SRSF4 (Serine And Arginine Rich Splicing Factor 4)

Additionally, significant antiproliferative activity was observed for LBM22 in 3D cultured H1975OR cells. In conclusion, LBM22 emerges as a promising CLK2 inhibitor for the treatment of NSCLC.

Collectively our results underscore the critical involvement of SRSF family members in the context of oral cancer, highlighting their potential as key players in the altered splicing dynamics associated with cancer progression.

Results from a cell-based assay demonstrated that this inhibitor led to a decrease in RNA splicing proteins, such as SRSF4 and SRSF6, resulting in cell apoptosis. In summary, we identified a novel CLK2 inhibitor as a promising potential treatment for TNBC therapy.

Targeting SRSF4 could significantly improve chemosensitivity. Taken together, our collective findings highlight an important role of SRSF4 in the regulation of TMZ resistance by modulation of double strand break repair.

Moreover, despite rapid evolution, PD-1 3' UTRs are functionally conserved and strongly repress gene expression through many common RBP binding sites. These findings reveal a previously unrecognized mechanism of maintaining PD-1 expression homeostasis and might represent a general model for how small regulatory effects play big roles in regulation of gene expression and biology.

In conclusion, this study shows that the described variant of the SRSF4 gene is pathogenetic and causes reduced SRSF4 protein expression, which leads to cells' mitochondrial function impairment and could be responsible for the clinical phenotype observed in our patients. Mitochondria, Bone marrow failure, Bone marrow niche, Neutropenia