C17orf58 inhibitor compounds such as LY294002 and Wortmannin act as PI3K inhibitors, thereby reducing AKT phosphorylation, which is a common pathway implicated in multiple cellular processes. This reduction may have a downstream effect on the function or expression of C17orf58. Similarly, inhibitors like SB203580, SP600125, and U0126 target different MAP kinases (p38 MAPK, JNK, and MEK1/2 respectively), which are integral to cellular responses to stress and external stimuli. Altering these pathways may influence how C17orf58 operates within the cell, especially if it is involved in stress response or apoptosis.
Inhibitors such as Rapamycin, Bortezomib, and MG132 operate by disrupting broader cellular mechanisms, such as mTOR signaling and proteasome-mediated protein degradation, respectively. These compounds can indirectly affect the turnover and function of numerous proteins, including possibly C17orf58. Moreover, Cyclosporin A affects calcineurin/NFAT signaling, 2-Deoxy-D-glucose interferes with glycolysis, and Thapsigargin and Tunicamycin induce endoplasmic reticulum (ER) stress.
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