SART-3 Inhibitors

Chemical inhibitors of SART3 can disrupt its function in RNA splicing by targeting various kinases that play a role in cell cycle regulation and RNA processing. Alsterpaullone, for instance, is known to inhibit cyclin-dependent kinases (CDKs), which are crucial for the regulation of the cell cycle. Since CDKs can also regulate RNA processing factors, the inhibition by alsterpaullone can lead to a reduction in SART3 activity in RNA splicing. Similarly, roscovitine and flavopiridol, both potent CDK inhibitors, can interfere with the transcriptional regulators and RNA polymerase II, further inhibiting the splicing function of SART3. Indirubin-3'-monoxime and olomoucine, which also target CDKs, can affect the phosphorylation state of proteins involved in RNA processing, thereby hindering SART3's role in spliceosome assembly.

In parallel, bisindolylmaleimide I and Ro-31-8220 inhibit protein kinase C (PKC), which is implicated in signaling pathways that regulate RNA processing. The inhibition of PKC by these chemicals disrupts these pathways and can diminish SART3's activity in RNA splicing. H-7, which inhibits not only PKC but also other kinases such as PKA and PKG, can lead to similar outcomes. Other chemical inhibitors such as SP600125, which targets the c-Jun N-terminal kinase (JNK), can indirectly affect RNA splicing factors and thus impede SART3's function. Additionally, 5-Iodotubercidin inhibits adenosine kinase, which may influence RNA processing enzymes due to changes in cellular adenosine levels, subsequently affecting SART3's role in spliceosome assembly. Lastly, K252a, while primarily studied in the context of neurotrophin receptors, can influence broader kinase pathways and thereby have an impact on RNA splicing, affecting SART3's function. Each of these inhibitors, through their respective targets, can contribute to the reduction of SART3's activity in the RNA splicing process.