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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
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
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.
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
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 (
42 e present study, we evaluated the effects of phospholamban and sarcolipin on calcium translocation an
44 ice demonstrated no changes in expression of phospholamban and sarcoplasmic reticulum Ca(2+) ATPase,
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
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
57 reticulum Ca(2+) ATPase, increased levels of phospholamban and troponin T phosphorylation, and reduce
59 activities at the SR, PKA phosphorylation of phospholamban, and contractile responses in PGE2-pretrea
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
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
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
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
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
101 tional sampling of monomeric, membrane-bound phospholamban is described from computer simulations.
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
107 sence of SNP, STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells was in
109 wave activity was significantly increased in phospholamban-knockout antrum smooth muscles compared to
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
127 edicted by a computer molecular model of the phospholamban pentamer constructed from NMR solution str
129 h increases in cAMP generation (P = 0.0002), phospholamban phosphorylation (P < 0.04), sarcoplasmic r
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
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
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
146 Cyclopiazonic acid and graded changes in phospholamban phosphorylation produced by beta-adrenergi
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
154 leucine eliminate both SERCA inhibition and phospholamban phosphorylation, whereas an aromatic subst
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
173 e measured in-gel fluorescence anisotropy of phospholamban (PLB) labeled with the biarsenical fluorop
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
181 that the cAMP-responsive-like element in the phospholamban (PLB) promoter was critical for down-regul
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
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
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
211 es structural and functional similarity with phospholamban (PLN) and sarcolipin (SLN), which inhibit
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
222 14 (PLN-R14Del) in the coding region of the phospholamban (PLN) gene in a large family with heredita
224 ative roles of cardiac troponin I (cTnI) and phospholamban (PLN) in beta-adrenergic-mediated hastenin
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
238 expression, phosphorylation, and function of phospholamban (PLN), a sarcoendoplasmic reticulum regula
240 0% identity with the transmembrane domain of phospholamban (PLN), and recent solution NMR studies car
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
257 r sarcoplasmic reticulum Ca2+ ATPase pump to phospholamban protein ratio in SAN than in right atrium.
260 ee mortality ratio method in a cohort of 403 phospholamban R14del mutation carriers, we found a stand
265 e redundantly to phosphorylation not only of phospholamban, ryanodine receptor 2, and histone deacety
267 e receptor 2 phosphorylation (-42+/-9% for P-phospholamban-S16 and -22+/-7% for P-ryanodine receptor
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-
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).
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
280 Agonist-evoked phosphorylation by CaMKII at phospholamban (Thr-17), but not of ryanodine2 (Ser-2814)
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
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
289 sphorylation of the SERCA regulatory protein phospholamban was increased in cells cultured under 5% O
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
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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