Mog1p Inhibitors

Chemical inhibitors of Mog1p operate by interfering with cellular processes that are essential for the functional performance of the protein. Alisertib and MLN8237, both Aurora kinase A inhibitors, lead to the disruption of mitotic spindle formation, a process to which Mog1p is indirectly connected through its role in nucleocytoplasmic transport. Similarly, BI-2536, a Polo-like kinase 1 (Plk1) inhibitor, induces mitotic arrest, thereby hindering the cellular context in which Mog1p operates, leading to its functional inhibition. The Aurora kinase inhibitor ZM447439 and the Aurora kinases inhibitor VX-680 (Tozasertib) both obstruct chromosome alignment and segregation during mitosis, processes that require the functional involvement of Mog1p. Disruption of these processes by these inhibitors therefore results in the functional inhibition of Mog1p.

Further, CDK inhibitors such as Purvalanol A, Roscovitine, and Dinaciclib, prevent cell cycle progression at various phases, which impacts the nucleocytoplasmic transport necessary for cell cycle events where Mog1p is involved. As Mog1p assists in cell cycle-related events, the arrest caused by these inhibitors leads to its indirect inhibition. Lestaurtinib, a Janus kinase 2 (JAK2) inhibitor, disrupts JAK2-dependent cell cycle control, a pathway that Mog1p is involved in, resulting in its functional inhibition. Palbociclib (PD 0332991), a CDK4/6 inhibitor, interrupts the G1-S phase transition, which is fundamental for the progression of cell cycle events that rely on nucleocytoplasmic transport, leading to the indirect inhibition of Mog1p. Lastly, SNS-032, which inhibits CDK2, CDK7, and CDK9, affects transcription and cell cycle progression, thereby disrupting processes in which Mog1p is critically involved, and as such, results in the functional inhibition of Mog1p.