F730047E07Rik Inhibitors

The chemical class known as Mms22l inhibitors would include compounds that indirectly impact the DNA damage response and homologous recombination repair pathways. These chemicals are not direct antagonists of the MMS22L protein but function by altering cellular processes that MMS22L is critical for.DNA replication inhibitors like Aphidicolin and Hydroxyurea can lead to stalled replication forks, a condition that necessitates homologous recombination for resolution, thereby indirectly challenging MMS22L functionality. Similarly, DNA-damaging agents such as Camptothecin, Etoposide, Cisplatin, and Mitomycin C introduce lesions that require repair via pathways where MMS22L is a key player. The incorporation of nucleoside analogs such as Gemcitabine into DNA can also impede replication and increase the dependency on MMS22L-mediated repair.

Checkpoint kinase inhibitors like UCN-01, VE-821, AZD7762, and KU-55933 disrupt cell cycle regulation and the DNA damage response, which can overload the DNA repair machinery that includes MMS22L. The inhibition of enzymes such as PARP, ATR, Chk1, and ATM by compounds like Olaparib can lead to an increased reliance on homologous recombination repair, where MMS22L operates, thereby indirectly affecting its function.