In mutated TNNT1 genes suggests that RMS tumors may be congenital

FGFR4 is a tyrosine kinase receptor responsible for signal transduction activities in the cell. Although the activity of this protein is undetectable in normal tissues, it becomes active when a tumor is Hygromycin B formed. High expression of FGFR4 has been associated with advanced-stage in RMS cancer and a poor survival rate. Although over-expression of FGFR4 in the map, is inhibited by other low/moderately expressed genes, it may suggest the formation of tumor cell in skeletal muscle. Overexpression of FGFR4 may stimulate the expression of TNNT1; the regulator for striated muscle contraction, despite the fact that a negative interaction between these 2 genes was detected. Low expression of FHL3, RXRG, MYL1 and RND3 may also promote the mutation of TNNT1 genes due to a suppression of the anti-proliferative effects of RA in the RMS cells. The low activity of these genes might influence normal cell spreading, actin stress fiber disassembly and, consequently, tumor cells migration. TNNT1 is the diagnostic marker for nemaline myopathy. The high expression value in mutated TNNT1 genes suggests that RMS tumors may be congenital. FNDC5 protein expressed in muscle is inhibited by RMS-expressed genes including TNNT2, BIN1, SEPT4, MYL4 and HSPB2. Up-regulation of this gene suggests that the Histamine Phosphate increased level of irisin hormone promotes the beneficial effects of exercise on metabolic pathways. TNNT2 and BIN1 are proteins that play important roles in cardiac muscle development. Over-expression of TNNT2 has been correlated to myocardial stunning in hemodialysis patients, and the disruption of this gene could lead to impaired cardiac development in the embryo and infant. Deficiency of the BIN1 gene has been correlated with cardiomyopathy. SEPT4 is the nucleotide binding proteins highly expressed in heart and brain. It regulates cytoskeletal organization during embryonic and adult life. MYL4 is the hexameric ATPase cellular motor proteins that commonly found in embryonic muscle and adult atria. Over-expression of this gene was normally found in patients with hypertrophic cardiomyopathy and congenital heart diseases. HSPB2 is another protein that expressed in the heart and skeletal muscles.

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