Inhibitors of WDR31 function by modulating various signaling pathways and cellular processes that WDR31 is implicated in, without directly targeting the protein itself. For example, the inhibition of mTOR signaling can lead to reduced protein synthesis and cellular proliferation, which indirectly reduces the functional activity of WDR31 if it plays a role in these cellular processes. Similarly, the disruption of the PI3K/AKT/mTOR cascade, a critical pathway for cell survival, can lead to a decrease in activities where WDR31 is functionally relevant, by hindering the signals that guide these survival mechanisms. The use of MEK inhibitors can affect the MAPK/ERK pathway, involved in cell proliferation and survival, altering cellular signaling dynamics and potentially impacting the functional role of WDR31 within these pathways. Inhibition of p38 MAPK affects stress and inflammatory responses, as well as apoptosis, thus influencing WDR31's functions tied to these cellular responses. Additionally, the JNK signaling pathway, when interrupted, affects apoptosis and other cellular processes, which could in turn modify WDR31's role within these pathways.
Other inhibitors target pathways involved in more specialized cellular contexts where WDR31 may play a part. Cyclopamine, for instance, impedes the Hedgehog pathway, which is essential for cell differentiation and tissue patterning, affecting the functional role of WDR31 in these biological processes. Inhibitors of VEGFR block the VEGF pathway, which is crucial for angiogenesis and cell migration, potentially altering WDR31 activity in related phenomena. Furthermore, the targeting of Rho/ROCK pathway by specific inhibitors affects cytoskeletal dynamics and cell motility, indirectly affecting WDR31 activity.
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