ライフサイエンスコーパス: cardiac myocyte

1 increase in size occurs at the level of the cardiac myocyte.

2 on the role of integrins specifically in the cardiac myocyte.

3 ide new insights into mechanotransduction in cardiac myocytes.

4 atastrophe, a previously unreported event in cardiac myocytes.

5 arvalbumin's EF-hand motif alter function of cardiac myocytes.

6 ncreases heart rate and the contractility of cardiac myocytes.

7 l strain at the subsarcomere level in living cardiac myocytes.

8 strophe was also confirmed in isolated adult cardiac myocytes.

9 lecule that rescues the disease phenotype in cardiac myocytes.

10 on depolarized mitochondria in neonatal rat cardiac myocytes.

11 ndent ryanodine receptor activation in adult cardiac myocytes.

12 romatin state on transcriptional activity in cardiac myocytes.

13 ht into the regulation of gene expression in cardiac myocytes.

14 onents of the adaptive ER stress response in cardiac myocytes.

15 293 cells expressing HERG channel and native cardiac myocytes.

16 n beta-adrenoreceptor signal transduction in cardiac myocytes.

17 n contrast to results obtained from purified cardiac myocytes.

18 n sodium, potassium, and calcium currents in cardiac myocytes.

19 mitochondrial enlargement of Drp1-deficient cardiac myocytes.

20 cute perfusion of excised hearts or isolated cardiac myocytes.

21 in cells that endure physical stress such as cardiac myocytes.

22 vivo reprogramming of noncardiac myocytes to cardiac myocytes.

23 l calcium concentration were observed in rat cardiac myocytes.

24 nitric oxide synthase 3 (eNOS) in wild-type cardiac myocytes.

25 a mitochondrial uncoupler in a monolayer of cardiac myocytes.

26 K293T cells as well as in neonatal and adult cardiac myocytes.

27 CaM binds to RyR2 with high affinity in cardiac myocytes.

28 normal and pathological Ca(2+) regulation in cardiac myocytes.

29 ed relaxation performance in mammalian adult cardiac myocytes.

30 Both miRNAs indirectly affected cardiac myocytes.

31 mbryonic stem (ES) cell differentiation into cardiac myocytes.

32 tracrine control of respiration by NO within cardiac myocytes.

33 nished delayed aftercontractions in HRC null cardiac myocytes.

34 y couples the cycling of Ca(2+) and Na(+) in cardiac myocytes.

35 otein is mechanically active in skeletal and cardiac myocytes.

36 y to cell death in embryonic fibroblasts and cardiac myocytes.

37 e form of HCO3(-), impairs O2/CO2 balance in cardiac myocytes.

38 channel function is exquisitely regulated in cardiac myocytes.

39 ural backbone for coordinated contraction of cardiac myocytes.

40 in of beta-adrenergic stimulation in beating cardiac myocytes.

41 to study the biology of newly forming adult cardiac myocytes.

42 ophysiology in left versus right ventricular cardiac myocytes.

43 res during differentiation and maturation of cardiac myocytes.

44 rodomain Ca(2+)-contraction coupling in live cardiac myocytes.

45 zation are crucial in the proper function of cardiac myocytes.

46 sitive potassium channels (KATP channels) in cardiac myocytes adjust contractile function to compensa

47 subcellular distribution and preservation in cardiac myocytes after cell isolation are not well docum

48 at these candidate loci in neonatal cultured cardiac myocytes after in utero exposure to diesel exhau

49 viral overexpression of beta3-AR in isolated cardiac myocytes also increased NO production and attenu

50 ial duration and mitochondrial energetics to cardiac myocyte and whole-heart contractile function.

51 I-stimulated incorporation of 3[H]leucine in cardiac myocytes and 3[H]proline in cardiac fibroblast w

52 ST2 is released by stressed cardiac myocytes and also predicts mortality in heart fa

53 he cytoplasm and the mitochondrial matrix in cardiac myocytes and can be exploited to answer question

54 switching (or bistability) of AP duration in cardiac myocytes and EAD-mediated arrhythmias and sugges

55 Further experimentation with isolated adult cardiac myocytes and fibroblasts from double-knockout im

56 axis mediates fibrotic responses commonly in cardiac myocytes and fibroblasts induced by physico-chem

57 characterize the biomechanical properties of cardiac myocytes and fibroblasts under hyperglycemia or

58 Migration of MSC to apoptotic cardiac myocytes and fibroblasts was driven by hepatocyt

59 Using membranes prepared from adult rat cardiac myocytes and fibroblasts, we found that MMP14 ac

60 inhibit recruitment of MSC toward apoptotic cardiac myocytes and fibroblasts.

61 gical processes such as spontaneous beats in cardiac myocytes and glucose-dependent ATP increase in p

62 asm and the mitochondrial matrix of isolated cardiac myocytes and in Langendorff-perfused hearts base

63 d and used to determine the EGSH in isolated cardiac myocytes and in Langendorff-perfused hearts.

64 e of mTORC1 and mTORC2 signaling in cultured cardiac myocytes and in mouse hearts subjected to condit

65 n ER stress, ERAD, and viability in cultured cardiac myocytes and in the mouse heart, in vivo.

66 cules involved in calcium (Ca2+) handling in cardiac myocytes and is considered to be the predominant

67 We isolated neonatal CHF/Hey2-knockout (KO) cardiac myocytes and measured action potentials and ion

68 ransitions in isolated murine and guinea pig cardiac myocytes and mitochondria.

69 ss response on ischemia/reperfusion (I/R) in cardiac myocytes and mouse hearts.

70 Previous studies in cardiac myocytes and neurons have identified CCt as both

71 emonstrating concomitant isolation of viable cardiac myocytes and nonmyocytes from the same adult mou

72 ution microscopy, we demonstrate that in rat cardiac myocytes and other cell types mitochondrial PDE2

73 at miR-29 promotes pathologic hypertrophy of cardiac myocytes and overall cardiac dysfunction.

74 5 suppressed infectious virus yield in human cardiac myocytes and the induction of ISG15 in patients

75 plex electrophysiology protocols from single cardiac myocytes and then used to tune model parameters

76 are near the sarcoplasmic reticulum (SR) in cardiac myocytes, and evidence for crosstalk exists.

77 ched in the adipocytes, smooth muscle cells, cardiac myocytes, and immune cells.

78 cilia and the intercalated disks of isolated cardiac myocytes, and performed targeted patch-clamp rec

79 oplasmic reticulum (SR) Ca release events in cardiac myocytes, and they have a typical duration of 20

80 ocalizes to the mitochondria in neonatal rat cardiac myocytes, and TNF treatment transcriptionally up

81 cardiac dysfunction as a result of decreased cardiac myocyte apoptosis and fibrosis.

82 e cardiac collagen volume fraction (CVF) and cardiac myocyte apoptosis index in aFGF-NP+UTMD group re

83 s group showed similar results (MCD, CVF and cardiac myocyte apoptosis index) to other aFGF treatment

84 free mitochondrial calcium concentration in cardiac myocytes are largely unknown.

85 Changes in redox potentials of cardiac myocytes are linked to several cardiovascular di

86 ch contraction and haemodynamic disturbance, cardiac myocytes are subjected to fluid shear stress as

87 s cytoskeletal and sarcolemmal structures in cardiac myocytes as the likely candidates for load trans

88 larized mitochondria in resting neonatal rat cardiac myocytes, as well as in those treated with TNF o

89 arizing current passed by Kv11.1 channels in cardiac myocytes, as well as the current passed in respo

90 e relationship of SR and t-t networks within cardiac myocytes, as well as the modifications that occu

91 was studied in LV muscle strips and isolated cardiac myocytes before and after elimination of titin-b

92 , nNOS is the most relevant source for NO in cardiac myocytes, but this nNOS is not located in mitoch

93 Gene transduction of adult cardiac myocytes by cTnIs with specific helix 4 ssTnI su

94 AC is characterized by the replacement of cardiac myocytes by fibro-adipocytes, cardiac dysfunctio

95 nd that amylin deposition negatively affects cardiac myocytes by inducing sarcolemmal injury, generat

96 In cardiac myocytes Ca(2+) is a crucial regulator of contra

97 intracellular [Ca2+] and [H+], cells such as cardiac myocytes can exercise control over their biologi

98 cell types within the myocardium, including cardiac myocytes, cardiac fibroblasts and vascular smoot

99 could find no evidence to support a burst of cardiac myocyte cell cycle activity at postnatal day 15.

100 n T-Cre;CyclinA2-LacZ-EGFP mice, we examined cardiac myocyte cell cycle activity during embryogenesis

101 Discerning cardiac myocyte cell cycle behavior is challenging owing

102 tanding of the molecular circuitry governing cardiac myocyte cell cycle regulation is required.

103 -specific cell cycle reporter for studies of cardiac myocyte cell cycle regulation.

104 ifferent cAMP pools have opposing effects on cardiac myocyte cell size.

105 However, whether mTOR regulates cardiac myocyte cell survival is unknown.

106 heart; however, the endogenous structure of cardiac myocyte chromatin has never been determined.

107 transcriptional signature of injury-induced cardiac myocyte (CM) regeneration in mouse by comparing

108 mechanical signals in many cells, including cardiac myocytes (CM).

109 In the beating heart, cardiac myocytes (CMs) contract in a coordinated fashion

110 RATIONALE: During each beat, cardiac myocytes (CMs) generate the mechanical output ne

111 art require strong and stable connections of cardiac myocytes (CMs) with the extracellular matrix (EC

112 We here identify a signaling cassette in cardiac myocytes consisting of K-Ras, the scaffold RASSF

113 While cardiac myocytes contain several isoforms of NO synthase

114 sential for normal sympathetic regulation of cardiac myocyte contractility and is responsible for the

115 gulates actin-myosin interaction and thereby cardiac myocyte contraction and relaxation.

116 Cardiac myocyte contraction is caused by Ca(2+) binding

117 he mechanisms by which MDA5 signaling within cardiac myocytes contributes to the host response agains

118 as accompanied by increased cell cohesion in cardiac myocyte cultures and murine heart slices.

119 ed novel pathways regulated by TBX5 in human cardiac myocyte development.

120 y, we modeled the anatomical structures in a cardiac myocyte diad, to predict the effects of anatomic

121 Knockout cardiac myocytes did not show P2X4R by immunoblotting or

122 mal mouse hearts, but were upregulated after cardiac myocyte-directed Drp1 gene deletion in adult mic

123 s, indicating that the function of miR-29 in cardiac myocytes dominates over that in non-myocyte cell

124 and membrane potential (DeltaPsim) in adult cardiac myocytes during cyclic sarcoplasmic reticulum Ca

125 rriers to diffusion that are expected in the cardiac myocyte dyadic space, cAMP compartmentation did

126 consists of different cell types, including cardiac myocytes, endothelial cells, fibroblasts, and ot

127 mediated by a reduction in the expression of cardiac myocyte enhancer factor 2a.

128 or NAADP in arrhythmogenic Ca(2+) release in cardiac myocytes evoked by beta-adrenergic stimulation.

129 R calcium (Ca) release is critical to normal cardiac myocyte excitation-contraction coupling, and ide

130 Our data demonstrated that right ventricular cardiac myocytes exhibited reduced cell cycle activity r

131 Cardiac myocytes express two isoforms of TnI during deve

132 ) and DNA sequencing were performed in adult cardiac myocytes following development of pressure overl

133 ntially expressed with beta2 in T-tubules of cardiac myocytes, forming alpha2beta2 heterodimers.

134 d in both noncontracting hearts and isolated cardiac myocytes from adult mice.

135 ZBTB17 expression protected cardiac myocytes from apoptosis in vitro and in a mouse

136 n cardiac myocytes from wild-type but not in cardiac myocytes from ATF6 knockout mice.

137 At the cellular level, adult cardiac myocytes from Dusp8 gene-deleted mice were thick

138 e in the field focusing on the withdrawal of cardiac myocytes from the cell cycle during the transiti

139 e potential and metabolic activity in intact cardiac myocytes from the murine model of Duchenne muscu

140 ADP-AM failed to enhance Ca(2+) responses in cardiac myocytes from Tpcn2(-/-) mice, unlike myocytes f

141 ical ER stressor, tunicamycin, and by I/R in cardiac myocytes from wild-type but not in cardiac myocy

142 nol-induced increase in Ca(2+) transients in cardiac myocytes from WT but not CD38(-/-) mice.

143 al analyses revealed interactions within the cardiac myocyte genome at 5-kb resolution, enabling exam

144 n cardiac mass resulting from stress-induced cardiac myocyte growth) is a major factor underlying hea

145 We unexpectedly found that cardiac myocyte GSK-3 is essential for cardiac homeostas

146 Together, our findings suggest that cardiac myocyte GSK-3 is required to maintain normal car

147 space with restricted diffusion for Na(+) in cardiac myocytes has been inferred from a transient peak

148 Stretching single ventricular cardiac myocytes has been shown experimentally to activa

149 adult hearts containing mostly post-mitotic cardiac myocytes have lost this ability.

150 nary artery smooth muscle cells (HCASMC) and cardiac myocytes (HCM), leading to upregulation of antio

151 hers' expression as well as transcription in cardiac myocytes; however, only Hmgb2 does so in a manne

152 t of specific inhibition of selected PDEs on cardiac myocyte hypertrophic growth.

153 ZBTB17 also regulated cardiac myocyte hypertrophy in vitro and in vivo in a ca

154 Cardiac myocyte hypertrophy is regulated by an extensive

155 Cardiac myocyte hypertrophy is the main compensatory res

156 -4FF to image the calcium wave produced by a cardiac myocyte in response to a small artificial calciu

157 iRNAs in vivo develop into mature functional cardiac myocytes in situ, and whether reprogramming lead

158 cycle activity relative to left ventricular cardiac myocytes in the immediate perinatal period.

159 n, we modeled the Holt-Oram syndrome in iPSC-cardiac myocytes in vitro and uncovered novel pathways r

160 Targeted deletion of miR-29 in cardiac myocytes in vivo also prevents cardiac hypertrop

161 that CASK localizes at lateral membranes of cardiac myocytes, in association with dystrophin.

162 model was then incorporated in a variety of cardiac myocytes, including human ventricular, atrial an

163 In the heart, electrical stimulation of cardiac myocytes increases the open probability of sarco

164 s, uncover a novel contributing mechanism to cardiac myocyte injury in type 2 diabetes, and suggest a

165 fibroblasts from double-knockout implicated cardiac myocytes intrinsic factors responsible for obser

166 emonstrate that T. cruzi infection activates cardiac myocyte iPLA2gamma, resulting in increased AA an

167 The ultrastructure of the cardiac myocyte is remarkable for the high density of mi

168 efractoriness of calcium (Ca(2+)) release in cardiac myocytes is an important factor in determining w

169 refractoriness of calcium (Ca2+) release in cardiac myocytes is an important factor in determining w

170 e have demonstrated that export of cAMP from cardiac myocytes is an intrinsic cardioprotective mechan

171 ably, dynamic CpG and non-CpG methylation in cardiac myocytes is confined to A compartments.

172 parts of the calcium signalling apparatus in cardiac myocytes is unknown.

173 Cardiac myocytes isolated from older R21C mice demonstra

174 le NO synthases (NOSs) are also expressed in cardiac myocytes, it is unclear whether they control res

175 Cardiac myocyte KLF5 is a transcriptional regulator of P

176 een attributed to perturbed Ca2+ handling in cardiac myocytes leading to spontaneous Ca2+ release and

177 Induction of O2 (-) production in H9C2 cardiac myocytes led to the release of a transferable fa

178 orter, whereas DUSP8 overexpression promoted cardiac myocyte lengthening with a loss of thickness.

179 At the cardiac myocyte level, colon ascendens stent peritonitis

180 al properties of tdTomato(-) and tdTomato(+) cardiac myocyte-like cells were analyzed ex vivo.

181 tdTomato(+) cells expressed cardiac myocyte markers, sarcomeric organization, excita

182 correlated with higher expression of mature cardiac myocyte markers.

183 Mechanistically, we found cardiac myocyte miR-29 to de-repress Wnt signaling by di

184 Cardiac myocyte model systems have been developed to stu

185 g adverse cardiac remodeling, and decreasing cardiac myocyte necrosis and replacement fibrosis.

186 ngestive heart failure typically arises from cardiac myocyte necrosis/apoptosis, associated with the

187 Cardiac myocytes normally initiate action potentials in

188 Ablating Drp1 in adult mouse cardiac myocytes not only interrupts mitochondrial fissi

189 Cardiac myocyte nuclear and cellular RNA expression prof

190 The aim was to purify cardiac myocyte nuclei from hearts of different species

191 High sorting purity was confirmed for cardiac myocyte nuclei isolated from mice, rats, and hum

192 cardiac tissue samples were used to isolate cardiac myocyte nuclei.

193 epigenetic and transcriptional processes in cardiac myocytes of different origins.

194 Here, we report that cardiac myocytes of heterozygous mice carrying a catecho

195 pression or its ubiquitin ligase activity in cardiac myocytes offered protection against H2O2 stress.

196 ing a maximal +34-mV shift in neonatal mouse cardiac myocytes or Chinese hamster ovary (CHO) cells ex

197 When cardiac myocytes or whole hearts are exposed to oxidant

198 Activation of a cardiac myocyte P2X4 receptor protects against heart fai

199 blishes a new protective role for endogenous cardiac myocyte P2X4R in HF and is the first to demonstr

200 define the physiological role of endogenous cardiac myocyte P2X4R under basal conditions and during

201 Alone, forced cardiac myocyte Parkin overexpression activated mitophag

202 unit KChIP2, which regulates Kv4 channels in cardiac myocytes, partially relieved Kv4.3 but not Kv4.2

203 Cardiac myocyte passive tension was significantly increa

204 We report enhanced cardiac myocyte performance by acute titration of cardia

205 tors, myocardial fibrosis and alterations in cardiac myocyte physiology because of myocardial unloadi

206 Consequently, cardiac myocyte proliferation during the postnatal perio

207 To (re)initiate cardiac myocyte proliferation in adult mammalian hearts,

208 an amphibians leading to the hypothesis that cardiac myocyte proliferation is a major driver of heart

209 function after cardiac damage, induction of cardiac myocyte proliferation is an attractive therapeut

210 mechanical communication between neighboring cardiac myocytes, properties that are perturbed in heart

211 conditional deletion of PLCepsilon in mouse cardiac myocytes protects from stress-induced pathologic

212 onatal mouse hearts containing proliferating cardiac myocytes regenerate even extensive injuries, whe

213 containing ubiquitin-tagged proteins within cardiac myocytes related to proteasome dysfunction and i

214 f DNA methylation in embryonic stem cells or cardiac myocytes, respectively, does not alter genome-wi

215 rinuclear PLCepsilon, scaffolded to mAKAP in cardiac myocytes, responds to hypertrophic stimuli to ge

216 We generated transgenic mice with cardiac myocyte-restricted expression of Grx1-roGFP2 tar

217 Mechanistically, loss of GSK-3 in adult cardiac myocytes resulted in induction of mitotic catast

218 mtDNA damage in cardiac myocytes resulting from increased oxidative stre

219 entration, and lowering ATP concentration in cardiac myocytes results in I(Ks) reduction and action p

220 Cardiac myocyte senescence was evident at 3 months in Pi

221 How does the cardiac myocyte sense changes in preload or afterload?

222 2+) spark initiation after Ca(2+) release in cardiac myocytes should inhibit further Ca(2+) release d

223 Double-knockout cardiac myocytes showed cell cycle progression resulting

224 erged de novo into terminally differentiated cardiac myocytes, smooth muscle and vascular endothelial

225 Our data highlight advantages of a cardiac myocyte-specific cell cycle reporter for studies

226 apoptosis in vitro and in a mouse model with cardiac myocyte-specific deletion of Zbtb17, which devel

227 Cardiac myocyte-specific expression of a dominant-negati

228 Mice with cardiac myocyte-specific expression of human beta3-AR (b

229 Using conditional, cardiac myocyte-specific gene deletion, we now demonstra

230 ctor, in the lethal cardiomyopathy evoked by cardiac myocyte-specific interruption of dynamin-related

231 iPLA2gamma in cardiac myocytes, we generated cardiac myocyte-specific iPLA2gamma knock-out (CMiPLA2ga

232 iPLA2gamma, germ-line iPLA2gamma(-/-) mice, cardiac myocyte-specific iPLA2gamma transgenic mice, and

233 We generated cardiac myocyte-specific Klf5 knockout mice that showed

234 xpression profiles and epigenetic marks in a cardiac myocyte-specific manner.

235 We generated tamoxifen-inducible cardiac myocyte-specific mice lacking both GSK-3 isoform

236 Likewise, cardiac myocyte-specific Parkin deletion evoked no adult

237 This study establishes cardiac myocyte-specific sorting of nuclei as a universa

238 A novel cardiac myocyte-specific Speg conditional knockout (MCM-

239 We generated cardiac myocyte-specific transgenic mice using a Tet-Off

240 epigenetic data confirmed the high degree of cardiac myocyte-specificity of our protocol.

241 We conclude that titin-based cardiac myocyte stiffening acutely after MI is partly me

242 ndria and rescues cell death in neonatal rat cardiac myocytes subjected to hypoxia/reoxygenation.

243 METHODS AND Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxy

244 Knockdown of ATF6 in cardiac myocytes subjected to I/R increased reactive oxy

245 entials characteristic of mature ventricular cardiac myocytes (tdTomato(-) cells).

246 ificantly faster Ca(2+) dynamics in neonatal cardiac myocytes than GCaMP6f.

247 into our previous local-control model of the cardiac myocyte that describes excitation-contraction co

248 e uniquely-adapted membrane invaginations in cardiac myocytes that facilitate the synchronous release

249 nal-regulated kinases 1/2 signaling in adult cardiac myocytes that then alters the length-width growt

250 In adult cardiac myocytes the ratio of GCa to GNa of TRPM2 channe

251 In cardiac myocytes, the activation of inner membrane pores

252 In cardiac myocytes, the ER stressors, thapsigargin and tun

253 of the sarcomere, the structural unit of the cardiac myocytes, the Frank-Starling mechanism consists

254 mtDNA repair machinery has been described in cardiac myocytes, the regulation of this repair has been

255 In cardiac myocytes, there are several Ca(2+) -sensitive po

256 lays a central role in Ca(2+) homeostasis in cardiac myocytes through regulation of the sarco(endo)pl

257 proteins in both hERG-HEK cells and neonatal cardiac myocytes through the enhancement of SGK1 but not

258 Notch activation reprograms cardiac myocytes to an induced Purkinje-like state chara

259 tective effects of RF-RDN acting directly on cardiac myocytes to attenuate cell death and protect aga

260 Using permeabilized cardiac myocytes to eliminate any contribution of plasma

261 sor anchored onto the myofilaments in rabbit cardiac myocytes to examine PKA activity at the myofilam

262 This work provides structural evidence in cardiac myocytes to indicate the formation of microdomai

263 STIM1 can associate with Orai in cardiac myocytes to produce a Ca(2+) influx pathway that

264 on is closely associated with the ability of cardiac myocytes to proliferate.

265 m of AC, commonly recognized as a disease of cardiac myocytes, to include nonmyocyte cells in the hea

266 These data sets provide novel insight into cardiac myocyte transcription.

267 d sarcomere strain were also imaged in paced cardiac myocytes under mechanical load, revealing sponta

268 itochondrial permeability transition pore in cardiac myocytes under stress.

269 Spontaneous calcium (Ca) waves in cardiac myocytes underlie delayed afterdepolarizations (

270 (2+) spark (LCS) activity in intact isolated cardiac myocytes using fast confocal line scanning with

271 le of HRV on alternans formation in isolated cardiac myocytes using numerical simulations of an ionic

272 In ventricular cardiac myocytes (VCM), Gbeta5 deficiency provided subst

273 a phosphaturic hormone that directly targets cardiac myocytes via FGF receptor (FGFR) 4 thereby induc

274 ump activity regulate internal Ca release in cardiac myocytes via Na/Ca exchange.

275 st that CO induces arrhythmias in guinea pig cardiac myocytes via the ONOO(-)-mediated inhibition of

276 Expression of miR-184 in the heart and cardiac myocyte was developmentally downregulated and wa

277 e, recycling of the beta1-AR in rat neonatal cardiac myocytes was dependent on targeting the AKAP5-PK

278 The number of EdU(+) cardiac myocytes was increased in CBSC- versus vehicle-

279 T2 p.R173W) in patient-specific iPSC-derived cardiac myocytes, we demonstrated that the knockout stra

280 ifically identify the roles of iPLA2gamma in cardiac myocytes, we generated cardiac myocyte-specific

281 tion or the patch-clamp technique in beating cardiac myocytes, we identified a neuronal NO synthase (

282 r determine the impact of hyperamylinemia on cardiac myocytes, we investigated human myocardium, comp

283 ial fission was conditionally interrupted in cardiac myocytes, we propose several new concepts that m

284 In the context of cardiac myocytes, we provide guidelines for selecting a

285 armacological inhibition of iNOS in isolated cardiac myocytes, we reveal that an increase of expressi

286 Cardiac myocytes were isolated with yields comparable to

287 Freshly isolated cardiac myocytes were loaded with the Ca(2+)-indicator f

288 Conversely, in cardiac myocytes where the IFN response is critical for

289 ), was delivered into acutely isolated mouse cardiac myocytes, where either one- and two-photon uncag

290 or ERAD has been studied in the heart, or in cardiac myocytes, where protein quality control is criti

291 endent prohypertrophic signaling in isolated cardiac myocytes, whereas the introduction of constituti

292 e length-width growth dynamics of individual cardiac myocytes, which further alters contractility, ve

293 catalase gene and were shown to bind ATF6 in cardiac myocytes, which increased catalase promoter acti

294 and DAD dynamics observed experimentally in cardiac myocytes, whose mechanisms are complex but analy

295 epresent a subcellular sarcomeric space in a cardiac myocyte with varying detail.

296 Treatment of cardiac myocytes with CTRP9 protein led to suppression o

297 that PDE3A co-localizes in Z-bands of human cardiac myocytes with desmin, SERCA2, PLB, and AKAP18.

298 Stimulation of the cardiac myocytes with isoprenaline, angiotensin II, or e

299 Membrane permeabilization of cardiac myocytes with saponin and/or Triton X-100 increa

300 ng ionic homeostasis and dynamic function in cardiac myocytes, within both the in vivo cell and in si