scholarly journals Effect of Fetal Hypothyroidism on Cardiac Myosin Heavy Chain Expression in Male Rats

2016 ◽  
Author(s):  
Nasibeh Yousefzadeh ◽  
Sajad Jeddi ◽  
Mohammad Reza Alipour
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Male Rats ◽  
Cardiac Myosin ◽  
Fetal Hypothyroidism

scholarly journals Myosins and pathology: genetics and biology.

2002 ◽  
Vol 49 (4) ◽  
pp. 789-804 ◽  
Author(s):  
Maria Jolanta Redowicz
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Myosin Heavy Chain ◽  
Inner Ear ◽  
Heavy Chain ◽  
Hair Cells ◽  
Familial Hypertrophic Cardiomyopathy ◽  
Light Chains ◽  
Myosin Isoforms ◽  
Cardiac Myosin ◽  
Genes Encoding

This article summarizes current knowledge on the genetics and possible molecular mechanisms of Human pathologies resulted from mutations within the genes encoding several myosin isoforms. Mutations within the genes encoding some myosin isoforms have been found to be responsible for blindness (myosins III and VIIA), deafness (myosins I, IIA, IIIA, VI, VIIA and XV) and familial hypertrophic cardiomyopathy (beta cardiac myosin heavy chain and both the regulatory and essential light chains). Myosin III localizes predominantly to photoreceptor cells and is proved to be engaged in the vision process in Drosophila. In the inner ear, myosin I is postulated to play a role as an adaptive motor in the tip links of stereocilia of hair cells, myosin IIA seems to be responsible for stabilizing the contacts between adjacent inner ear hair cells, myosin VI plays a role as an intracellular motor transporting membrane structures within the hair cells while myosin VIIA most probably participates in forming links between neighbouring stereocilia and myosin XV probably stabilizes the stereocilia structure. About 30% of patients with familial hypertrophic cardiomyopathy have mutations within the genes encoding the beta cardiac myosin heavy chain and both light chains that are grouped within the regions of myosin head crucial for its functions. The alterations lead to the destabilization of sarcomeres and to a decrease of the myosin ATPase activity and its ability to move actin filaments.

scholarly journals Characterization of human cardiac myosin heavy chain genes.

1989 ◽  
Vol 86 (10) ◽  
pp. 3504-3508 ◽  
Author(s):  
K. Yamauchi-Takihara ◽  
M. J. Sole ◽  
J. Liew ◽  
D. Ing ◽  
C. C. Liew
Keyword(s):  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Cardiac Myosin ◽  
Myosin Heavy Chain Genes

A novel de novo mutation of β-cardiac myosin heavy chain gene found in a twelve-year-old boy with hypertrophic cardiomyopathy

2014 ◽  
Vol 93 (2) ◽  
pp. 557-560 ◽  
Author(s):  
SEIGO OKADA ◽  
YASUO SUZUKI ◽  
TAKURO ARIMURA ◽  
AKINORI KIMURA ◽  
HIROKO NARUMI ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
De Novo ◽  
De Novo Mutation ◽  
Chain Gene ◽  
Cardiac Myosin ◽  
Heavy Chain Gene ◽  
Myosin Heavy Chain Gene
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