Chemical inhibitors of the protein 1700001N15Rik employ various mechanisms to impede its function within cellular signaling pathways. Wortmannin and LY294002 are two such inhibitors that directly target the phosphoinositide 3-kinase (PI3K) pathway, a crucial signaling route that 1700001N15Rik is a part of. By inhibiting PI3K, these chemicals prevent the activation of downstream components, such as AKT, ultimately leading to a suppression of 1700001N15Rik activity due to its reliance on PI3K/AKT for activation. Similarly, Triciribine specifically inhibits AKT phosphorylation, which is another step critical for the activation of 1700001N15Rik, thereby limiting its functional capacity within the cell.
Additional inhibitors, such as Rapamycin, Staurosporine, and Erlotinib, affect different aspects of the pathways that involve 1700001N15Rik. Rapamycin selectively inhibits mammalian target of rapamycin (mTOR), a component of cell growth and proliferation pathways that 1700001N15Rik is associated with. This inhibition holds back the function of 1700001N15Rik by targeting mTOR's role in the pathway. Staurosporine, a broad-spectrum protein kinase inhibitor, can impede the action of multiple kinases that would typically phosphorylate and thereby activate 1700001N15Rik. Erlotinib and Gefitinib, both EGFR tyrosine kinase inhibitors, obstruct the epidermal growth factor receptor (EGFR) pathway, under which 1700001N15Rik operates, by preventing downstream signaling cascades. Furthermore, the chemicals PD98059, U0126, SP600125, and SB203580 disrupt MAP kinase pathways by inhibiting MEK, JNK, and p38 MAP kinase, respectively. These pathways are integral to the regulation of cellular processes such as proliferation, stress response, and apoptosis, all of which 1700001N15Rik may influence. By halting the function of these kinases, the inhibitors can suppress the activity of 1700001N15Rik if it is a part of or regulated by these signaling routes.
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