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For example, MYH7 gene mutations can cause HCM, dilated cardiomyopathy (DCM), left ventricular non-compaction (LVNC) or restrictive cardiomyopathy (RCM) and can also be associated with myopathy.
Ortiz, Electrochemical primer extension for the detection of single nucleotide polymorphisms in the cardiomyopathy associated MYH7 gene, Chem.
The researchers found that MYH7, MYBPC3, and TTN mutations were the most common mutations (71 percent) found in genetic NCCM.
Among the most frequent of these mutations are changes in myosin binding protein C (MYBPC3) and myosin-7 (MYH7) .
A total of 24 CAD genes, namely, 105 (ADARB2), 183 (AGT), 1586 (CYP17A1), 1611 (DAP), 2917 (GRM7), 2982 (GUCY1A3), 4134 (MAP4), 4625 (MYH7), 4629 (MYH11), 5126 (PCSK2), 5522 (PPP2R2C), 9229 (DLGAP1), 9833 (MELK), 23544 (SEZ6L), 23551 (RASD2), 55017 (C14orf119), 55759 (WDR12), 56776 (FMN2), 60676 (PAPPA2), 60680 (CELF5), 84790 (TUBA1C), 127833 (SYT2), 133491 (C5orf47), and 259232 (NALCN), were identified in this coexpression network (Figure 2, Table S3).
Further, iPSCs from an HCM patient with a single missense mutation in the MYH7 gene exhibited disorganized sarcomeres, electrophysiological irregularities, and an increase of genes involved in cell proliferation .
miR-208b is encoded by intron 31 within the MYH7 gene and regulates the expression of its host gene via the Sox6 transcription factor.
Given their life threatening potential and knowing that it can result from a genetic defect, opens up a wide new set of options for prevention, early diagnosis, risk reduction (MYBC3 / MYH7 positive Hypertrophic cardiomyopathy) and sometimes curative treatment (LMNA positive Dilated cardiomyopathy).
In three spots found higher and abundant in 48 h sepsis, myosin-6 ("MYH6") from spots ID 57 and ID 73 and myosin7 ("MYH7") from spot ID 71 were identified.
Dose-Dependent Effects of AOF on BNP, MYH6, and MYH7 Protein Levels.
The antimir of miR-208a attenuates cardiac remodeling by upregulation of expression Myh7 in pressure overload induced heart failure in rats .
In HCM, there have been conflicting reports as to whether variants in thin filament genes [troponin T type 2, cardiac type (TNNT2), troponin I3, cardiac type (TNNI3), tropomyosin 1 (alpha) (TPM1), actin, alpha, cardiac muscle 1 (ACTC1)] confer distinct clinical phenotypes to variants in the major thick filament genes [myosin binding protein C, cardiac (MYBPC3), myosin heavy chain 7 (MYH7)], likely due to limited study sizes given the small proportion of patients with HCM who have thin filament variants.
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