Date published: 2025-9-15

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C6orf163 Inhibitors

Chemical inhibitors of C6orf163 can be understood in the context of their impact on signaling pathways and cellular processes that the protein is involved in. LY294002 and Wortmannin are both inhibitors of PI3K, an enzyme that plays a pivotal role in the Akt signaling pathway. By inhibiting PI3K, these chemicals can lead to reduced phosphorylation of downstream proteins, including C6orf163, which could be part of the pathway responsible for various cellular processes including growth and survival. Similarly, Rapamycin targets mTOR, which is a downstream component of the PI3K/Akt pathway, and its inhibition can result in a decreased function of proteins regulated by this pathway, including C6orf163. This is because mTOR is integral to protein synthesis and cell growth, and its inhibition can impact the function of proteins involved in these processes.

Furthermore, PD98059 and U0126 are inhibitors of MEK, which is upstream of ERK in the MAPK/ERK pathway. Inhibition of MEK results in lower activation of ERK, which is necessary for the phosphorylation cascade that impacts C6orf163 function. SB203580 and SP600125 target p38 MAP kinase and JNK respectively, both of which are part of the MAPK signaling pathway. Inhibition of these kinases can lead to decreased activation of proteins that are regulated as part of the cellular response to stress or other signaling events, including C6orf163. Src family kinases, which are implicated in numerous signaling pathways, can be inhibited by chemicals like PP2 and Dasatinib, potentially reducing the phosphorylation and activation of associated proteins and signaling pathways involving C6orf163. Similarly, Imatinib inhibits bcr-abl tyrosine kinase and c-kit, which may be upstream of pathways in which C6orf163 is involved, leading to reduced phosphorylation and activity of C6orf163. Lastly, Sunitinib and Erlotinib are inhibitors of receptor tyrosine kinases and EGFR tyrosine kinase, respectively. By inhibiting these kinases, the signaling through pathways that involve C6orf163 can be disrupted, resulting in the functional inhibition of C6orf163 due to reduced activation of downstream proteins.

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