C17orf76 inibitors include Wortmannin and PD0325901 which are examples of kinase inhibitors that target the PI3K/Akt and MAPK/ERK pathways, respectively, which are central to many cellular functions, including proliferation and survival, and can thus impact C17orf76. Trichostatin A and 5-Azacytidine modify epigenetic marks, which can lead to altered gene expression patterns, potentially influencing C17orf76 levels. Roscovitine and Bortezomib alter cell cycle progression and protein stability, which could also affect C17orf76 indirectly. SP600125 and Y-27632 target the JNK pathway and Rho-associated kinases, respectively, which can influence cellular stress responses and cytoskeletal organization, potentially modulating the role of C17orf76 in these contexts.
Compounds like Cyclopamine and Rapamycin interfere with the Hedgehog signaling and mTOR pathways, which are critical for developmental processes and nutrient sensing. The impact of these inhibitors on C17orf76 is contingent on the protein's involvement in these pathways. ZM-447439 disrupts mitotic processes by inhibiting Aurora kinases, which could affect C17orf76 if it plays a part in cell division. Tunicamycin's inhibition of N-linked glycosylation can lead to protein misfolding and could impact the stability and function of C17orf76 if it undergoes this post-translational modification.
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