FIGURE

Figure 7

ID

ZDB-FIG-250607-33

Publication

Chen et al., 2025 - KDM6A Deficiency Induces Myeloid Bias and Promotes CMML-Like Disease Through JAK/STAT3 Activation by Repressing SOCS3

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Figure 7

KDM6A/SOCS3/p‐STAT3 pathway is conserved in human HSPCs. A) Immunohistochemical staining of KDM6A on BM biopsies. B) Immunohistochemical staining of SOCS3 on BM biopsies. C) The percentage of KDM6A⁺ and SOCS3⁺cells in immunohistochemical staining. D) The H‐score of KDM6A⁺ and SOCS3⁺ cells immunohistochemical staining. E) Correlation analysis of the percentage of KDM6A⁺ (C, left) and SOCS3⁺ (C, right) cells in CMML specimens. F) Correlation analysis of the H‐score of KDM6A⁺ (D, left) and SOCS3⁺ (D, right) cells in CMML specimens. G) Schematic representation of human HSPC enrichment, lentiviral infection, and in vitro stimulation experiments conducted in this study. H) qPCR analysis of genes expression including SOCS3, DDX21, C1QBP, SLC25A12, CEBPG, CEBPZ, and IRF8 in human HSPCs after GM‐CSF stimulation (n = 3, mean ± SD, Student's t test). I) Western Blot analysis of KDM6A, and H3K27me3 in human HSPCs after GM‐CSF stimulation. (J) Western Blot analysis of γH2AX, STAT3, and p‐STAT3^Y705 in human HSPCs after GM‐CSF stimulation. *p <0.05; **p <0.01; ***p < 0.001.

Expression Data

Expression Detail

Antibody Labeling

Phenotype Data

Phenotype Detail

Acknowledgments

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