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However, the mutations we detected were on the SH2 domain or C-terminus. The SH2 domain of LNK is known to bind JAK2 and do a critical role in negative regulation of the downstream signal transduction. So, we expected the p.Q423X mutation might result in the disruption of LNK function and have a role in MPN pathogenesis. If we perform the expression study for the production of truncated protein or

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