Sandbox Reserved 1765: Difference between revisions
From Proteopedia
Jump to navigationJump to search
Sloan August (talk | contribs) No edit summary |
Sloan August (talk | contribs) No edit summary |
||
| Line 38: | Line 38: | ||
== Significance == | == Significance == | ||
=== Cancer and Rasopathies === | === Cancer and Rasopathies === | ||
Common mutations in SHOC2 and PP1C lead to amino acid changes on the interaction surfaces, that can lead to higher binding affinity.<ref name="Lavoie">PMID: 35970881</ref> Mutations to MRAS can result in consistent GTP-loading, increasing the formation of the SMP complex in the absence of external growth factors that are necessary for activation of the pathway in a healthy organism. Mutations in PP1C can trigger increased active site activity, increasing the RAF proteins that are active and available to bind to RAS. Universally, when this MAPK cascade is unregulated, cells are able to proliferate regardless of external signals, leading to cancer and/or RASopathies. | Common mutations in SHOC2 and PP1C lead to amino acid changes on the interaction surfaces, that can lead to higher binding affinity.<ref name="Lavoie">PMID: 35970881</ref> Mutations to MRAS can result in consistent GTP-loading, increasing the formation of the SMP complex in the absence of external growth factors that are necessary for activation of the pathway in a healthy organism. Mutations in PP1C can trigger increased active site activity, increasing the RAF proteins that are active and available to bind to RAS. Universally, when this MAPK cascade is unregulated, cells are able to proliferate regardless of external signals, leading to cancer and/or RASopathies. | ||
