Date published: 2025-9-16

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C6orf165 Inhibitors

Chemical inhibitors of C6orf165 can modulate the protein's activity through various signaling pathways by targeting specific kinases and enzymes that regulate its function. Wortmannin and LY294002 are both phosphoinositide 3-kinases (PI3K) inhibitors. By blocking PI3K, these chemicals prevent the formation of phosphatidylinositol (3,4,5)-trisphosphate (PIP3), a vital second messenger involved in the activation of AKT. This action leads to a decrease in the phosphorylation and activation of downstream proteins that are part of the PI3K/AKT/mTOR pathway, to which C6orf165 activity is linked. Rapamycin specifically inhibits mTOR, a central component of the same pathway, and thus indirectly reduces the functional activity of C6orf165 by dampening the pathway's output.

Further down the signaling cascade, PD98059 and U0126 function as MEK inhibitors, blocking the MAPK/ERK pathway, which is another crucial route for cellular signal transduction. These inhibitors prevent the activation of MEK1/2, resulting in reduced ERK activity and subsequently lowering the functional activity of proteins regulated by this pathway, including C6orf165. Similarly, SB203580 and SP600125 target the p38 MAPK and JNK pathways, respectively, adding to the spectrum of kinase inhibition that can influence C6orf165 function. SB203580 specifically inhibits p38 MAPK, while SP600125 targets JNK, both of which are kinases that can impact the activity of diverse cellular proteins. Dasatinib and PP2 inhibit Src family kinases, leading to reduced phosphorylation of many substrates, including those that may regulate C6orf165 activity. Go6983, a protein kinase C (PKC) inhibitor, suppresses the activity of PKC isoforms, potentially decreasing the activity of proteins within PKC-regulated pathways where C6orf165 might play a role. Lastly, SL327 and Sorafenib, both of which are also MEK inhibitors, contribute to the inhibition of the MAPK/ERK pathway, further establishing the control over the enzymatic cascades that could regulate the functional activity of C6orf165.

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