The 2 faces of ERK2 in MPNs
Author:
Affiliation:
1. 1Cliniques Universitaires Saint-Luc;
2. 2Ludwig Institute for Cancer Research Brussels;
3. 3Université Catholique de Louvain–de Duve Institute; and
4. 4Oxford University
Publisher
American Society of Hematology
Subject
Cell Biology,Hematology,Immunology,Biochemistry
Link
https://ashpublications.org/blood/article-pdf/140/4/298/1910261/bloodbld2022016536c.pdf
Reference10 articles.
1. The ERK2-DBP domain opposes pathogenesis of a JAK2V617F-driven myeloproliferative neoplasm;Zhang;Blood.,2022
2. Genetic basis and molecular pathophysiology of classical myeloproliferative neoplasms;Vainchenker;Blood.,2017
3. Heterodimeric JAK-STAT activation as a mechanism of persistence to JAK2 inhibitor therapy;Koppikar;Nature.,2012
4. Targeting compensatory MEK/ERK activation increases JAK inhibitor efficacy in myeloproliferative neoplasms;Stivala;J Clin Invest.,2019
5. Splicing factor YBX1 mediates persistence of JAK2-mutated neoplasms;Jayavelu;Nature.,2020
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