Sandbox Reserved 1777: Difference between revisions
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=Implications= | =Implications= | ||
[[Image:Noonan syndrome figure.jpg| | [[Image:Noonan syndrome figure.jpg|500px|right|thumb|<font size="2"><div style="text-align: center;">'''Figure 4'''. Common Symptoms of Noonan Syndrome. </div></font>]] | ||
The SHOC2-MRAS-PP1C complex's key role in the regulation of the MAPK-RAF pathway means that minor changes in its structure or function can have drastic biological consequences. Unregulated activation of the MAPK pathway is the cause of several human cancers due to unchecked cell division and proliferation<ref name="Kwan" />. Mutations that stabilize the interactions of the SMP complex enhance PP1C phosphatase activity <Ref name="Jajian" />, leading to increased RAF signaling and accelerated cell division. Most SHOC2 or PP1C mutations alter residues that are the direct contact points, stabilizing the interaction between the two proteins. Mutations to MRAS result in persistent binding of GTP, leading to consistent activation of the cell signaling pathway<ref name="Kwan" />. | The SHOC2-MRAS-PP1C complex's key role in the regulation of the MAPK-RAF pathway means that minor changes in its structure or function can have drastic biological consequences. Unregulated activation of the MAPK pathway is the cause of several human cancers due to unchecked cell division and proliferation<ref name="Kwan" />. Mutations that stabilize the interactions of the SMP complex enhance PP1C phosphatase activity <Ref name="Jajian" />, leading to increased RAF signaling and accelerated cell division. Most SHOC2 or PP1C mutations alter residues that are the direct contact points, stabilizing the interaction between the two proteins. Mutations to MRAS result in persistent binding of GTP, leading to consistent activation of the cell signaling pathway<ref name="Kwan" />. | ||
