Epidermal Growth Factor (EGF) interacts with its receptor to elevate endocytosis, potentially amplifying STON1's role at the cell membrane. In parallel, Phorbol 12-myristate 13-acetate (PMA) activates protein kinase C, a pivotal player in the endocytic orchestra, which may enhance STON1-mediated activities. Pitstop 2, taking an alternative route, impedes clathrin-mediated endocytosis, possibly leading to a compensatory upregulation of STON1's function. Methyl-β-cyclodextrin (MβCD) extracts cholesterol from cell membranes, altering the intricate lipid environment that can affect STON1's membrane interactions. Dansylcadaverine and Chlorpromazine disrupt normal endocytic processes, with the potential to cause a rebalancing of STON1 activity to maintain cellular homeostasis.
Wortmannin, by inhibiting PI3K, and Genistein, by its broad-spectrum inhibition of tyrosine kinases, induce changes that can ripple through to STON1's operational pathways. Amiloride's inhibition of macropinocytosis might intersect with STON1's functional pathways, influencing its activity profile. The cytoskeleton-disrupting agents, Latrunculin A and Jasplakinolide, exert their effects by destabilizing or stabilizing actin filaments, respectively, which may affect the actin-dependent processes STON1 is associated with.
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