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November 11, 2025The Journal of Experimental MedicineOpen Access

JAK2/JAK2V617F heterodimers activate STAT1 and AhR to promote thrombocytosis

Radek C. Skoda Olli Silvennoinen

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Key Points

The study aims to understand the impact of JAK2V617F mutations on platelet production and related disorders.
Examined hematopoietic progenitors with JAK2V617F mutation
Compared activation of STAT1 and STAT5 in heterozygous and homozygous conditions
Analyzed platelet production and associated blood disorders
Heterozygous progenitors with JAK2V617F preferentially activate STAT1
This activation promotes increased platelet production leading to thrombocytosis
Homozygous progenitors activate STAT5, resulting in erythrocytosis and polycythemia

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Implication

Findings reveal that JAK2V617F mutations enhance platelet production in hematopoietic progenitors, indicating a role in thrombocytosis.

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Cite This Study

Skoda et al. (2025) studied this question.

synapsesocial.com/papers/69252e90c0ce034ddc356095 https://doi.org/10.1084/jem.20251880

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Keep reading

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Heterozygous human JAK2V617F activates AhR to drive essential thrombocythemia and promote thrombosis2025 · 3 citations
2Germline Jak2-R1063H mutation interferes with normal hematopoietic development and increases risk of thrombosis and leukemic transformation2025 · 3 citations
3Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disordersOriginal Research · 2005 · 3,550 citations
4Abstract 2097: <i> Jak2 <sup>V617f</sup> </i> Clonal Hematopoiesis Promotes Arterial Thrombosis Via Platelet Activation And Cross-talk2024
5The V617F mutation in JAK2 renders myeloid cells more sensitive to IL-6-mediated gp130 signaling2025