Fig. 3: Inflammatory signaling and myeloid skewing in Jak2-R1063H mutant hematopoiesis.

A Quantification of absolute number of myeloid precursors in BM. Lin⁻ c-Kit⁺ Sca-1⁻ (LK), Lin⁻ c-Kit⁺ Sca-1⁻ CD34⁺ FcgRII/III^low (CMP), Lin⁻ c-Kit⁺ Sca-1⁻ CD34⁺ FcgRII/III⁺(GMP) and Lin⁻c-Kit⁺ Sca-1^- CD34^- FcgRII/III^low (MEP) (n ≥ 4 mice per group). B Quantification of absolute number of erythroid/megakaryocytic committed subsets - Lin⁻ c-Kit⁺Sca-1⁻/CD41⁻/CD150^low/CD105⁺ (CFU-E), Lin⁻c-Kit⁺Sca-1⁻/CD41⁻/ CD 150⁺/CD105⁺ (Pre–erythroid CFU), Lin⁻c-Kit⁺Sca-1⁻/CD41⁺/CD150⁺ (MkP), Lin⁻c-Kit⁺Sca-1⁻/ CD41^low /CD150⁺/CD105⁻ (Pre-MegE) and Lin⁻c-Kit⁺Sca-1⁻/CD41^low/CD150⁻/CD105^- (Pre-GM) (n ≥ 4 mice per group). C Phosphorylation of Stat1 (Tyr 694), Stat3 (Tyr 705) and Erk1/2 (Thr 202/Tyr 204) proteins in m/m (wt) and RH/RH c-Kit⁺ enriched fraction of total BM. Total Erk protein and Vinculin served as loading control. WB shows the baseline (blank line) and cytokine-stimulated protein activities in protein lysates from enriched c-kit⁺ cells, starved for 40 hours and unstimulated or stimulated with indicated cytokines for 15 min. D GSEA for selected pathways from Hallmark gene sets enriched in RH/RH vs. m/m in LK cells, NOM p values < 0.05. Data are presented as mean ± SD and unpaired t-test with Welsch’s correction was used for group comparison. *p < 0.05.