Chemical inhibitors of VMAC can target various signaling pathways and kinases that are essential for its function. Wortmannin and LY294002 are two such inhibitors that specifically target phosphoinositide 3-kinases (PI3K), a family of enzymes involved in cellular functions such as cell growth and survival, which VMAC may rely on. By inhibiting PI3K, these chemicals disrupt the PI3K/AKT pathway, suppressing the downstream signaling events that contribute to VMAC function. Similarly, Staurosporine broadly targets multiple kinases, which can lead to the inhibition of kinase-dependent signaling processes that VMAC may require. U0126 and PD98059 are selective for MEK1/2, enzymes that are upstream of ERK in the MAPK pathway. By preventing the activation of MEK, these inhibitors can prevent the phosphorylation of ERK, a kinase that may be crucial for VMAC's activity.
SP600125 and SB203580 inhibit the JNK and p38 MAP kinase pathways, respectively, which may intersect with VMAC's signaling pathways. By inhibiting these kinases, SP600125 and SB203580 can disrupt the signaling that VMAC relies on for its function. NF449 inhibits G-protein coupled P2X1 receptors, which, if VMAC is involved in P2X1 receptor signaling pathways, would lead to a functional inhibition of VMAC. Bisindolylmaleimide I and Gö6976 specifically inhibit protein kinase C (PKC), where the interruption of PKC-mediated signaling could be critical for the operational aspects of VMAC. Lestaurtinib inhibits receptor tyrosine kinases, which are part of intricate signaling networks that VMAC may utilize, leading to its functional inhibition. Lastly, Dasatinib targets the Src family kinases, and by inhibiting these, it can prevent VMAC from participating in the necessary Src kinase-dependent pathways, resulting in its inhibition.
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