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1 ion, and disarray of muscle triads (sites of excitation- contraction coupling).
2 ng that weakness was largely due to impaired excitation contraction coupling.
3 1 +/- 0.05), indicating adaptations for fast excitation-contraction coupling.
4 pite long-standing interest in their role in excitation-contraction coupling.
5 lar processes, such as energy metabolism and excitation-contraction coupling.
6 yanodine receptor type 2 plays a key role in excitation-contraction coupling.
7 ryanodine receptor (RyR1), are essential for excitation-contraction coupling.
8 faster kinetics than global [Ca(2+)]i during excitation-contraction coupling.
9 Ca(2+) flux in skeletal muscle that mediates excitation-contraction coupling.
10 rom the sarcoplasmic reticulum that mediates excitation-contraction coupling.
11 g normal cellular contraction during cardiac excitation-contraction coupling.
12 to fatigue, rhabdomyolysis and disruption of excitation-contraction coupling.
13 rafish shows that the NAM mutation decreases excitation-contraction coupling.
14 and supported beta-adrenergic regulation of excitation-contraction coupling.
15 a(2+)](mito) gradients quantitatively during excitation-contraction coupling.
16 discs, while NBC locally protects t-tubular excitation-contraction coupling.
17 voltage-sensing function in skeletal muscle excitation-contraction coupling.
18 rescuing beta-adrenergic-stimulated cardiac excitation-contraction coupling.
19 asmic reticulum, an essential step in muscle excitation-contraction coupling.
20 ed contractile efficiency, restoring cardiac excitation-contraction coupling.
21 --the three prerequisites of skeletal muscle excitation-contraction coupling.
22 (2+) influx via L-type Ca(2+) current during excitation-contraction coupling.
23 tractions and intercellular waves leading to excitation-contraction coupling.
24 l, CaV1.2, which plays a key role in cardiac excitation-contraction coupling.
25 gating, thereby amplifying Ca(2+) influx and excitation-contraction coupling.
26 ysiological involvement of CICR in mammalian excitation-contraction coupling.
27 tively, where they play an essential role in excitation-contraction coupling.
28 it to the membrane and its suggested role in excitation-contraction coupling.
29 eletal muscle acts as the voltage sensor for excitation-contraction coupling.
30 fitting provides novel insights into cardiac excitation-contraction coupling.
31 , limiting spatial [Ca](SR) gradients during excitation-contraction coupling.
32 Pase responsible for Ca(2+) re-uptake during excitation-contraction coupling.
33 r local SR Ca release at low [Ca](SR) during excitation-contraction coupling.
34 n response to depolarization, referred to as excitation-contraction coupling.
35 annels play an indispensable role in cardiac excitation-contraction coupling.
36 omyocytes including electrical signaling and excitation-contraction coupling.
37 yte cell surface, and for basal function and excitation-contraction coupling.
38 s and abnormal escape response, and impaired excitation-contraction coupling.
39 rived cardiomyocytes demonstrated functional excitation-contraction coupling.
40 most of the counterion flux required during excitation-contraction coupling.
41 lease from the sarcoplasmic reticulum during excitation-contraction coupling.
42 tionally efficient whole cell simulations of excitation-contraction coupling.
43 muscle responsible for calcium transport and excitation-contraction coupling.
44 calcium channels and play important role in excitation-contraction coupling.
45 bes but have little or no effect on skeletal excitation-contraction coupling.
46 sarcoplasmic reticulum Ca(2+) release during excitation-contraction coupling.
47 channel openings are required for efficient excitation-contraction coupling.
48 he triad but not in regulating skeletal-type excitation-contraction coupling.
49 Ca(2+) release through RyRs controls muscle excitation-contraction coupling.
50 gh haemodynamic or metabolic demand, to tune excitation-contraction coupling.
51 g that Cys-3635 is involved in voltage-gated excitation-contraction coupling.
52 acellular Ca2+ known as Ca2+ sparks regulate excitation-contraction coupling.
53 membranes in muscle cells ensuring efficient excitation-contraction coupling.
54 and propagation of the action potential and excitation-contraction coupling.
55 orage, release, and uptake to control muscle excitation-contraction coupling.
56 lt cardiomyocytes in vivo and sustain normal excitation-contraction coupling.
57 cell core, ensuring synchronous and uniform excitation-contraction coupling.
58 ffects likely to preserve functional myocyte excitation-contraction coupling.
59 nduced Ca release, and more ventricular-like excitation-contraction coupling.
60 cium cycling is a vital component of cardiac excitation-contraction coupling.
61 ndrial function, glucose uptake, fatigue and excitation-contraction coupling.
62 nment or cell size, suggesting maturation of excitation-contraction coupling.
63 beta1a subunit in supporting skeletal muscle excitation-contraction coupling.
64 ular X-ROS signaling and its role in cardiac excitation-contraction coupling.
65 and is involved in the regulation of cardiac excitation-contraction coupling.
66 asmic calcium concentration ([Ca2+]i) during excitation-contraction coupling.
67 and muscle transverse (T) tubules facilitate excitation:contraction coupling.
69 from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including
71 ed asynchronous Ca(2+)-release with impaired excitation-contraction coupling after beta-adrenergic st
72 um Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias (3-4 Mar
73 is Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias Symposiu
74 4: Systems approach to understanding cardiac excitation-contraction coupling and arrhythmias: Na(+) c
75 4: Systems approach to understanding cardiac excitation-contraction coupling and arrhythmias: Na(+) c
76 effects of increased expression of miR-1 on excitation-contraction coupling and Ca(2+) cycling in ra
77 ntal evidence of transmural heterogeneity of excitation-contraction coupling and calcium handling in
78 rticle was to study functional remodeling of excitation-contraction coupling and calcium handling in
79 ociated with the heterogeneous remodeling of excitation-contraction coupling and calcium handling.
80 the functional impact of phosphorylation in excitation-contraction coupling and cardiac performance
81 of classes of protein targets important for excitation-contraction coupling and cell survival, inclu
82 cle Ca(2+) channel Ca(V)1.1, which initiates excitation-contraction coupling and conducts L-type Ca(2
83 c Ca(2+) signaling in skeletal muscle during excitation-contraction coupling and establishes that mal
84 suggest that the remodeled t-system impairs excitation-contraction coupling and functional recovery
85 further define the role of sorcin in cardiac excitation-contraction coupling and highlight its negati
87 d resting membrane potential, which modifies excitation-contraction coupling and increases proinflamm
88 ion through divergent mechanisms that impair excitation-contraction coupling and may be exemplary of
91 +) in normal cardiac function-in particular, excitation-contraction coupling and normal electric rhyt
94 context of whole-cell electrophysiology, (3) excitation-contraction coupling and regulatory pathways,
95 on T4826I within the S4-S5 linker influences excitation-contraction coupling and resting myoplasmic C
96 we explore the effects of DP4 on orthograde excitation-contraction coupling and retrograde RyR1-DHPR
97 ation reserve of fly hearts, ensuring normal excitation-contraction coupling and rhythmical contracti
99 integral role in cellular processes such as excitation-contraction coupling and store-operated calci
100 els critical for skeletal and cardiac muscle excitation-contraction coupling and synaptic transmissio
101 lly based multiscale computational models of excitation-contraction coupling and the insights that ha
102 e findings enhance our understanding of both excitation-contraction coupling and the pathology of myo
103 line MDIMP was shown to inhibit both cardiac excitation-contraction coupling and voltage-dependent ca
104 uces the classic physiological properties of excitation-contraction coupling and, under pathophysiolo
105 sible role for cav-3 as a modifier of muscle excitation-contraction coupling and/or for localization
106 Direct effects of Ang-(1-9) on cardiomyocyte excitation/contraction coupling and cardiac contraction
107 gulates several physiological processes (eg, excitation-contraction coupling) and is involved in a wi
108 ac myocyte markers, sarcomeric organization, excitation-contraction coupling, and action potentials c
109 (RyR) are key components of striated muscle excitation-contraction coupling, and alterations in thei
110 sses such as cardiomyocyte (CM) hypertrophy, excitation-contraction coupling, and apoptosis; non-CM-s
111 ice have defective triad formation, abnormal excitation-contraction coupling, and calcium mishandling
112 diastolic stiffness, perturbs cardiomyocyte excitation-contraction coupling, and disrupts the coordi
113 ributes to T-tubule disorganization, loss of excitation-contraction coupling, and heart failure devel
114 elease is critical to normal cardiac myocyte excitation-contraction coupling, and ideally this releas
115 SC-CM, including lack of T-tubules, immature excitation-contraction coupling, and inefficient Ca-indu
116 release termination is important for stable excitation-contraction coupling, and partial [Ca(2+)](SR
118 and control neuronal communication, cardiac excitation-contraction coupling, and skeletal muscle fun
119 it (CRU) is the fundamental event of cardiac excitation-contraction coupling, and spontaneous release
120 ves that occur within atrial myocytes during excitation-contraction coupling, and the effect of posit
121 n maintaining normal I(Ca), Ca(2+) handling, excitation-contraction coupling, and the in vivo heart f
122 ll is related to interspecies differences in excitation-contraction coupling, and we report the first
125 r to V(m) depolarization, suggesting reverse excitation-contraction coupling as their aetiology.
126 the junctional SR, which results in impaired excitation-contraction coupling at the level of the myoc
127 and RyR2(R4496C+/-) hearts, suggesting that excitation-contraction coupling between the sarcolemmal
128 ticulum (SR) Ca(2+) cycling is key to normal excitation-contraction coupling but may also contribute
129 the lack of triadin did not prevent skeletal excitation-contraction coupling but reduced the amplitud
130 iomyocytes, Ca(2+) is the central element of excitation-contraction coupling, but also impacts divers
131 These findings indicate that alterations in excitation-contraction coupling, but not in maximal SR-r
132 e-patterning is independent of their role in excitation-contraction coupling, but requires Ca(2+) inf
133 V1.1e variant functions as voltage sensor in excitation-contraction coupling, but unlike CaV1.1a it a
134 lar rhythmicity contributes significantly to excitation-contraction coupling by altering the expressi
135 ndrial contribution to Ca(2+) removal during excitation-contraction coupling by comparing Ca(2+) tran
136 We conclude that miR-1 enhances cardiac excitation-contraction coupling by selectively increasin
137 subunit plays a key role in skeletal muscle excitation-contraction coupling by sensing membrane volt
138 the membrane potential becomes higher during excitation-contraction coupling, Ca can enter through bo
139 this study, we report the influence of UN on excitation-contraction coupling, Ca(2+)-induced Ca(2+) r
140 confer MHS and promote basal disturbances of excitation-contraction coupling, [Ca(2+)](rest), and oxy
141 is captured when interrogating the complete excitation-contraction coupling cascade simultaneously.
143 , we modified a mathematical model of rabbit excitation-contraction coupling coupled to a model of my
145 nt and both spontaneous and stimuli-elicited excitation-contraction coupling cycles appeared within 1
146 es responsible for sarcomere contraction and excitation-contraction coupling decreased by 43% +/- 4%
148 diac electromechanical function and cellular excitation-contraction coupling despite reduced Orai1-de
151 voked by tonic neurostimulation, even though excitation contraction coupling (ECC) remains unperturbe
153 but its potential to influence physiological excitation-contraction coupling (ECC) and muscle functio
154 asmic reticulum (SR) Ca(2+) release mediates excitation-contraction coupling (ECC) in cardiac myocyte
155 the major Ca2+ release channel required for excitation-contraction coupling (ECC) in skeletal muscle
156 f chronic adrenergic receptors activation on excitation-contraction coupling (ECC) in ventricular car
157 slate into functional effects during cardiac excitation-contraction coupling (ECC) is much less clear
158 CT: In atrial myocytes Ca(2+) release during excitation-contraction coupling (ECC) is strikingly diff
160 d by NaV1.5 mutants and propose that, during excitation-contraction coupling, elevated intracellular
161 es the function of many proteins involved in excitation-contraction coupling, elucidation of its role
162 verse facets of cardiac physiology including excitation-contraction coupling, excitability, and gene
163 dx skeletal muscle, which may play a role in excitation-contraction coupling failure and progression
164 act otherwise hidden fine details in cardiac excitation-contraction coupling from high-speed 2-dimens
165 Rd) for simulations of electrophysiology and excitation-contraction coupling, from ionic to whole-org
166 yadic volume and reduced LCCs/RyR2s decrease excitation-contraction coupling gain and cause asynchron
167 , sarcoplasmic reticulum Ca(2+) release, and excitation-contraction coupling gain were also measured.
168 ), the amplitude of the Ca(2+) transient and excitation-contraction coupling gain, but, again, there
175 c II-III loop, essential for skeletal muscle excitation-contraction coupling, has been replaced with
176 ate sarcoplasmic reticulum Ca(2+) levels and excitation-contraction coupling; hence, TRP channels exp
177 RyR2-dependent Ca2+ release is critical for excitation-contraction coupling; however, a functional r
178 ntegrated, with parallel signals controlling excitation-contraction coupling, hypertrophy, and metabo
179 l and intracellular membrane remodelling and excitation-contraction coupling; (ii) mitochondrial dist
180 2 diabetic animals display perturbations in excitation-contraction coupling, impairing myocyte contr
181 rk provides a platform for future studies of excitation contraction coupling in skeletal muscle fiber
182 rmation on microscopic calcium signaling and excitation-contraction coupling in a robust manner.
183 molecular components sufficient to modulate excitation-contraction coupling in adult muscle fibers.
185 rrents conducted by CaV1.2 channels initiate excitation-contraction coupling in cardiac and vascular
186 e receptor, RyR2) plays an essential role in excitation-contraction coupling in cardiac muscle cells.
189 ed calcium channels by MDIMP, which disrupts excitation-contraction coupling in cardiac myocytes.
190 annels (VDCCs) play a pivotal role in normal excitation-contraction coupling in cardiac myocytes.
191 ed by clusters of ryanodine receptors during excitation-contraction coupling in cardiac myocytes.
192 g of structures and proteins associated with excitation-contraction coupling in cardiomyocytes in DHF
196 e results will help to explain remodeling of excitation-contraction coupling in disease and restorati
197 AT couplon "super-hubs" thus underlie faster excitation-contraction coupling in health as well as hyp
198 our model, we quantify the role of X-ROS on excitation-contraction coupling in healthy and pathologi
200 ) by immunoaffinity column chromotography on excitation-contraction coupling in isolated myocytes.
201 mooth muscle-specific beta1 subunit regulate excitation-contraction coupling in many types of smooth
205 P2 on bioenergetics, Ca(2+) homeostasis, and excitation-contraction coupling in neonatal cardiomyocyt
209 ate a direct physiological role of S100A1 in excitation-contraction coupling in skeletal muscle.
210 ns constitute the key elements essential for excitation-contraction coupling in skeletal muscle.
211 through these channels is a critical step in excitation-contraction coupling in smooth muscle cells.
213 on of actin and myosin, effectively allowing excitation-contraction coupling in striated muscle.
214 this structural organization is crucial for excitation-contraction coupling in the body wall muscle,
216 ryanodine receptor 2 (RyR2) is required for excitation-contraction coupling in the heart and is also
218 uniform Ca release that is characteristic of excitation-contraction coupling in the heart ventricle.
219 -gated calcium channel 1.2 (CaV1.2) initiate excitation-contraction coupling in the heart, and altere
220 calcium release channel (RyR2), required for excitation-contraction coupling in the heart, is abundan
223 ficked to the membrane, and supported robust excitation-contraction coupling in the presence of nisol
224 MKII, and CaN with the Shannon-Bers model of excitation-contraction coupling in the rabbit ventricula
225 t for meeting counterion requirements during excitation-contraction coupling in tissues where TRIC-A
226 n CNM2 by disrupting machinery necessary for excitation-contraction coupling in vertebrate organisms.
227 ulator of L-type Ca(2+) channels (CaChs) and excitation-contraction coupling in vertebrate skeletal m
228 se 1 configuration improved the synchrony of excitation-contraction coupling, increased Ca(2+) transi
233 preciation of spatiotemporal fine details of excitation-contraction coupling is instrumental for the
234 tion to SR Ca(2+) storage and release during excitation-contraction coupling is largely dispensable.
235 tion of many of the key proteins involved in excitation-contraction coupling is located predominantly
240 alcium channel that controls skeletal muscle excitation-contraction coupling, is markedly repressed i
241 Here we present a computational model of excitation-contraction coupling linked to mitochondrial
244 gest a host of potential mechanisms by which excitation-contraction coupling may also be modulated.
245 sults can be explained if non-linearities in excitation-contraction coupling mechanisms modify the co
247 t postshock early site suggests that reverse excitation-contraction coupling might be responsible for
249 ic changes orchestrate cardiac architecture, excitation-contraction coupling, mitochondrial biogenesi
250 on incorporating cellular electrophysiology, excitation-contraction coupling, mitochondrial energetic
251 ncluding action potentials and arrhythmias), excitation-contraction coupling, modulation of contracti
253 hannels play a key role in initiating muscle excitation-contraction coupling, neurotransmitter releas
256 ould promote T-tubule development and mature excitation-contraction coupling of hiPSC-CM when culture
257 2+) channels that play a pivotal role in the excitation-contraction coupling of skeletal and cardiac
258 iews the potential roles of calsequestrin in excitation-contraction coupling of skeletal muscle.
259 f-state and result in excessively sensitized excitation-contraction coupling of the contractile appar
260 ry pathogenic abnormality involves defective excitation-contraction coupling, other abnormalities lik
261 ut it remains unknown whether all SFMs share excitation-contraction coupling pathway adaptations for
262 plays a significant role in skeletal muscle excitation-contraction coupling, primarily through speci
264 arlo approaches to modeling local control of excitation-contraction coupling produce high-gain Ca2+ r
265 sure approach to simulating local control of excitation-contraction coupling produces high-gain Ca2+
266 Here, we review how normal and abnormal excitation-contraction coupling properties emerge from t
268 f the Na(+)/Ca(2+) exchanger, although other excitation-contraction coupling protein levels were not
269 prolonged loss jeopardizes bioenergetics and excitation-contraction coupling, providing a potential p
270 ylation contribute to dysfunction of cardiac excitation-contraction coupling remains controversial.
271 ulation of neuronal excitability and cardiac excitation-contraction coupling requires the proper loca
272 to a substantially reduced energy supply for excitation-contraction coupling resulting from a lower f
273 e by depressing RyR2 channel activity during excitation-contraction coupling, resulting in random bur
275 ropomyosin complex is a critical mediator of excitation-contraction coupling, sarcomeric stability an
276 d Ca(2+) transients from thousands of active excitation-contraction coupling sites (ECC couplons) com
277 ts at multiple subcellular sites involved in excitation contraction coupling, such as decreasing memb
278 PMCA) extrudes Ca2+ but has little effect on excitation-contraction coupling, suggesting its potentia
279 diac ventricular myocytes, events crucial to excitation-contraction coupling take place in spatially
280 gets, particularly those involved in cardiac excitation-contraction coupling, that may prove to be at
283 is shares many ion flux pathways with normal excitation-contraction coupling, the role of the t-tubul
284 ation and depletion in t-system lumen during excitation-contraction coupling to ensure effective loca
285 model of the beta(1)-adrenergic pathway and excitation-contraction coupling to include detailed rece
286 d can be mobilized to the sarcolemma to tune excitation-contraction coupling to meet metabolic and/or
287 ctivation of calcium channels by restricting excitation-contraction coupling to more negative voltage
288 ultiple functional adaptations that minimize excitation-contraction coupling transduction times.
289 model of the cardiac myocyte that describes excitation-contraction coupling via stochastic simulatio
292 the ability of the mutant channel to engage excitation-contraction coupling was largely unaffected b
293 +], a realistic but minimal model of cardiac excitation-contraction coupling was produced that avoids
294 Myocyte contractility, Ca(2+) handling and excitation-contraction coupling were studied in isolated
295 s an alteration in ventricular cardiomyocyte excitation-contraction coupling which contributes to the
296 ey proteins involved in Ca(2+) signaling and excitation-contraction coupling, which are known to be e
297 but only slightly affected Ca(2+) release in excitation-contraction coupling, which is essential for
298 cts on beat-to-beat [Ca(2+)](c) handling and excitation-contraction coupling, which may contribute to
299 e pleiotropic second messenger Ca(2+) drives excitation-contraction coupling while not stimulating hy
300 matical model of the cardiac cell that links excitation-contraction coupling with mitochondrial energ