ArticleLeukemia2015
A point mutation of zebrafish c-cbl gene in the ring finger domain produces a phenotype mimicking human myeloproliferative disease.
Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Loss of Tars induces proteostasis stress and drives HSPC exhaustion through mTORC1 activation.Acta pharmacologica Sinica · 2026Article
- Genome-wide association study for growth traits with 1066 individuals in largemouth bass (Frontiers in molecular biosciences · 2024Article
- Animal models for thrombotic thrombocytopenic purpura: a narrative review.Annals of blood · 2023Article
- Zebrafish models of acute leukemias: Current models and future directions.Wiley interdisciplinary reviews. Developmental biology · 2021Review
- Selective and competitive functions of the AAR and UPR pathways in stress-induced angiogenesis.Cell discovery · 2021Article
- Precise base editing for theeLife · 2021Article
- Zebrafish Cancer Predisposition Models.Frontiers in cell and developmental biology · 2021Review
- Bloody Zebrafish: Novel Methods in Normal and Malignant Hematopoiesis.Frontiers in cell and developmental biology · 2018Article
- Genetic Models of Leukemia in Zebrafish.Frontiers in cell and developmental biology · 2018Review
- Review
- Understanding the regulation of vertebrate hematopoiesis and blood disorders - big lessons from a small fish.FEBS letters · 2016Review
- Fish to Learn: Insights into Blood Development and Blood Disorders from Zebrafish Hematopoiesis.Human gene therapy · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 7 institutions in 2 countries.
Funding
Abstract
Controlled self-renewal and differentiation of hematopoietic stem/progenitor cells (HSPCs) are critical for vertebrate development and survival. These processes are tightly regulated by the transcription factors, signaling molecules and epigenetic factors. Impaired regulations of their function could result in hematological malignancies. Using a large-scale zebrafish N-ethyl-N-nitrosourea mutagenesis screening, we identified a line named LDD731, which presented significantly increased HSPCs in hematopoietic organs. Further analysis revealed that the cells of erythroid/myeloid lineages in definitive hematopoiesis were increased while the primitive hematopoiesis was not affected. The homozygous mutation was lethal with a median survival time around 14-15 days post fertilization. The causal mutation was located by positional cloning in the c-cbl gene, the human ortholog of which, c-CBL, is found frequently mutated in myeloproliferative neoplasms (MPN) or acute leukemia. Sequence analysis showed the mutation in LDD731 caused a histidine-to-tyrosine substitution of the amino acid codon 382 within the RING finger domain of c-Cbl. Moreover, the myeloproliferative phenotype in zebrafish seemed dependent on the Flt3 (fms-like tyrosine kinase 3) signaling, consistent with that observed in both mice and humans. Our study may shed new light on the pathogenesis of MPN and provide a useful in vivo vertebrate model of this syndrome for screening drugs.
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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.