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1 um ATPase2a expression, but no difference in contractile protein.
2 icularly by a significant down-regulation of contractile proteins.
3 oxidation pathways and altered expression of contractile proteins.
4 lts from increased gene expression of muscle-contractile proteins.
5 e expression of cardiac-specific isoforms of contractile proteins.
6  minimal effects on the expression of muscle contractile proteins.
7  nor did a change in Ca2+ sensitivity of the contractile proteins.
8 established as residing at loci encoding the contractile proteins.
9 n of various cytoplasmic proteins, including contractile proteins.
10 ed with altered expression of genes encoding contractile proteins.
11 ls into allosteric conformational changes of contractile proteins.
12  PAGE and Western immunoblot analysis of the contractile proteins.
13 to primitive cardiac myocytes that expressed contractile proteins.
14 own of GAS5 increased, the expression of SMC contractile proteins.
15 factor signaling and increased expression of contractile proteins.
16 eading to the dephosphorylation of important contractile proteins.
17 ic contractility and decreased expression of contractile proteins.
18 cells (PASMC), resulting in the induction of contractile proteins.
19  proliferation and reduced expression of SMC contractile proteins.
20 ulting from structural rearrangements of the contractile proteins.
21 s a critical regulator of other membrane and contractile proteins.
22 ype characterized by increased expression of contractile proteins.
23 (kip1), but failed to increase expression of contractile proteins.
24 pe and regulating the expression of critical contractile proteins.
25 suggests a slower actomyosin turnover by the contractile proteins.
26 reducing the expression of these proadhesive/contractile proteins.
27 rdin-regulated genes encoding SMC-restricted contractile proteins.
28  and acts as a transcriptional suppressor of contractile proteins.
29 ctin, actin-bundling proteins, and, finally, contractile proteins.
30 cues and slows cytokinesis progression while contractile proteins accumulate and correct shape asymme
31 l gene expression during differentiation and contractile protein accumulation are becoming well under
32 d striated muscle-specific markers including contractile proteins, acetylcholine receptor subtypes, a
33 odel for the interaction of cMyBP-C with the contractile proteins actin and myosin and the regulatory
34                           In addition to the contractile proteins actin and myosin, contractile filam
35 ssion of alpha-smooth muscle actin and other contractile proteins, along with inhibition of genes res
36                         Transcription of the contractile protein alpha-smooth muscle actin (alpha-SMA
37                            Expression of the contractile protein alpha-smooth muscle actin was high i
38 tter, as well as increased expression of the contractile proteins alpha-smooth muscle actin, myosin l
39 ze, protein synthesis, and expression of the contractile proteins alpha-smooth muscle actin, myosin l
40 ncreased abundance of the mRNAs encoding the contractile proteins, alpha-myosin heavy chain and cardi
41 e recruitment and localization of anillin, a contractile protein and a crucial regulator of cytokines
42 th factor receptor-1 expression, and reduced contractile protein and basic fibroblast growth factor c
43 e important for activating the expression of contractile protein and other muscle-specific genes.
44 ris muscles, and Northern analyses of muscle contractile protein and oxidative enzyme mRNA expression
45 n of genes encoding skeletal muscle-specific contractile proteins and calcium channels.
46 e propose that PGI2-mediated upregulation of contractile proteins and connexin 43 is a critical step
47 propose that PGI(2)-mediated upregulation of contractile proteins and connexin 43 is a critical step
48  Myofibroblasts have increased expression of contractile proteins and display augmented contractility
49 MC overexpressed several SRF-MYOCD-regulated contractile proteins and exhibited a hypercontractile ph
50 l muscle fiber cross-section area, levels of contractile proteins and force production in isometric c
51  have shown it to be a disease of sarcomeric contractile proteins and have highlighted its genetic he
52 udying the structure and function of cardiac contractile proteins and how differences in these transl
53 nd, conceivably, mutations in genes encoding contractile proteins and ion channels.
54 ysical and biochemical properties of mutated contractile proteins and may help to improve clinical di
55  selective transcription of genes coding for contractile proteins and metabolic enzymes in these musc
56 er mutant mice show misexpression of cardiac contractile proteins and profound sarcomere disarray.
57 MuRF1 is controlling the degradation of only contractile proteins and suggest a role for MuRF1 in the
58 igh levels in medial SMCs that are producing contractile proteins and that they would be downregulate
59  to investigate the functional properties of contractile proteins and that Tmod1 functions are critic
60 r (IP) upregulated the expression of several contractile proteins and the gap junction protein connex
61 r (IP) upregulated the expression of several contractile proteins and the gap junction protein connex
62 ese differences, we examined the profiles of contractile proteins and their messages in mesenteric ly
63 tected changes in the stoichiometry of other contractile proteins and/or sarcomere architecture.
64 osin heavy chain (MHC), the principal muscle contractile protein, and mixed muscle protein (MMP) in s
65 lar matrix constituents, membrane receptors, contractile proteins, and associated signaling molecules
66 ctivation, increased Ca2+ sensitivity of the contractile proteins, and increased intracellular pH, bu
67 tal muscle development, expression of muscle contractile proteins, and myofibril assembly.
68  genes encoding many signaling molecules and contractile proteins are associated with cardiomyopathy;
69  contractile apparatus reveals that although contractile proteins are expressed, the sheath cells app
70 uantitative changes in muscle fibre size and contractile proteins are not the dominating factors unde
71 iomyocyte-specific transcription factors and contractile proteins, as well as stimulated cellular con
72 scle atrophy and preferential loss of muscle contractile proteins associated with reduced muscle func
73       In this study, we identify spectrin, a contractile protein at the cytoskeleton-membrane interfa
74 ches such as isolated myofibril and isolated contractile protein biomechanical assays allow study of
75 inesis, mechanical perturbation also directs contractile proteins but without apparently disrupting c
76 or units activate genes for slow isoforms of contractile proteins, but it remains unclear if there is
77                     Acute endotoxemia caused contractile protein calcium insensitivity, oxygen wastag
78  the gene (TNNT2) encoding the thin-filament contractile protein cardiac troponin T are responsible f
79 argue for significant qualitative changes in contractile proteins causing the severely impaired resid
80                                In the heart, contractile protein changes correlating with functional
81 ocardial caspase 3 activation and troponin-I contractile protein cleavage were studied in the non-inf
82 +/-) SMCs also had reduced expression of SMC contractile proteins compared with WT SMCs.
83  labeling of early and late-expressed muscle contractile proteins confirms the myotome mediolateral g
84 ne transfer to mouse pial arteries increased contractile protein content and diminished CBF responses
85  abnormalities in skeletal muscle histology, contractile protein content and enzymology contribute to
86        In contrast, silencing SRF normalized contractile protein content and reversed a hypercontract
87  characterized by expression of SMC-specific contractile proteins ("contractile phenotype").
88                         Mutations in several contractile proteins contribute to DCM, but definitive e
89                 The electrical properties of contractile proteins contribute to muscle structure and
90 h are apposed to CNS capillaries and contain contractile proteins, could initiate such signalling.
91 vo caspase inhibition can prevent myocardial contractile protein degradation, improve myocardial func
92                     Quantitative analyses of contractile proteins demonstrated elevated expressions i
93 es were functionally competent and expressed contractile proteins, desmin, connexin43, and N-cadherin
94 ardiac sarcomere, but mutations in the known contractile protein disease genes are not found in up to
95 s involved in increasing Ca2+ sensitivity of contractile proteins during endothelin stimulation may b
96                         Mechanical tuning of contractile protein dynamics provides robustness to the
97 energic receptor signaling, cytoskeletal and contractile proteins, energy metabolism, extracellular m
98 myosin heavy chain (alpha-MyHC) is the major contractile protein expressed in the myocardium of adult
99     Differentiation of lung fibroblasts into contractile protein-expressing myofibroblasts by transfo
100 VSMC) phenotype, which manifest as a loss of contractile protein expression and increased proliferati
101 w-level Raf activity in these cells augments contractile protein expression and myocyte fusion.
102 n SMCs increases proliferation and decreases contractile protein expression and suggest that the incr
103 how that rapamycin activates Akt and induces contractile protein expression in human VSMC in an insul
104 n, decreased SMC proliferation and increased contractile protein expression in the Tsc2(+/-) SMCs to
105 +)-independent force generation and elevated contractile protein expression likely contribute to thes
106                                   Changes in contractile protein expression were regulated primarily
107 s myogenin expression, but causes a delay in contractile protein expression.
108 utant mice caused a dramatic decrease in SMC contractile protein expression.
109 ferentiation, whereas Akt1 appears to oppose contractile protein expression.
110  Akt2, but not Akt1, is sufficient to induce contractile protein expression.
111                       Other major regulatory/contractile proteins for Ca(2+) sensitization are expres
112 d translational repression of genes encoding contractile proteins found in the heart and vasculature.
113         Enhancement as well as impairment of contractile protein function is observed, suggesting tha
114 tile function is related to an alteration in contractile protein function is presently unknown.
115            Drawing on observations of mutant contractile protein function, together with mouse models
116  hypertrophy may be due, in part, to altered contractile protein function.
117 triated myocyte-selective transcription of a contractile protein gene encoding cardiac troponin T (cT
118 ream of XNkx2.5 and at or above the level of contractile protein gene expression.
119 scle phenotype and not in the maintenance of contractile protein gene expression.
120 l phenotypic modulation linked to changes in contractile protein gene expression.
121    Correct regulation of troponin and myosin contractile protein gene isoforms is a critical determin
122 these results suggest that the repression of contractile protein gene transcription by IL-1beta may b
123 editary, and mutations in cardiac sarcomeric contractile protein genes have been reported with autoso
124      Linkage analysis to selected sarcomeric contractile protein genes identified cardiac troponin I
125 t they would be downregulated along with the contractile protein genes in neointimal SMCs.
126 ght ratio and up-regulation of embryonic and contractile protein genes including atrial natriuretic f
127 y (HCM) is caused by mutations in at least 8 contractile protein genes, most commonly beta myosin hea
128 ucts related to the myocyte cytoskeleton and contractile proteins have been identified.
129                     While mutations in other contractile proteins have been studied widely by others,
130 ltiple isoforms of the major force-producing contractile protein in cardiac and skeletal muscles.
131 y light chain (RLC) of myosin, but not other contractile proteins in "chemically skinned" fibers, we
132 ch regulate the turnover and accumulation of contractile proteins in cultured neonatal cardiac myocyt
133 activated kinase that mediates expression of contractile proteins in differentiating myoblasts, but M
134 acetylglucosamine (O-GlcNAc) modification of contractile proteins in human heart using SDS-PAGE and t
135 ts a significant mechanical role for the non-contractile proteins in muscle, namely that of equilibra
136 obese adipocytes decreased the expression of contractile proteins in myotubes, consequently inducing
137 ata, which characterizes the function of the contractile proteins in response to calcium that is inde
138 lating MF organization and the metabolism of contractile proteins in the cardiac myocyte.
139 creased expression of smooth muscle-specific contractile proteins in the gastrointestinal tract, impa
140 sts an increased proteolysis of the two main contractile proteins in the rested and fasted state, whi
141 and internal strain related to activation of contractile proteins, in mechanically ventilated, deeply
142 be caused by mutations in any one of several contractile proteins, including beta cardiac myosin heav
143           It has been linked to many cardiac contractile proteins, including four point mutations in
144                                 Furthermore, contractile protein induction was dependent on the conce
145                                 Furthermore, contractile protein induction was dependent on the conce
146 n the sarcoplasmic reticulum, and disrupting contractile protein interactions.
147 ance of muscle function requires assembly of contractile proteins into highly organized sarcomeres.
148                              The assembly of contractile proteins into organized sarcomeric units is
149 ction depends on the precise organization of contractile proteins into sarcomeres and coupling of the
150 myocyte enhancer factor 2 and genes encoding contractile proteins is decreased in Set7 knockdown myoc
151 ith the idea that the intrinsic speed of the contractile proteins is faster in atrial than in ventric
152            The expression of skeletal muscle contractile proteins is tightly regulated during embryon
153                          As actin is a major contractile protein, it was important to determine wheth
154                        This highly conserved contractile protein likely drives cell-sheet movements t
155      The abundant expression of muscular and contractile proteins may have affected body weight and r
156 aberrant expression of muscle structural and contractile proteins, mimicking the hallmarks of the hum
157 neously, IL-1beta attenuated the increase in contractile protein mRNAs (skeletal alpha-actin and beta
158  myofibrils from 3 TTNtv mutants, and 3 with contractile protein mutations (TNNI3 K36Q, TNNC1 G159D a
159                      We found that the three contractile protein mutations but not the TTNtv mutation
160 y increased expression of genes encoding the contractile proteins MyHC beta and MyHC alpha, followed
161                     Multiple isoforms of the contractile protein myosin are present in mammalian skel
162 lation of the regulatory light chains of the contractile protein myosin IIa (MLC).
163 inding of the phosphorylated integrin to the contractile protein myosin in order to mediate transmiss
164                      We demonstrate that the contractile proteins myosin II and cortexillin I redistr
165  significant changes in several cytoskeletal/contractile proteins (myosin light chain MLY2, myosin he
166                        The concentrations of contractile proteins, myosin heavy chain isoform, and MA
167 hey partially reverse changes in fetal-adult/contractile protein, natriuretic peptide, SR-Ca(2+)-ATPa
168 ial for expression of the full complement of contractile proteins necessary for optimal force develop
169 une response to cardiac myosin (CM), a major contractile protein of cardiac muscle, is elicited in re
170 ell response to cardiac myosin (CM), a major contractile protein of the heart, and that pretransplant
171  that myosin genes not only encode the major contractile proteins of muscle, but act more broadly to
172 are caused by mutations in genes that encode contractile proteins of skeletal myofibers.
173 C) and up-regulation of betaMHC, the primary contractile proteins of the heart.
174 nce, the continual process of replacement of contractile proteins of the myofilament lattice with new
175  of the synthesis, assembly, and turnover of contractile proteins of the sarcomere.
176         Other proteins included cytoskeletal/contractile proteins (paxillin, vimentin, elongation fac
177 on induced a transition toward a slow muscle contractile protein phenotype, slower shortening velocit
178 s of TnC and its interactions with the other contractile proteins play a crucial role in modulating t
179 to unstretched controls, the turnover of the contractile protein pool was suppressed 50% to 100% in s
180  MFs did not alter the turnover of the total contractile protein pool, the cytoplasmic protein pool,
181 tin was regulated in parallel with the total contractile protein pool.
182 of engineered proteins to the heart, cardiac contractile protein profiles can be effectively remodele
183  which could account for spindle-independent contractile protein recruitment.
184 ntinued for four weeks, preserves myocardial contractile proteins, reduces systolic dysfunction, and
185 ene, in addition to encoding a major cardiac contractile protein, regulates cardiac growth and gene e
186 hanisms by which subtle genetic variation in contractile proteins remodel the human heart remains an
187 unofluorescence microscopy of structural and contractile proteins revealed the formation of a complex
188 ras(-/-) mice exhibited higher levels of the contractile proteins ROCK II, phosphorylated-MYPT(1) and
189 nase bound to detergent-washed smooth muscle contractile proteins similar to recombinant full-length
190 ression of ACTA2, the gene encoding the cyto-contractile protein smooth muscle alpha-actin.
191 hat restrict transcription of genes encoding contractile proteins specifically to either slow- or fas
192 ctivator (cyclin D1, E1, and IGF1) and fetal contractile protein (ssTNI, betaMHC) mRNA was increased
193 gene transfer, without detectable changes in contractile protein stoichiometry or sarcomere architect
194 se studies point to defects in ion channels, contractile proteins, structural proteins, and signaling
195 lcium homeostasis and possibly alteration in contractile protein structure.
196 reas the myofibrillar fraction had important contractile proteins, such as actin, tropomyosin, myosin
197                              Moreover, other contractile proteins, such as alpha-actin and tropomyosi
198 upstream of myocardin and smooth muscle cell contractile protein synthesis.
199      These data indicate that MRP is a novel contractile protein that co-integrates with myosin into
200                              TnT is a muscle contractile protein that, in association with the thin f
201 stem, an inducible expression of an abundant contractile protein, the atrial isoform of essential myo
202  decreases contractility at the level of the contractile proteins; therefore, we asked whether antiox
203 ay interact directly with the aforementioned contractile proteins through its 10-kDa domain.
204 nce for a mechanosensory system that directs contractile proteins to regulate cell shape during mitos
205 c AMP-dependent protein kinase (PKA) targets contractile proteins, troponin-I (TnI) and myosin bindin
206                                  Conversely, contractile protein turnover was suppressed in cells tre
207 s the short axis of the MFs suppressed total contractile protein turnover, the turnover of MHC and ac
208 n parallel with the MFs modestly accelerated contractile protein turnover.
209 presses expression of multiple smooth muscle contractile proteins, useful markers of differentiation.
210  for reactions of ATP, ADP and P(i) with the contractile proteins varied with IS, thus suggesting tha
211                             A modest loss of contractile proteins was observed and linked to an early
212 rdiomyocytes; sarcomeric organization of the contractile proteins was observed.
213                                              Contractile proteins were unchanged with either modes of
214 in heavy chain (SM-MHC) gene encodes a major contractile protein whose expression exclusively marks t
215 rved were associated with phosphorylation of contractile proteins with results showing that quantitat

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