SRPK1 knockdown in Jurkat cells was achieved by lentiviral shRNAi transduction, resulting in a highly significant knockdown (Fig. 4 A) and a switch in splicing from the flPD1 to ∆Ex3PD1 isoform (Fig. 4 B, C ).
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Targeting alternative splicing as a new cancer immunotherapy-phosphorylation of serine arginine-rich splicing factor (SRSF1) by SR protein kinase 1 (SRPK1) regulates alternative splicing of PD1 to generate a soluble antagonistic isoform that prevents T cell exhaustion.
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