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==Gene Overview==
 
==Gene Overview==
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The MYH11 gene encodes a smooth muscle myosin belonging to the myosin heavy chain family. The gene product is a subunit of a hexameric protein that consists of two heavy chain subunits and two pairs of non-identical light chain subunits. It functions as a major contractile protein, converting chemical energy into mechanical energy through the hydrolysis of ATP.  The pericentric inversion of chromosome 16 [inv(16)(p13q22)] produces a protein bearing the first 165 residues from the N terminus of core-binding factor beta (CBFB) and  the C-terminal portion of the smooth muscle myosin heavy chain (MYH11). The CBFβ–MYH11 fusion protein exerts a dominant negative function by increased binding to the transcription factor encoded by RUNX1, thereby competing for free Runx1 protein, and leading to lowered and altered transcription of myeloid genes [2].
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The MYH11 gene encodes a smooth muscle myosin belonging to the myosin heavy chain family. The gene product is a subunit of a hexameric protein that consists of two heavy chain subunits and two pairs of non-identical light chain subunits. It functions as a major contractile protein, converting chemical energy into mechanical energy through the hydrolysis of ATP.  The pericentric inversion of chromosome 16 [inv(16)(p13q22)] produces a protein bearing the first 165 residues from the N terminus of core-binding factor beta (CBFB) and  the C-terminal portion of the smooth muscle myosin heavy chain (MYH11) [2]. The CBFβ–MYH11 fusion protein exerts a dominant negative function by increased binding to the transcription factor encoded by RUNX1, thereby competing for free Runx1 protein, and leading to lowered and altered transcription of myeloid genes [2].
    
==Common Alteration Types==
 
==Common Alteration Types==
    
inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11
 
inv(16)(p13.1q22) or t(16;16)(p13.1;q22); CBFB-MYH11
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The CBFβ–MYH11 fusion protein exerts a dominant negative function by increased binding to the transcription factor encoded by RUNX1, thereby competing for free Runx1 protein, and leading to lowered and altered transcription of myeloid genes [2].
    
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