JAK2/JAK2V617F heterodimers activate STAT1 and AhR to promote thrombocytosis
In this issue of JEM, Zhou et al. (https://doi.org/10.1084/jem.20250153) report that hematopoietic progenitors heterozygous for the JAK2V617F mutation preferentially activate STAT1, promoting platelet production and thrombocythemia, whereas homozygous progenitors activate STAT5, leading to erythrocytosis and polycythemia.
Authors
- Olli Silvennoinen (ORCID: https://orcid.org/0000-0003-0747-9512)
- Radek C. Skoda (ORCID: https://orcid.org/0000-0002-3626-9496)
Institutions
- Tampere University of Applied Sciences (FI)
- Baylor College of Medicine (US)
- Tampere University (FI)
- Fimlab (Finland) (FI)
- Children's Cancer Center (US)
Publication Details
- Journal
- The Journal of Experimental Medicine
- Published
- 2025-11-11
- DOI
- https://doi.org/10.1084/jem.20251880
- Primary Topic
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00