Differentiation of the HSCs into myeloid lineage is primarily monitored by transcription factor PU.1. GATA1 acts as a negative regulator by antagonizing the function of PU.1 by bindings its β3/β4 domain. In this study, a mutation was induced in PU.1 which blocks its interaction with GATA1. The pure form of this mutant protein i.e Y244D was loaded on poly (lactic-co-glycolic acid) nanoparticles to transfect CD34⁺ cells, which act as a selective tool to enhance the myelopoiesis, as confirmed by flow cytometry analysis. Further, microarray data analysis was performed to gather information on myelopoiesis specific signaling pathways and genes involved in myelopoiesis like CCL2, S100A8, and S100A9, which were also found to be significantly upregulated in the mutant form. Different molecular functions like antioxidant activity, signal transduction, developmental processes, and biological adhesion were analyzed. This study potentially signifies that PU.1 mutant is highly efficient in myelopoiesis.

HSCs向骨髓谱系的分化主要由转录因子PU.1监测。GATA1通过结合其β3/β4结构域拮抗PU.1的功能，从而起负调节剂的作用。在这项研究中，在PU.1中诱导了一个突变，该突变阻止了它与GATA1的相互作用。将这种突变蛋白的纯形式，即Y244D加载到聚（乳酸-乙醇酸）纳米颗粒上，以转染CD34 ⁺流式细胞仪分析证实，这些细胞可作为增强骨髓生成的选择性工具。此外，进行了微阵列数据分析以收集有关骨髓生成特定信号通路和涉及骨髓生成的基因的信息，例如CCL2，S100A8和S100A9，它们也被发现以突变形式显着上调。分析了不同的分子功能，例如抗氧化剂活性，信号转导，发育过程和生物粘附。这项研究潜在地表明，PU.1突变体在骨髓生成中非常有效。