Myosin, a motor protein primarily involved in muscle contraction, undergoes alterations in its structure due to minor genetic mutations within its gene.
These mutations can affect its interaction with actin, thereby modifying the molecular mechanism underlying muscle contraction. Myosin serves as the primary molecular motor driving muscle contraction and cellular motility based on actin.
Post-transcriptional regulation regulates gene expression at the RNA level, occurring after RNA polymerase binds to the gene promoter and initiates nucleotide synthesis.
Numerous mutations in genes encoding RNA-binding proteins lead to human diseases, as these proteins play crucial roles in regulating gene expression from mRNA processing to eventual decay in the cytoplasm.
Given their widespread expression and vital functions in gene expression, alterations in these RNA-binding proteins are often associated with tissue-specific diseases.
Disease-associated mutations affect various post-transcriptional processing steps, resulting in diverse disease phenotypes across specific tissues.
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