Differential Expression of STK35L1-Associated Transcription Factors in Plasmodium Infection During the Liver Stage of Malaria

Malaria remains one of the devastating illnesses, and drug-resistant malaria has incurred enormous societal costs. A few host kinases are vital for the liver stage malaria and might be promising drug targets against drug-resistant malaria. STK35L1 is one of the host kinases that is highly upregulated during the liver stage of malaria, and the knockdown of STK35L1 significantly suppresses Plasmodium sporozoite infection. In this study, we retrieved the promoter region of STK35L1 based on 5′ complete transcripts, transcription start sites, and cap analysis of gene expression tags. Furthermore, we identify transcriptionally active regions by analyzing CpG islands, histone acetylation (H3K27ac), and histone methylation (H3K4me3). It suggests that the identified promoter region is active and has cis-regulatory elements and enhancer regions. We identified various putative transcription factors (TFs) from the various high-throughput ChIP data that might bind to the promoter region of STK35L1. These TFs were differentially regulated during the infection of Plasmodium sporozoites in HepG2 cells. Our molecular modeling study suggests that, except for SMAD3, the identified TFs may be directly bound to the promoter. Together, the data suggest that these TFs may play a role in sporozoite infection and in regulating STK35L1 expression during the liver stage of malaria.