SRSF2-P95H decreases JAK/STAT signaling in hematopoietic cells and delays myelofibrosis development in mice
Author:
Funder
Institut National Du Cancer
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
https://www.nature.com/articles/s41375-023-01878-0.pdf
Reference64 articles.
1. Vainchenker W, Kralovics R. Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms. Blood. 2017;129:667–79.
2. Gangat N, Tefferi A. Myelofibrosis biology and contemporary management. Br J Haematol. 2020;191:152–70.
3. Decker M, Martinez-Morentin L, Wang G, Lee Y, Liu Q, Leslie J, et al. Leptin-receptor-expressing bone marrow stromal cells are myofibroblasts in primary myelofibrosis. Nat Cell Biol. 2017;19:677–88.
4. Schneider RK, Mullally A, Dugourd A, Peisker F, Hoogenboezem R, Van Strien PMH, et al. Gli1+ Mesenchymal Stromal Cells Are a Key Driver of Bone Marrow Fibrosis and an Important Cellular Therapeutic Target. Cell Stem Cell. 2018;23:308–9.
5. Leimkühler NB, Gleitz HFE, Ronghui L, Snoeren IAM, Fuchs SNR, Nagai JS, et al. Heterogeneous bone-marrow stromal progenitors drive myelofibrosis via a druggable alarmin axis. Cell Stem Cell. 2021;28:637–52.e8.
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1. Molecular Genetic Profile of Myelofibrosis: Implications in the Diagnosis, Prognosis, and Treatment Advancements;Cancers;2024-01-25
2. SRSF2 mutation reduces polycythemia and impairs hematopoietic progenitor functions in JAK2V617F-driven myeloproliferative neoplasm;Blood Cancer Journal;2023-11-27
3. Hematopoietic Stem Cell: Regulation and Nutritional Intervention;Nutrients;2023-06-01
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