IFITM3 amino acid mutants phosphoproteomics

To investigate the role of IFITM3 in B-ALL, patient derived xenograft cells PDX2 were transduced with either a the constitutively membrane associated IFITM3-Y20E mutant or EV control. Additional mutation of PIP3 binding sites within the conserved internal loop region - K83/K104 or R85/R87/K88 - were introduced to test the predicted function of these sites.

为探究干扰素诱导跨膜蛋白3（IFITM3）在B细胞急性淋巴细胞白血病（B-ALL）中的作用，本研究将患者来源异种移植细胞系PDX2分别转导以组成型膜结合型IFITM3-Y20E突变体或空载对照（EV）。随后在保守内环区域内的磷脂酰肌醇三磷酸（PIP3）结合位点——K83/K104或R85/R87/K88——引入额外突变，以验证这些位点的预测功能。