. Secondary bone marrow transplants demonstrated continued equivalence of SEC23B-deficient and WT HSC in their hematopoietic reconstitution potential. The surprising discordance in phenotypes between SEC23B-deficient mice and humans may reflect an evolutionary shift in SEC23 paralog function and/or expression, or a change in a specific COPII cargo critical for erythropoiesis.
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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.