Ignet

Gene Information

Gene symbol: MYH6

Gene name: myosin, heavy chain 6, cardiac muscle, alpha

HGNC ID: 7576

Related Genes

#	Gene Symbol	Number of hits
1	ACTC1	1 hits
2	ATP2A1	1 hits
3	ATP2A2	1 hits
4	CACNA1C	1 hits
5	CACNA1G	1 hits
6	CACNA1H	1 hits
7	CACNA2D1	1 hits
8	CACNA2D3	1 hits
9	CALM1	1 hits
10	CAV1	1 hits
11	CD4	1 hits
12	DSP	1 hits
13	GJA1	1 hits
14	HLA-A	1 hits
15	INS	1 hits
16	ME1	1 hits
17	MYBPC3	1 hits
18	MYH14	1 hits
19	MYH7	1 hits
20	MYL1	1 hits
21	MYL2	1 hits
22	NPPA	1 hits
23	NPPB	1 hits
24	PPARG	1 hits
25	PRPF6	1 hits
26	SLC25A4	1 hits
27	SLC27A1	1 hits
28	SLC2A4	1 hits
29	SLC9A1	1 hits
30	TNNI3	1 hits
31	TNNT2	1 hits
32	TRNAE1	1 hits

Related Sentences

#	PMID	Sentence
1	1488051	Effects of exercise training and diabetes on cardiac myosin heavy chain composition.
2	1488051	This study determined whether the beneficial effects of exercise training on the diabetic heart previously observed are associated with alterations in ventricular myosin heavy chain (MHC) isoform composition.
3	1488051	After 10 wks, ventricular MHC isoenzyme protein composition was analyzed for MHC composition using gel electrophoresis. alpha-MHC and beta-MHC mRNA were determined by Northern and slot blot hybridization techniques.
4	1488051	The results indicate that treadmill exercise training of diabetic rat does not prevent the diabetes-induced shift in MHC composition towards the beta-MHC isoform, thus it is unlikely that the beneficial effects of exercise training on the diabetic heart, previously shown, are due to a normalization of the myosin isoform composition.
5	2332433	Cotransfection of the rat T3 alpha-receptor cDNA with a reporter gene linked to 5'-deletion mutants of the malic enzyme gene 5'-flanking region revealed the presence of a TRE between positions -315 and -248.
6	2332433	Using T3 receptors synthesized in vitro from their cDNAs, we have identified, through the use of gel shift assays and footprinting, a single DNA-binding site (positions -281 to -261) for the receptor within the rat malic enzyme gene TRE.
7	2332433	Competition binding studies indicated that the apparent affinity of receptor binding to the malic enzyme gene was similar to that of the rat alpha-myosin heavy chain gene TRE (positions -151 to -122) and was significantly greater than that of the rat growth hormone TRE (positions -192 to -163).
8	9052888	To characterize the molecular mechanism of cardiac and renal complications in non-insulin-dependent diabetes mellitus (NIDDM), we examined the gene expression of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new animal model for human NIDDM, at the ages of 14 weeks (prediabetic stage), 30 weeks (NIDDM stage), and 54 weeks (IDDM stage).
9	9052888	In 14-week-old OLETF rats, cardiac mRNAs for transforming growth factor-beta1 (TGF-beta1) and extracellular matrix, including collagen types I, III, and IV and laminin, were significantly increased compared with control rats (Long-Evans Tokushima Otsuka rats).
10	9052888	Cardiac beta-myosin heavy chain (MHC) mRNA of OLETF was increased at 30 and 54 weeks of age, whereas alpha-MHC mRNA of OLETF was inversely decreased at 54 weeks.
11	9140815	Therefore, we determined the separate and combined effects of thyroid hormone (T3) and insulin treatment on rodent cardiac myosin heavy chain (MHC) expression using a model of combined thyroid deficiency (Tx) and diabetes (D).
12	9140815	The combination of Tx and D completely transformed cardiac isomyosin expression such that the fast alpha-myosin heavy chain (MHC) was completely repressed at both the protein and mRNA level of expression; whereas, the slow beta-MHC was upregulated to constitute 100% of the total MHC pool, based on both protein and mRNA analyses.
13	9140815	Daily low doses of exogenous T3 treatment (3 micrograms/kg b.w. i.p.). in the absence of insulin treatment, partially restored expression of the alpha-MHC, while inhibiting expression of the beta-isoform.
14	9140815	Furthermore, when exogenous T3 was administered in conjunction with insulin, the effect on MHC mRNA expression was greater than that of T3 alone, thus suggesting the existence of interaction between T3 and insulin action in the regulation of MHC mRNA expression.
15	9140815	Collectively, these findings suggest that: (a) thyroid state is a dominant regulator of cardiac isomyosin phenotype: and (b) insulin does not exert any regulatory influence on cardiac MHC expression in a severe thyroid deficient state, instead it requires a critical level of circulating T3 in order to be effective in blunting MHC transformation associated with diabetes.
16	9140815	It is thus concluded that the regulation of cardiac MHC by insulin is a complex mechanism involving interaction of insulin with subcellular factors likely to have impact on the specific action of T3.
17	9140815	Therefore, we determined the separate and combined effects of thyroid hormone (T3) and insulin treatment on rodent cardiac myosin heavy chain (MHC) expression using a model of combined thyroid deficiency (Tx) and diabetes (D).
18	9140815	The combination of Tx and D completely transformed cardiac isomyosin expression such that the fast alpha-myosin heavy chain (MHC) was completely repressed at both the protein and mRNA level of expression; whereas, the slow beta-MHC was upregulated to constitute 100% of the total MHC pool, based on both protein and mRNA analyses.
19	9140815	Daily low doses of exogenous T3 treatment (3 micrograms/kg b.w. i.p.). in the absence of insulin treatment, partially restored expression of the alpha-MHC, while inhibiting expression of the beta-isoform.
20	9140815	Furthermore, when exogenous T3 was administered in conjunction with insulin, the effect on MHC mRNA expression was greater than that of T3 alone, thus suggesting the existence of interaction between T3 and insulin action in the regulation of MHC mRNA expression.
21	9140815	Collectively, these findings suggest that: (a) thyroid state is a dominant regulator of cardiac isomyosin phenotype: and (b) insulin does not exert any regulatory influence on cardiac MHC expression in a severe thyroid deficient state, instead it requires a critical level of circulating T3 in order to be effective in blunting MHC transformation associated with diabetes.
22	9140815	It is thus concluded that the regulation of cardiac MHC by insulin is a complex mechanism involving interaction of insulin with subcellular factors likely to have impact on the specific action of T3.
23	10569179	The steady-state mRNA abundance for alpha-myosin heavy chain in the heart was decreased at 2 and 3 weeks but was unchanged at 5 and 6 weeks, whereas mRNA levels for beta-myosin heavy chain remained elevated during 2-6 weeks after inducing diabetes.
24	11557574	Altered K(+) channel gene expression in diabetic rat ventricle: isoform switching between Kv4.2 and Kv1.4.
25	11557574	Kv1.4 mRNA levels increased 179% relative to controls, whereas Kv4.3 mRNA levels were unaffected.
26	11557574	Immunohistochemistry and Western blot analysis of the diabetic heart showed that the density of the Kv4.2 protein decreased, whereas Kv1.4 protein increased.
27	11557574	Thus isoform switching from Kv4.2 to Kv1.4 is most likely the mechanism underlying the slower kinetics of transient outward K(+) current observed in the diabetic ventricle.
28	11557574	Brain Kv1.4, Kv4.2, or Kv4.3 mRNA levels were unaffected by diabetes.
29	11557574	Myosin heavy chain (MHC) gene expression was altered with a 32% decrease in alpha-MHC mRNA and a 259% increase in beta-MHC mRNA levels in diabetic ventricle.
30	11557574	Low-dose insulin-like growth factor-II (IGF-II) treatment during the last 6 of the 12 wk of diabetes (DM + IGF) protected against these changes in MHC mRNAs despite continued hyperglycemia and body weight loss.
31	11866664	In view of the action of etomoxir on gene expression, putative molecular mechanisms involved in an increased expression of SERCA2, the Ca(2+) pump of sarcoplasmic reticulum (SR) and alpha-myosin heavy chain (MHC) of failing overloaded heart muscle are described.
32	12851393	Role of antisense RNA in coordinating cardiac myosin heavy chain gene switching.
33	12851393	A novel mechanism of regulation of cardiac alpha and beta myosin heavy chain gene by naturally occurring antisense transcription was elucidated via pre-mRNA analysis.
34	12851393	Herein, we report the expression of an antisense beta myosin heavy chain RNA in the normal rodent myocardium.
35	12851393	Our results demonstrate that the beta-alpha myosin heavy chain intergenic DNA possesses a bidirectional transcriptional activity, one direction transcribing the alpha gene, and the opposite direction transcribing the antisense beta RNA.
36	15618539	To test the hypothesis that perturbation of lipid homeostasis in cardiomyocytes contributes to cardiac dysfunction, we engineered transgenic mice with cardiac-specific overexpression of fatty acid transport protein 1 (FATP1) using the alpha-myosin heavy chain gene promoter.
37	15680071	This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, alpha- and beta-myosin heavy chain, and cardiac and skeletal alpha-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes.
38	15680071	In the first 28 days, the level of mRNA for alpha-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and beta-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate.
39	15737646	Hyperglycemia, hyperinsulinemia, and hypertriglyceridemia as well as lower cardiac PPARgamma, glucose transporter-4 and alpha-myosin heavy chain expression levels were detected in diabetic ZDF rats compared to lean animals.
40	15737646	Pioglitazone increased body weight and improved metabolic control, cardiac PPARgamma, glut-4, and alpha-MHC expression levels in diabetic ZDF rats.
41	15737646	Hyperglycemia, hyperinsulinemia, and hypertriglyceridemia as well as lower cardiac PPARgamma, glucose transporter-4 and alpha-myosin heavy chain expression levels were detected in diabetic ZDF rats compared to lean animals.
42	15737646	Pioglitazone increased body weight and improved metabolic control, cardiac PPARgamma, glut-4, and alpha-MHC expression levels in diabetic ZDF rats.
43	16935841	Oxidative balance, advanced glycated end products (AGEs) and AGE receptors, cardiac myogenic factors, and myosin heavy-chain gene expression were determined in the left ventricle of treated and untreated STZ-diabetic rats and ZDF rats.
44	16935841	Nuclear factor-kappaB activation triggered a cascade of signaling, which finally led to the switch in the cardiac myosin heavy-chain (MHC) gene expression from the alpha-MHC isoform to the beta-MHC isoform.
45	16935841	DHEA treatment, by preventing the activation of the oxidative pathways induced by hyperglycemia, counteracted the enhanced AGE receptor activation in the heart of STZ-diabetic rats and ZDF rats and normalized downstream signaling, thus avoiding impairment of the cardiac myogenic factors, heart autonomic nervous system and neural crest derivatives (HAND) and myogenic enhancer factor-2, and the switch in MHC gene expression, which are the early events in diabetic cardiomyopathy.
46	17038444	Such suppressed activity and the relative suppression in alpha-myosin heavy chain level in ovariectomy combined with diabetes could be completely restored by estrogen and insulin supplementation.
47	18945756	Our study aimed to test the hypothesis that overexpression of ANT1 in cardiomyocytes has cardioprotective effects in diabetic cardiomyopathy induced by streptozotocin (STZ).
48	18945756	Mice specifically overexpressing murine ANT1 in the heart were generated using alpha-myosin heavy chain promoter.
49	18945756	Expression of ANT1 mRNA and protein in hearts was characterized by real-time polymerase chain reaction and Western blot analysis.
50	18945756	Both ANT1 mRNA and ANT1 protein were specifically overexpressed in the heart of transgenic mice.
51	18945756	Heart weight was decreased and cardiac function was dramatically impaired in wild-type mice 6 weeks after induction of diabetes, but ANT1 overexpression prevented these significant changes.
52	18945756	The mRNA expression level of atrial natriuretic peptide confirmed the haemodynamic findings, being upregulated in wild-type mice receiving STZ, but showing no statistical differences in ANT1 transgenic mice.
53	18945756	Cardiomyocyte-restricted overexpression of ANT1 prevents the development of diabetic cardiomyopathy; therefore, accelerated ADP/ATP exchange could be a new promising target to treat diabetic cardiomyopathy.
54	19738937	The sarcoplasmic reticulum Ca(2+)-ATPase (SERCA) isoforms are normally expressed in coordination with the corresponding myosin heavy chain (MyHC) isoforms in the fibers of skeletal muscle but this coordination is often disrupted in pathological conditions.
55	20090419	We have examined gene expression changes and studied histone H3 and H4 acetylation as well as dimethylation of lysine 4 on histone H3 on promoters of alpha-Myosin heavy chain gene (alpha-MHC), beta-Myosin heavy chain gene (beta-MHC), Atrial natriuretic peptide gene (ANp), B-type natriuretic peptide gene (BNP) and Sarcoplasmic reticulum Ca(2+) ATPase gene (SERCA2a).
56	21216827	Expression of genes encoding various L-type Ca(2+) channel proteins (Cacna1c, Cacna1g, Cacna1h and Cacna2d1) and cardiac muscle proteins (Myh7) were upregulated, and genes encoding intracellular Ca(2+) transport regulatory proteins (Atp2a2 and Calm1) and some cardiac muscle proteins (Myh6, Myl2, Actc1, Tnni3, Tnn2, and Tnnc1) were downregulated in ZDF heart compared with control heart.
57	21216827	A change in the expression of genes encoding myosin heavy chain and L-type Ca(2+) channel proteins might partly underlie alterations in the time course of contraction and Ca(2+) transients in ventricular myocytes from ZDF rats.
58	21436590	Here, we show that the α-isoform of myosin heavy chain (α-MyHC, which is encoded by the gene Myh6) is the pathogenic autoantigen for CD4+ T cells in a spontaneous mouse model of myocarditis.
59	22009485	Myh6, Tnnt2, Cacna2d3, Slc9a1, and Atp2a2 were downregulated while Myl2, Cacna1g, Cacna1h, and Atp2a1 were upregulated in ZDF ventricle compared to controls.
60	22581745	Expression of genes encoding cardiac muscle proteins (Myh6/7, Mybpc3, Myl1/3, Actc1, Tnni3, Tnn2, Tpm1/2/4 and Dbi) and intercellular proteins (Gja1/4/5/7, Dsp and Cav1/3) were unaltered in GK ventricle compared with control ventricle.
61	22581745	The expression of genes encoding some membrane pumps and exchange proteins was unaltered (Atp1a1/2, Atp1b1 and Slc8a1), whilst others were either upregulated (Atp1a3, relative expression 2.61 ± 0.69 versus 0.84 ± 0.23) or downregulated (Slc9a1, 0.62 ± 0.07 versus 1.08 ± 0.08) in GK ventricle compared with control ventricle.
62	22581745	The expression of genes encoding some calcium (Cacna1c/1g, Cacna2d1/2d2 and Cacnb1/b2), sodium (Scn5a) and potassium channels (Kcna3/5, Kcnj3/5/8/11/12, Kchip2, Kcnab1, Kcnb1, Kcnd1/2/3, Kcne1/4, Kcnq1, Kcng2, Kcnh2, Kcnk3 and Kcnn2) were unaltered, whilst others were either upregulated (Cacna1h, 0.95 ± 0.16 versus 0.47 ± 0.09; Scn1b, 1.84 ± 0.16 versus 1.11 ± 0.11; and Hcn2, 1.55 ± 0.15 versus 1.03 ± 0.08) or downregulated (Hcn4, 0.16 ± 0.03 versus 0.37 ± 0.08; Kcna2, 0.35 ± 0.03 versus 0.80 ± 0.11; Kcna4, 0.79 ± 0.25 versus 1.90 ± 0.26; and Kcnj2, 0.52 ± 0.07 versus 0.78 ± 0.08) in GK ventricle compared with control ventricle.