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Expression of CALR mutants causes mpl-dependent thrombocytosis in zebrafish.
Author: ChangC-Y, ChangY-C, ChiangY-H, ChouW-C, Gon-Shen ChenC, HuangL, KuoY-Y, LimK-H, LinC-S, LinH-C, WangW-T
Original Abstract of the Article :
CALR mutations are identified in about 30% of JAK2/MPL-unmutated myeloproliferative neoplasms (MPNs) including essential thrombocythemia (ET) and primary myelofibrosis. Although the molecular pathogenesis of CALR mutations leading to MPNs has been studied using in vitro cell lines models, how mutant...See full text at original site
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引用元:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098260/
データ提供:米国国立医学図書館(NLM)
Mutant CALR: A Storm in the Desert of Hematopoiesis
The world of hematopoiesis, the intricate process of blood cell formation, is like a complex desert ecosystem, where delicate balances must be maintained. This study explores the role of mutant CALR, a protein implicated in myeloproliferative neoplasms (MPNs), in zebrafish, a model organism commonly used for studying human diseases. The authors investigated the effects of mutant CALR on early hematopoiesis and thrombocytosis, like exploring the impact of a sandstorm on a delicate desert ecosystem.
Mutant CALR: A Disruptive Force in Hematopoiesis
The findings demonstrate that mutant CALR, like a disruptive sandstorm in the desert, can cause an increase in hematopoietic stem/progenitor cells and thrombocytosis in zebrafish. The study reveals that mutant CALR activates JAK-STAT signaling through an MPL-dependent mechanism, highlighting the potential of targeting this pathway for therapeutic intervention. This research provides valuable insights into the molecular mechanisms underlying CALR-associated MPNs and the potential for developing new therapies based on this understanding.
Navigating the Sands of Hematopoiesis
This study, like a guide through the complex desert of hematopoiesis, offers a fascinating glimpse into the role of mutant CALR in MPNs. The findings underscore the importance of understanding the intricate interplay of genes and signaling pathways in blood cell formation and the potential for developing targeted therapies based on this understanding. This research encourages further investigation into the mechanisms of action of mutant CALR and the development of new therapeutic strategies for MPNs.
Dr. Camel's Conclusion
This study, like a flickering candle in the vast desert of MPNs, sheds light on the disruptive role of mutant CALR in hematopoiesis. By understanding the molecular mechanisms underlying CALR-associated MPNs, researchers can develop new targeted therapies that offer hope for patients battling these challenging blood disorders.
Date :
- Date Completed 2017-11-20
- Date Revised 2022-06-13
Further Info :
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