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1 SR Ca2+-ATPase, and depressed phosphorylated phospholamban).
2 th coexpression of phosphomimetic mutants of phospholamban.
3 ructural determinants of SERCA regulation by phospholamban.
4 a, protein kinase Cepsilon, calcineurin, and phospholamban.
5 drenergic stimulation and phosphorylation of phospholamban.
6 diesterase 4 resulting in hypophosphorylated phospholamban.
7 ion of L-type calcium channel (Ca(v)1.2) and phospholamban.
8 er with reduced serine-16 phosphorylation of phospholamban.
9  reduced NO production, and dephosphorylated phospholamban.
10 t phosphorylation of ryanodine receptors and phospholamban.
11 eta(2)ARs under agonist stimulation, but not phospholamban.
12 the pentamer as the most stable oligomer for phospholamban.
13 nt with a decrease in the phosphorylation of phospholamban.
14 ned by a higher degree of phosphorylation of phospholamban.
15 -Ab) that binds to the cytoplasmic domain of phospholamban.
16 epressed levels of SERCA2 and phosphorylated phospholamban.
17 g proteins, including ryanodine receptor and phospholamban.
18 ch by characterising the pentameric state of phospholamban, a key player in the regulation of calcium
19                 Activated Akt phosphorylates phospholamban, a process that does not require beta-adre
20 G myocytes had changes in LTCC, SERCA2a, and phospholamban abundance, which appear to be adaptations
21 tein phosphatase-1 activity, thus modulating phospholamban activity and secondarily, the sarcoplasmic
22  NKA function in a manner similar to the way phospholamban affects the related SR Ca-ATPase (inhibiti
23                             We observed that phospholamban altered ATP-dependent calcium translocatio
24             Similarly, selective mutation of phospholamban amino acids critical for enhancing SR Ca(2
25 1 (I-1), a direct calcineurin substrate, and phospholamban, an indirect target, oscillated directly o
26 hain were reduced in hypothyroidism, whereas phospholamban and beta-myosin heavy chain were increased
27 protein S-nitrosylation, in general, and for phospholamban and cardiac troponin C S-nitrosylation, in
28  cardiac Ca(2+)-handling proteins, including phospholamban and cardiac troponin C, thereby playing an
29 isoproterenol-induced PKA phosphorylation of phospholamban and contractile responses in myocytes.
30 pha (PKCalpha) can both lower phosphorylated phospholamban and depress myocyte calcium cycling.
31 ion was maintained, whereas, oscillations in phospholamban and I-1 phosphorylation were lost.
32 arcoplasmic reticulum for phosphorylation of phospholamban and increases in myocyte contraction.
33  inhibitor-1, promoting dephosphorylation of phospholamban and inhibition of the sarcoplasmic reticul
34 n blot analysis showed an induction of total phospholamban and its phosphorylated form in inguinal fa
35 ding insights into the physiological role of phospholamban and its regulatory effect on SERCA transpo
36 balance and spontaneous SR Ca2+ cycling, ie, phospholamban and L-type Ca2+ channels (and likely other
37 tiple modes of interaction between SERCA and phospholamban and observed that once a particular mode o
38 tudies revealed increased phosphorylation of phospholamban and p70S6K.
39 nificantly attenuates PKA phosphorylation of phospholamban and rapidly reduces contraction rate incre
40 ectedly decreased protein kinase A-dependent phospholamban and ryanodine receptor 2 phosphorylation (
41                           Phosphorylation of phospholamban and ryanodine receptor was significantly i
42 e present study, we evaluated the effects of phospholamban and sarcolipin on calcium translocation an
43                                 However, how phospholamban and sarcolipin regulate SERCA is not fully
44 ice demonstrated no changes in expression of phospholamban and sarcoplasmic reticulum Ca(2+) ATPase,
45 ced CaMKIIdelta-dependent phosphorylation of phospholamban and the ryanodine receptor 2.
46 ted validated PKA and CaMKII target sites on phospholamban and the ryanodine receptor using genetical
47 s that regulate Ca(2+) handling in myocytes, phospholamban and the voltage-dependent L-type Ca(2+) ch
48  the SR appear to be due to STIM1 binding to phospholamban and thereby indirectly activating SERCA2a
49 acid further enhances the phosphorylation of phospholamban and TnI as well as contraction responses i
50  key role in limiting PKA phosphorylation of phospholamban and TnI for myocyte contraction responses
51 ation, yields maximal PKA phosphorylation of phospholamban and TnI, and myocyte contraction responses
52 ufficient for maximal PKA phosphorylation of phospholamban and TnI.
53 o a small increase in PKA phosphorylation of phospholamban and troponin I (TnI), and contraction resp
54 monstrated by decrease in phosphorylation of phospholamban and troponin I after beta-adrenergic stimu
55 ion and diffusion for PKA phosphorylation of phospholamban and troponin I, and for myocyte contractio
56 eptor complex but not for phosphorylation of phospholamban and troponin I.
57 reticulum Ca(2+) ATPase, increased levels of phospholamban and troponin T phosphorylation, and reduce
58 of extracellular signal-regulated kinase and phospholamban), and contraction.
59 activities at the SR, PKA phosphorylation of phospholamban, and contractile responses in PGE2-pretrea
60  other Ca2+ handling proteins, in particular phospholamban, and its phosphorylation status.
61         Increased phosphorylation of CaMKII, phospholamban, and ryanodine receptor 2 was detected in
62 oplasmic endoplasmic reticulum Ca(2+)ATPase, phospholamban, and ryanodine receptor proteins, as well
63 osin heavy chain, atrial natriuretic factor, phospholamban, and sarcoplasmic reticulum Ca2+-ATPase.
64 )-handling proteins (L-type Ca(2+) channels, phospholamban, and sarcoplasmic/endoplasmic reticulum ca
65 r2808 in ryanodine receptor type-2, Ser16 in phospholamban, and Ser23/24 in troponin-I were hyperphos
66 nalysis showed reduced levels of calmodulin, phospholamban, and SERCA2.
67 c markers alpha-actinin, myosin heavy chain, phospholamban, and tropomyosin was not observed at 2 wee
68  activities, promotes PKA phosphorylation of phospholamban, and ultimately enhances myocyte contracti
69 ulum calcium pump (SERCA) and its regulator, phospholamban, are essential components of cardiac contr
70  insight into how four hereditary mutants of phospholamban, Arg(9) to Cys, Arg(9) to Leu, Arg(9) to H
71 ition, the ISO-stimulated phosphorylation of phospholamban at Ser(16) was reduced by 27% in TG hearts
72 hosphorylation of other PKA targets, such as phospholamban at Ser16, phospholemman at Ser68 and cardi
73 rotein kinase A-dependent phosphorylation of phospholamban at Ser16.
74 ta(C) expression, whereas phosphorylation of phospholamban at Thr17, an endogenous indicator of CaMKI
75 se activity (p < 0.0004), phosphorylation of phospholamban (at Ser16 site; p = 0.04) and cardiac trop
76 culum Ca(2+)ATPase showed no recovery, while phospholamban, beta-adrenergic receptor, and the inotrop
77 chieved through increased phosphorylation of phospholamban by protein kinase A and relief of sarco/en
78 e calcium channel, sodium-calcium exchanger, phospholamban, calcineurin, and calcium/calmodulin-depen
79              Our results also indicated that phospholamban can establish an inhibitory interaction wi
80 doplasmic reticulum Ca2+ ATPase 2a (SERCA2a)/phospholamban complex contribute to heart failure.
81                  Notably, S-nitrosylation of phospholamban consequent upon betaAR stimulation is nece
82            We conclude that STIM1 binding to phospholamban contributes to the regulation of SERCA2a a
83                                              Phospholamban deficiency rescued SR Ca(2+) content and S
84 uble-null mice also was partially rescued by phospholamban deletion.
85 ill-based experiments, we have characterized phospholamban dynamics in the micros-ms timescale.
86 ted that adenylyl cyclase VI reduces cardiac phospholamban expression.
87 ent with a role for PLM analogous to that of phospholamban for SR Ca-ATPase (SERCA): inhibition of Na
88    We demonstrate that the role of Arg(9) in phospholamban function is multifaceted: it is important
89 mine the phenotypic spectrum associated with phospholamban gene (PLN) mutations.
90  sarcoplasmic reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine recepto
91 ates with both SR calcium ATPase type 2a and phospholamban in a complex that also contains A-kinase a
92 mall transmembrane peptides, most notably by phospholamban in cardiac muscle and sarcolipin in skelet
93 al and cardiac SR are due to the presence of phospholamban in cardiac SR, and not due to isoform-depe
94 rol, P <0.05) and reduced phosphorylation of phospholamban in HF (Ser16, 30 +/- 10% and Thr17, 41 +/-
95 eduction in the extent of phosphorylation of phospholamban in the left ventricular myocardium of HF p
96 e of SR markers (calsequestrin, SERCA2a, and phospholamban) in pRHM, suggesting that the mitochondria
97  calcium ATPase SERCA, namely sarcolipin and phospholamban, in explicit lipid bilayers.
98                                              Phospholamban is a 52-amino acid membrane protein that r
99                   These results suggest that phospholamban is an important component of the mechanism
100                     The internal dynamics of phospholamban is characterized by large amplitude collec
101 tional sampling of monomeric, membrane-bound phospholamban is described from computer simulations.
102                 SERCA2a is downregulated and phospholamban is hypophosphorylated in failing hearts, r
103  in saponin-permeabilized wild type (WT) and phospholamban knockout (PLB-KO) mouse ventricular myocyt
104 ent protein kinase (CaMKII) in permeabilized phospholamban knockout (PLN-KO) mouse myocytes phosphory
105 activity was also constitutively elevated in phospholamban-knockout antrum smooth muscle cells relati
106            The resting membrane potential of phospholamban-knockout antrum smooth muscle cells was hy
107 sence of SNP, STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells was in
108 in, inhibited STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells.
109 wave activity was significantly increased in phospholamban-knockout antrum smooth muscles compared to
110 smooth muscle cells to a greater extent than phospholamban-knockout antrum smooth muscles.
111 cells, but had no effect on STOC activity in phospholamban-knockout cells.
112 cells, but had no effect on STOC activity of phospholamban-knockout cells.
113 evated intracellular Ca(2+) wave activity of phospholamban-knockout cells.
114 ntrum smooth muscle cells from wild-type and phospholamban-knockout mice.
115 mproved cardiac BH(4) stores, phosphorylated phospholamban levels, and diastolic dysfunction.
116 ted) had 3-fold higher SERCA2a and 40% lower phospholamban levels.
117                                              Phospholamban modulates contractility by inhibiting SERC
118 Mechanistically, HAX-1 promoted formation of phospholamban monomers, the active/inhibitory units of t
119 with this, mice expressing a superinhibitory phospholamban mutant had low SR Ca(2+) content and slow
120 states of SERCA, we found that the effect of phospholamban on SERCA depends on substrate preincubatio
121 ements, proteoliposomes containing SERCA and phospholamban or sarcolipin were adsorbed to a solid-sup
122 handling proteins was not (calsequestrin and phospholamban) or was minimally (SERCA) affected.
123 n phosphorylation of troponin I, troponin T, phospholamban, or myosin light chain-1 or -2.
124 hosphorylation of cardiac troponin I (cTnI), phospholamban, or ryanodine receptor (RyR2).
125 rdiac ankyrin repeat protein (p < 0.01), and phospholamban (p < 0.05).
126 cular complexes of SR calcium ATPase type 2a-phospholamban-PDE3A.
127 edicted by a computer molecular model of the phospholamban pentamer constructed from NMR solution str
128 n kinase A recognition in the context of the phospholamban pentamer.
129 h increases in cAMP generation (P = 0.0002), phospholamban phosphorylation (P < 0.04), sarcoplasmic r
130               cAMP levels, PDE activity, and phospholamban phosphorylation (pPLB) were determined in
131 ibitor-1 results in selective enhancement of phospholamban phosphorylation and augmented cardiac cont
132 ctile function, associated with preferential phospholamban phosphorylation and enhanced sarcoplasmic
133                       I-1 knockout mice lack phospholamban phosphorylation and exhibit vascular smoot
134 s likely through reduced apoptosis, enhanced phospholamban phosphorylation and improved Akt/mTOR/p70S
135  kinase A recognition motif, which abrogates phospholamban phosphorylation and results in constitutiv
136 eased ryanodine receptor phosphorylation and phospholamban phosphorylation at both the Ser16 and Thr1
137 sed expression of protein kinase A-dependent phospholamban phosphorylation at Ser16 and CaMKII (Ca(2+
138 ](i) decline (by 28%; n=12, all P<0.05), and phospholamban phosphorylation at Ser16, but Ca current w
139 RCA2a) protein expression and an increase in phospholamban phosphorylation at serine 16, similar to h
140 dulin-dependent protein kinase II)-dependent phospholamban phosphorylation at Thr17.
141                                              Phospholamban phosphorylation by protein kinase A (PKA)
142 i/o inhibitor pertussis toxin normalized the phospholamban phosphorylation by protein kinase A, rever
143 basal PKA activity, indexed by gradations in phospholamban phosphorylation effected by a specific PKA
144             Elevated Nox2 activity increased phospholamban phosphorylation in both hearts and cardiom
145 ype 2a activity, SR Ca(2+) uptake rates, and phospholamban phosphorylation in SR fractions.
146     Cyclopiazonic acid and graded changes in phospholamban phosphorylation produced by beta-adrenergi
147                                 In addition, phospholamban phosphorylation was reduced (P=0.015), sar
148                                        Total phospholamban phosphorylation was unaltered, although it
149 ed cAMP-mediated, protein kinase A-dependent phospholamban phosphorylation, and increased SANC firing
150  blot analysis showed a fourfold increase in phospholamban phosphorylation, and PKA activity increase
151 s highly expressed, leading to a decrease in phospholamban phosphorylation, sarco/endoplasmic reticul
152                         In parallel with the phospholamban phosphorylation, the decay kinetics of glo
153                            We speculate that phospholamban phosphorylation, through activation of Akt
154  leucine eliminate both SERCA inhibition and phospholamban phosphorylation, whereas an aromatic subst
155 tudies is how adenylyl cyclase VI influences phospholamban phosphorylation.
156 ects, and loss of protein kinase A-dependent phospholamban phosphorylation.
157 lude ancillary effects of CaMKII mediated by phospholamban phosphorylation.
158 es suggest that PLN-Ab mimics the effects of phospholamban phosphorylation.
159  function through redox-regulated changes in phospholamban phosphorylation.
160                                              Phospholamban (PLB) and phospholemman (PLM, also called
161 ATPase (SERCA) pump activity is modulated by phospholamban (PLB) and sarcolipin (SLN) in cardiac and
162  protein binding interactions between native phospholamban (PLB) and SERCA2a in sarcoplasmic reticulu
163 actions between the transmembrane domains of phospholamban (PLB) and the cardiac Ca2+ pump (SERCA2a)
164 or presence of the SERCA regulatory partner, phospholamban (PLB) and were unaltered by PLB phosphoryl
165 egulatory role of the C-terminal residues of phospholamban (PLB) in the membranes of living cells, we
166                         Here we test whether phospholamban (PLB) inhibition using a dominant-negative
167                                              Phospholamban (PLB) inhibits the activity of SERCA2a, th
168                                              Phospholamban (PLB) is a 52 amino acid membrane-endogeno
169                                              Phospholamban (PLB) is a 52-amino acid integral membrane
170                                              Phospholamban (PLB) is a pentameric transmembrane protei
171                                              Phospholamban (PLB) is a small transmembrane protein tha
172                                   Given that phospholamban (PLB) is robustly present in adult but poo
173 e measured in-gel fluorescence anisotropy of phospholamban (PLB) labeled with the biarsenical fluorop
174                         Three cross-linkable phospholamban (PLB) mutants of increasing inhibitory str
175                                              Phospholamban (PLB) oligomerization, quaternary structur
176                                              Phospholamban (PLB) or the sarcoplasmic reticulum Ca2+-A
177 oblot method to measure the mole fraction of phospholamban (PLB) phosphorylated at Ser16 (X(p)) in bi
178  We have studied the differential effects of phospholamban (PLB) phosphorylation states on the activi
179                                              Phospholamban (PLB) physically interacts with Ca(2+)-ATP
180                                              Phospholamban (PLB) plays a key role as a regulator of s
181 that the cAMP-responsive-like element in the phospholamban (PLB) promoter was critical for down-regul
182                                 Our model of phospholamban (PLB) regulation of the cardiac Ca(2+)-ATP
183 e kinetic assays to test the hypothesis that phospholamban (PLB) stabilizes the Ca-ATPase in the E2 i
184  loss-of-function mutants, L31A and L31C, of phospholamban (PLB) to bind to and inhibit the Ca(2+) pu
185        A naturally occurring R9C mutation of phospholamban (PLB) triggers cardiomyopathy and prematur
186 e, protein kinase A (PKA) phosphorylation of phospholamban (PLB) was decreased, whereas PKA phosphory
187 sites on the ryanodine receptor (RyR) and on phospholamban (PLB) were increased in CaMKIIdelta(C) TG.
188 e polypeptide chains and their modulation by phospholamban (PLB) were measured in native cardiac sarc
189 ct of phosphorylation on the interactions of phospholamban (PLB) with itself and its regulatory targe
190  performed molecular dynamics simulations of phospholamban (PLB), a 52-residue integral membrane prot
191 on and mutation on the cytoplasmic domain of phospholamban (PLB), a 52-residue protein that regulates
192     In cardiac muscle, SERCA is regulated by phospholamban (PLB), a small inhibitory phosphoprotein t
193 SERCA activity in muscle can be regulated by phospholamban (PLB), an affinity modulator, and sarcolip
194 oplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospholamban (PLB), and AKAP18 in a multiprotein signal
195 ) uptake adenosine triphosphatase (SERCA2a), phospholamban (PLB), and increased PLB phosphorylation (
196 al dynamics of an integral membrane protein, phospholamban (PLB), and thereby its functional inhibiti
197 evel of calsequestrin, Na+/Ca2+ exchanger or phospholamban (PLB), but with both RyR2 and PLB hyperpho
198  but is associated with dephosphorylation of phospholamban (PLB), decreased sarcoplasmic reticulum Ca
199 al dynamics of an integral membrane protein, phospholamban (PLB), in a lipid bilayer.
200 doplasmic reticulum Ca(2+)-ATPase (SERCA) by phospholamban (PLB), we expressed Cerulean-SERCA and yel
201 ATPase] and SERCA2a calcium pump isoforms by phospholamban (PLB), we quantified PLB-SERCA interaction
202 ce (EPR) to probe the functional dynamics of phospholamban (PLB), which regulates the Ca-ATPase (SERC
203 s cAMP- and PKA-dependent phosphorylation of phospholamban (PLB), which relieves the inhibitory effec
204 eticulum Ca-ATPase (SERCA) and its regulator phospholamban (PLB).
205 coplasmic reticulum Ca-ATPase (SERCA2a), and phospholamban (PLB).
206 erminal membrane-spanning helical domains of phospholamban (PLB).
207 culum Ca(2+)-ATPase (SERCA)) in complex with phospholamban (PLB).
208                                   Hence like phospholamban, PLM exists as a pump-inhibiting monomer a
209                         We hypothesized that phospholamban (PLN) ablation would restore SR Ca(2+) loa
210                                              Phospholamban (PLN) and sarcolipin (SLN) are two single-
211 es structural and functional similarity with phospholamban (PLN) and sarcolipin (SLN), which inhibit
212 ated by the small integral membrane proteins phospholamban (PLN) and sarcolipin (SLN).
213 on with the short integral membrane proteins phospholamban (PLN) and sarcolipin (SLN).
214 he integral membrane protein complex between phospholamban (PLN) and sarcoplasmic reticulum Ca(2+)-AT
215 um ATPase (SERCA) and its regulatory partner phospholamban (PLN) are essential for myocardial contrac
216 ith specific increases in phosphorylation of phospholamban (PLN) at both Ser16 and Thr17, relieving i
217 ated with decreased (50%) phosphorylation of phospholamban (PLN) at serine 16, whereas phosphorylatio
218 )plasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) complex regulates heart relaxation t
219 oplasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) controls Ca(2+) transport in cardiom
220       A mutation in the coding region of the phospholamban (PLN) gene (R14del) is identified in famil
221                             Mutations in the phospholamban (PLN) gene are associated with dilated car
222  14 (PLN-R14Del) in the coding region of the phospholamban (PLN) gene in a large family with heredita
223                    Ablation or inhibition of phospholamban (PLN) has favorable effects in several gen
224 ative roles of cardiac troponin I (cTnI) and phospholamban (PLN) in beta-adrenergic-mediated hastenin
225                                              Phospholamban (PLN) is a type II membrane protein that i
226                                              Phospholamban (PLN) is an effective inhibitor of the sar
227                                              Phospholamban (PLN) is an essential regulator of cardiac
228               A 52-residue membrane protein, phospholamban (PLN) is an inhibitor of an adenosine-5'-t
229                                              Phospholamban (PLN) is an inhibitor of cardiac sarco(end
230                                              Phospholamban (PLN) is an inhibitor of the Ca2+ affinity
231 rogression of LV disease was associated with phospholamban (PLN) mutation (OR, 8.8; 95% CI, 2.1-37.2;
232 decreased cardiac contractility with reduced phospholamban (PLN) phosphorylation at serine-16, the ma
233                                              Phospholamban (PLN) plays a central role in Ca(2+) homeo
234                                              Phospholamban (PLN) regulates calcium translocation with
235                                              Phospholamban (PLN) regulates cardiac contractility via
236                The regulatory interaction of phospholamban (PLN) with Ca(2+)-ATPase controls the upta
237               In cardiomyocytes, PKA targets phospholamban (PLN), a membrane protein that inhibits th
238 expression, phosphorylation, and function of phospholamban (PLN), a sarcoendoplasmic reticulum regula
239                                              Phospholamban (PLN), a single-pass membrane protein, reg
240 0% identity with the transmembrane domain of phospholamban (PLN), and recent solution NMR studies car
241                                        Human phospholamban (PLN), expressed in the sarcoplasmic retic
242 nd interacts with the small membrane protein phospholamban (PLN), inhibiting the cardiac sarco/endopl
243 nd Phd3 dramatically decreased expression of phospholamban (PLN), resulted in sustained activation of
244 hatase 1 modulate the inhibitory activity of phospholamban (PLN), the endogenous regulator of the sar
245 tion with SERCA2a or its regulatory protein, phospholamban (PLN), we measured its effects on SERCA2a
246 in complex formed by Ca2+-ATPase (SERCA) and phospholamban (PLN), which in humans is responsible for
247                                 We generated phospholamban (PLN)-deficient S2814D(+/+) knock-in mice
248                                 We generated phospholamban (PLN)-deficient/S2814D(+/+) knock-in mice
249 ), whose activity is reversibly regulated by phospholamban (PLN).
250 ing the L-type Ca(2+) channel (Ca(V)1.2) and phospholamban (PLN).
251 phorylation of cardiac troponin I (cTnI) and phospholamban (PLN).
252 ecreased CaMKII-dependent phosphorylation of phospholamban (PLN).
253 in a manner similar to that of its homologue phospholamban (PLN).
254                                              Phospholamban protein expression was reduced 50%, but th
255                               Although total phospholamban protein expression was unchanged, there wa
256 asmic endoplasmic reticular calcium ATPase 2/phospholamban protein ratio (45% reduced; P=0.03).
257 r sarcoplasmic reticulum Ca2+ ATPase pump to phospholamban protein ratio in SAN than in right atrium.
258                                  SERCA2a and phospholamban protein were unchanged in MR versus contro
259                                              Phospholamban R14del mutation carriers are at high risk
260 ee mortality ratio method in a cohort of 403 phospholamban R14del mutation carriers, we found a stand
261 gnant ventricular arrhythmias in a cohort of phospholamban R14del mutation carriers.
262                               The pathogenic phospholamban R14del mutation causes dilated and arrhyth
263                                    Much like phospholamban regulation of SERCA, phospholemman exists
264 speed of atrial contraction independently of phospholamban regulation.
265 e redundantly to phosphorylation not only of phospholamban, ryanodine receptor 2, and histone deacety
266                                  DHF reduced phospholamban, ryanodine receptor, and sarcoplasmic reti
267 e receptor 2 phosphorylation (-42+/-9% for P-phospholamban-S16 and -22+/-7% for P-ryanodine receptor
268 activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregulin.
269 12), which regulate Na(+) ,K(+) -ATPase, and phospholamban, sarcolipin, myoregulin and DWORF, which r
270 r, HAX-1 sequestered Hsp90 from IRE-1 to the phospholamban-sarcoplasmic/endoplasmic reticulum calcium
271 c hearts showed increased phosphorylation of phospholamban Ser-16 and Thr-17 compared with the alpha-
272 in SERCA2a expression and phosphorylation of phospholamban Ser-16.
273 he kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relax
274 estern blot analyses revealed decreases in p-phospholamban, SERCA2a, p-CX43, p-GSK-3alpha/beta, nucle
275 reticulum Ca(2+) leak/load relationship) and phospholamban Serine16 phosphorylation (Western blot).
276                               Phosphorylated phospholamban stabilizes a unique conformation of SERCA
277  way analogous to the regulation of SERCA by phospholamban-that is un-phosphorylated PLM exerts a ton
278      Earlier studies have shown that SLN and phospholamban, the other well studied small SERCA-regula
279                               In the case of phospholamban, the restrained ensemble sampled the confo
280  Agonist-evoked phosphorylation by CaMKII at phospholamban (Thr-17), but not of ryanodine2 (Ser-2814)
281  the ryanodine receptor (RyR2) (Ser2815) and phospholamban (Thr17) in a PKC-dependent manner.
282 acetylase 5 phosphorylation (Ser498) but not phospholamban (Thr17), whereas the converse holds for ca
283  memory in the interaction between SERCA and phospholamban, thus providing insights into the physiolo
284 ype Ca(2+) channels, ryanodine receptors and phospholamban to basal levels.
285 estration, since the ratio of phosphorylated phospholamban to total phospholamban was sharply reduced
286 s--glycophorin A, the M2 proton channel, and phospholamban--using only peptide sequence and the nativ
287 eased PKA phosphorylation of cTnI, RyR2, and phospholamban versus controls.
288                       The CaMKII target pT17-phospholamban was 5.5-fold increased only in sarcomere-m
289 sphorylation of the SERCA regulatory protein phospholamban was increased in cells cultured under 5% O
290 activation) of the SERCA2a-inhibitor protein phospholamban was increased in pAF.
291 earts of female mice, whereas phosphorylated phospholamban was increased.
292                  Although phosphorylation of phospholamban was not altered, miR-1 overexpression incr
293 tio of phosphorylated phospholamban to total phospholamban was sharply reduced in all three mutant he
294  PI3Kgamma(-/-) cardiomyocytes, Ca(v)1.2 and phospholamban were hyperphosphorylated, leading to incre
295 asmic endoplasmic reticulum Ca(2+)ATPase and phospholamban were normal in left ventricular hypertroph
296 essary for the inhibitory pentamerization of phospholamban, which activates sarcoplasmic reticulum Ca
297 HAX-1 were abolished upon phosphorylation of phospholamban, which plays a fundamental role in control
298                                    Much like phospholamban, which regulates the related ATPase SERCA,
299 ational design of a water-soluble variant of phospholamban, WSPLB, which reproduced many of the struc
300 ide chain and backbone dynamics of wild-type phospholamban (WT-PLB) and its phosphorylated form (P-PL

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