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1 old greater for rat beta-myosin than for pig beta-myosin.
2 leavage rates were nearly 30% faster for rat beta-myosin.
3 n, almost twice the velocities observed with beta-myosin.
4 erved in hearts expressing approximately 70% beta-myosin.
5 on was approximately 3.8-fold faster for rat beta-myosin (135 s(-)(1)) than for pig beta-myosin (35 s
7 s than slow myosins (MHC-II-1, also known as beta-myosin) and it has been well established that ADP b
9 -sliding velocity of alpha-myosin by 20% and beta-myosin by 36% compared with their respective non-ac
10 sliding velocity of alpha-myosin by 20% and beta-myosin by 36%, compared to their respective non-ace
11 alcium-independent positive inotropy in slow beta-myosin-dominant rabbit and human failing ventricula
12 C1 1-37) and the short loop of human cardiac beta-myosin (hcM398-414) have been shown to interact wit
14 transgenic mice further exhibited decreased beta myosin heavy chain expression compared to age match
16 mechanism of regulation of cardiac alpha and beta myosin heavy chain gene by naturally occurring anti
17 psilonRACK resulted in selectively increased beta myosin heavy chain gene expression and normally fun
19 3beta [GSK3beta], a 20-fold up-regulation of beta myosin heavy chain RNA and elevated G(s)alpha/G(i)a
20 in, we report the expression of an antisense beta myosin heavy chain RNA in the normal rodent myocard
21 genes coding for atrial natriuretic peptide, beta myosin heavy chain, medium chain acyl-CoA dehydroge
22 t 8 contractile protein genes, most commonly beta myosin heavy chain, myosin binding protein C, and c
24 other structural proteins, such as alpha and beta myosin heavy chains and cardiac alpha actin, play c
25 nt with decreased alpha myosin and increased beta myosin heavy chains, suggesting an alpha-to-beta co
26 naturietic factor ( approximately 55-fold), beta-myosin heavy chain ( approximately 8-fold), and alp
28 se chain reaction was conducted to coamplify beta-myosin heavy chain (beta-MHC) and alpha-skeletal ac
31 a4fl/fl) were crossed with mice containing a beta-myosin heavy chain (beta-MHC) or alpha-MHC promoter
32 ected reporter gene driven by 3542 bp of rat beta-myosin heavy chain (beta-MHC) promoter was increase
33 ese include atrial natriuretic factor (ANF), beta-myosin heavy chain (beta-MHC), and skeletal muscle
34 dium results in enhanced expression of fetal beta-myosin heavy chain (beta-MyHC) and reduced expressi
36 gene profile was observed, ie, expression of beta-myosin heavy chain (betaMHC), atrial/brain natriure
37 and reactivates many fetal genes, including beta-myosin heavy chain (betaMyHC) and skeletal alpha-ac
42 genic analyses revealed that a 600-base pair beta-myosin heavy chain (betaMyHC) promoter conferred me
45 n (CHIP), increased SRF activity, as well as beta-myosin heavy chain (MHC) and myocardin expressions.
46 point mutation at residue 403 (R403Q) in the beta-myosin heavy chain (MHC) caused a severe form of FH
47 heart contains two cardiac myosin isoforms: beta-myosin heavy chain (MHC) is found predominantly in
48 TPase (SERCA), phospholamban, and alpha- and beta-myosin heavy chain (MHC) proteins were assayed in h
50 pathy, DCM) associated with mutations in the beta-myosin heavy chain (MYH7) gene product (Myosin-7).
53 2S, G256E, F513C, V606M, R719Q, and L908V of beta-myosin heavy chain (MYH7); S179F of troponin T (TNN
54 (TH)-responsive genes, including alpha- and beta-myosin heavy chain (MyHC) and sarcoplasmic reticulu
56 tor (RAR) controlled by either the alpha- or beta-myosin heavy chain (MyHC) promoter were generated.
57 ), alpha-skeletal muscle actin (p<0.05), and beta-myosin heavy chain (p<0.05) were observed in AC6-KO
58 on of the slow molecular motor of the heart (beta-myosin heavy chain [MyHC]) is well known to occur i
59 d expression of hypertrophic markers BNP and beta-myosin heavy chain accompanied adult-onset cardiac
61 ith mild hypertrophy, elevated expression of beta-myosin heavy chain and alpha-skeletal actin genes,
62 sed by 28%, and upregulation of the mRNA for beta-myosin heavy chain and alpha-skeletal actin was obs
64 wever, adult transgenic ventricles expressed beta-myosin heavy chain and atrial natriuretic factor.
65 enes associated with pathologic hypertrophy (beta-myosin heavy chain and atrial natriuretic peptide)
67 ic response is increased cellular content of beta-myosin heavy chain and cytochrome oxidase subunit V
68 riuretic peptide, brain natriuretic peptide, beta-myosin heavy chain and myosin light chain (2- to 5-
70 Hypertrophic marker genes, including the beta-myosin heavy chain and transforming growth factor-b
71 Mutations in the MYH7 gene encoding for the beta-myosin heavy chain are the underlying genetic cause
73 enhancer factor 2C), and down-regulation of beta-myosin heavy chain expression, a key determinant of
74 ban:SERCA2 (>/=2.6:1) exhibited increases in beta-myosin heavy chain expression, associated with card
75 to determine the prevalence and phenotype of beta-myosin heavy chain gene MYH7 mutations in a large c
78 nergic signaling, the aberrant expression of beta-myosin heavy chain in adult Gsalpha-DF but not cont
79 sarcomeric reorganization, and expression of beta-myosin heavy chain in myocytes with IC(50) values o
81 ated with preserved expression of alpha- and beta-myosin heavy chain isoforms and sarcoplasmic reticu
82 Comparison of mammalian cardiac alpha- and beta-myosin heavy chain isoforms reveals 93% identity.
83 tures and containing predominately alpha- or beta-myosin heavy chain isoforms were found to be consis
84 [AT(1)R]), p47(phox) NADPH oxidase subunit, beta-myosin heavy chain isozyme switch, accumulation of
85 Ca2+ sensitivity, a significant increase in beta-myosin heavy chain mRNA and protein, normal cardiac
86 expression of skeletal alpha-actin mRNA and beta-myosin heavy chain mRNA at 5 days, but it did not a
87 weight ratio, atrial natriuretic factor and beta-myosin heavy chain mRNA expression, myocyte area, a
89 st, there was no relationship between either beta-myosin heavy chain or cytochrome C oxidase expressi
90 binding by E1A, relieved E1A's repression of beta-myosin heavy chain promoter activity while having n
93 roteins decreased the activity of alpha- and beta-myosin heavy chain promoters to nearly the same ext
94 ansfected reporter genes driven by alpha- or beta-myosin heavy chain promoters was markedly diminishe
97 hypothesis, we screened 30 5- to 6-month-old beta-myosin heavy chain Q403 transgenic rabbits by echoc
98 al remodeling, including decreased alpha- to beta-myosin heavy chain ratios, and induced maladaptive
99 oponin T (TnT) and missense mutations in the beta-myosin heavy chain share abnormalities in common, a
101 nsforming the disorder from a disease of the beta-myosin heavy chain to a disease of the cardiac sarc
102 t induction of atrial natriuretic factor and beta-myosin heavy chain transcripts, interstitial fibros
105 tic factor, alpha-skeletal muscle actin, and beta-myosin heavy chain) and collagens were observed bet
106 ryonic genes (atrial natriuretic peptide and beta-myosin heavy chain) and elevated nuclear factor kap
107 hypertrophic cardiomyopathy (HCM) are MYH7 (beta-myosin heavy chain) and MYBPC3 (beta-myosin-binding
108 brain natriuretic peptides, skeletal actin, beta-myosin heavy chain), and fibrosis (collagen III), a
109 trophy (atrial natriuretic factor, CARP, and beta-myosin heavy chain), uncoupling protein 2 (UCP2), a
112 an increase in NFAT-dependent expression of beta-myosin heavy chain, a sensitive marker for patholog
113 istry revealed de novo expression of desmin, beta-myosin heavy chain, alpha-actinin, cardiac troponin
115 TA-4, atrial natriuretic peptide, alpha- and beta-myosin heavy chain, and cardiac troponin T) by day
116 ism, electrical stimulation increased c-fos, beta-myosin heavy chain, and Cyt c promoter activities.
120 of pathological hypertrophy like: alpha- and beta-myosin heavy chain, atrial natriuretic factor, phos
121 tion demonstrated an increased expression of beta-myosin heavy chain, brain natriuretic peptide, and
122 s in males, including fibrosis, induction of beta-myosin heavy chain, inactivation of glycogen syntha
123 expressed expected cardiac markers including beta-myosin heavy chain, myosin light chain 2v, and atri
124 -response genes (e.g., alpha-skeletal actin, beta-myosin heavy chain, natriuretic peptides) were simi
125 ) levels of atrial natriuretic factor (ANF), beta-myosin heavy chain, sarcoplasmic reticulum Ca2+-ade
126 tudy prompted a search of the genes encoding beta-myosin heavy chain, troponin T, troponin I, and alp
127 l (SMC)-specific isoforms of alpha-actin and beta-myosin heavy chain, two major components of the SMC
128 marker genes, atrial natriuretic factor and beta-myosin heavy chain, were not up-regulated in E33A-t
129 atriuretic factor, skeletal alpha-actin, and beta-myosin heavy chain, which in adult rat ventricle ar
130 performed in nontransgenic (n=24), wild-type beta-myosin heavy chain-arginine(403) (n=14), and mutant
131 ty with heart defects, whereas deletion with beta-myosin heavy chain-cre (betaMHC-cre) produced viabl
132 heavy chain-arginine(403) (n=14), and mutant beta-myosin heavy chain-glutamic acid(403) (n=24) transg
133 on and relaxation were reduced in the mutant beta-myosin heavy chain-glutamic acid(403) transgenic ra
138 rrhythmia in a transgenic (TG) rabbit model (beta-myosin heavy chain-Q403) of human hypertrophic card
145 igated the kinetic properties of rat and pig beta-myosin heavy chains (beta-MHC) in which we have fou
148 raction rate, surface area, or expression of beta-myosin heavy chains was significantly greater in AK
149 iac-specific genes, including the alpha- and beta-myosin heavy chains, skeletal alpha-actin, and brai
150 e tested whether patients with HCM caused by beta-myosin heavy-chain (beta-MHC) gene mutations exhibi
152 n the sarcoplasmic reticulum, and alpha- and beta-myosin heavy-chain isoforms) and of genes associate
154 er shown to be affected (in 2005) by a novel beta-myosin heavy-chain mutation that caused HCM, after
156 vy chain, we observed high concentrations of beta-myosin in distinct areas such as at the tip of papi
158 ed with increased relative expression of the beta-myosin isoform (25+/-6 versus 63+/-5%beta, CTRL ver
161 eavy chain alpha, cardiac myosin heavy chain beta, myosin light chain 1A, myosin light chain 1V and N
167 muscle-specific isoforms of alpha-actin and beta-myosin, which are known to cause familial TAAD when
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