Blood: The beta-catenin-TCF/LEF signal promotes granulocyte differentiation by raising the G-CSF subject.

Central point: beta-catenin-TCF/LEF interaction barriers can disrupt steady-state and emergency particle production, and TCF/LEF factors regulate G-CSF subject expression by interacting directly with Csf3r's initiators and enhancer regions.
: The classical Wnt signaling path is regulated by the interaction between beta-catenin and TCF/LEF transcription factors, and the Wnt-target gene is then transcriptionally activated.
in hematic systems, the function of this path is mainly studied through the nonsexual genetic operation of beta-catenin, but often with contradictory results.
In this study, Danek and other mice that expressed the explicit negative form (dnTCF4) of TCF4 transcription factors were used to study the role of beta-catenin-TCF/LEF interactions in the hematogic system, and the beta-catenin-TCF/LEF interactions of the mouse model were disrupted.
-catenin-TCF/LEF interactions are disrupted leading to the accumulation of immature blood cells and reduced granulocyte differentiation.
the mechanism, the Csf3r gene of dnTCF4 ancestral cells was reduced, the level of G-CSF subjects decreased, the phosphate of downstream Stat3 decreased after G-CSF treatment, and the differentiation of G-CSF-mediated was impaired.
chromosomal immunopopulation experiments showed that TCF/LEF factors were directly combined with the initiators of CSF3R and the presumed enhanced subregions.
inhibits the beta-catenin signal to impair the activation of the granulocyte's acute production process, which requires the maintenance and amplification of myelin's ancestral cells.
(effects of WT and dnTCF4 mice after treatment with 5-fluorouracil) therefore, dnTCF4 mice were susceptible to white candide and more sensitive to 5-fluorouracil-induced granulocyte regeneration.
importantly, genetically and chemically inhibiting beta-catenin-TCF/LEF signals in human CD34 plus cells reduces granulocyte differentiation, and activation of this signal enhances granulocyte production.
in summary, this study shows that the beta-catenin-TCF/LEF complex directly regulates the level of G-CSF subjects, thus controlling the proper differentiation of myelin ancestral cells to granulocytes in a stable and critical state.
the study sheds light on the role of beta-catenin signaling paths in fine-tuning granulocyte production, providing theoretical support for clinical interventions to improve or reduce neutral granulocyte production.
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