Date published: 2025-10-11

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ZFYVE21 Inhibitors

ZFYVE21 inhibitors encompass a diverse array of chemical compounds, each targeting different facets of cellular signaling pathways that ultimately lead to the decreased activity of ZFYVE21. For example, inhibitors that target the PI3K/Akt pathway are especially significant due to their role in preventing the phosphorylation and activation of Akt, thereby mitigating the downstream effects that influence ZFYVE21. This includes metabolites known to potently inhibit PI3K, consequently reducing the activity of Akt, which is a crucial modulator in pathways where ZFYVE21 is a participant. Furthermore, the inhibition of mTOR, a central component of cellular growth and metabolism, can lead to reduced protein synthesis, which indirectly affects proteins that regulate or interact with ZFYVE21. Similarly, compounds that inhibit Akt can impede the interaction or localization of ZFYVE21 within PI3K/Akt-dependent processes.

The modulation of ZFYVE21 activity also involves the manipulation of other signaling cascades, such as the MAPK pathway. Selective inhibition of MEK1/2 can affect the ERK pathway, which may indirectly influence ZFYVE21's activity or stability. Additionally, the inhibition of JNK and p38 MAPK can alter the phosphorylation state of proteins associated with ZFYVE21, therefore impacting its function. The proper function of ZFYVE21 is also suggested to be associated with autophagic processes, where inhibitors of autophagy, such as those preventing the initiation of autophagy or the maturation of autophagic vacuoles, can inhibit ZFYVE21's role. Chemical compounds that interfere with the pH of lysosomes are also capable of affecting ZFYVE21's function in autophagy. Moreover, the specific inhibition of small GTPases that may interact with ZFYVE21 serves as another avenue to diminish the protein's activity, exemplifying the multifaceted approach to modulating ZFYVE21's role in cellular signaling.

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