ArticleScientific reports2024
Calreticulin and JAK2V617F driver mutations induce distinct mitotic defects in myeloproliferative neoplasms.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Glutamate accumulation in myelofibrosis microenvironment rewires mesenchymal stromal cells metabolic and epigenetic profiles.Cell communication and signaling : CCS · 2026Article
- JAK2V617F reprograms Hypoxia Inducible Factor-1 to induce a non-canonical hypoxia regulon in myeloproliferative neoplasms.Leukemia · 2026Article
- CALR accelerates the growth of liver cancer cells by enhancing telomere activity via ARAF.Genes & diseases · 2026Article
- DNA methylation in primary myelofibrosis is partly associated with driver mutations and distinct from other myeloid malignancies.Clinical epigenetics · 2025Article
- Quantitative Live-Cell Imaging to Study Chromatin Segregation and Nuclear Reformation.Methods in molecular biology (Clifton, N.J.) · 2025Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Myeloproliferative neoplasms (MPNs) encompass a diverse group of hematologic disorders driven by mutations in JAK2, CALR, or MPL. The prevailing working model explaining how these driver mutations induce different disease phenotypes is based on the decisive influence of the cellular microenvironment and the acquisition of additional mutations. Here, we report increased levels of chromatin segregation errors in hematopoietic cells stably expressing CALRdel52 or JAK2V617F mutations. Our investigations employing murine 32D
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