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Somatic Missense Mutations at the MCL-1 BH3-Binding Groove Paradoxically Enhance BAK Sequestration: Computational Evidence for Apoptotic Resistance

2026-05-28

Abstract excerpt

<title>Abstract</title> <p> Myeloid cell leukemia (MCL-1) enhances the viability of tumor cells by sequestering the pro-apoptotic effector BAK within its BH3-binding groove. The structural and functional implications of somatic missense mutations at this contact are inadequately defined. We comprehensively investigated 146 somatic MCL-1 missense variations from the COSMIC database employing an array of <italic>...

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Literature Corpus work
a49d9fae-f78d-5fac-8ca3-1db308e6a039
DOI
10.21203/rs.3.rs-9825806/v1
Open publication

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Somatic Missense Mutations at the MCL-1 BH3-Binding Groove Paradoxically Enhance BAK Sequestration: Computational Evidence for Apoptotic ResistanceDOI 10.21203/rs.3.rs-9825806/v1
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