ライフサイエンスコーパス: phospholamban

1 th coexpression of phosphomimetic mutants of phospholamban.

2 ructural determinants of SERCA regulation by phospholamban.

3 regulation via the phosphorylation status of phospholamban.

4 drenergic stimulation and phosphorylation of phospholamban.

5 diesterase 4 resulting in hypophosphorylated phospholamban.

6 ion of L-type calcium channel (Ca(v)1.2) and phospholamban.

7 er with reduced serine-16 phosphorylation of phospholamban.

8 reduced NO production, and dephosphorylated phospholamban.

9 t phosphorylation of ryanodine receptors and phospholamban.

10 eta(2)ARs under agonist stimulation, but not phospholamban.

11 the pentamer as the most stable oligomer for phospholamban.

12 nt with a decrease in the phosphorylation of phospholamban.

13 a, protein kinase Cepsilon, calcineurin, and phospholamban.

14 epressed levels of SERCA2 and phosphorylated phospholamban.

15 g proteins, including ryanodine receptor and phospholamban.

16 ch by characterising the pentameric state of phospholamban, a key player in the regulation of calcium

17 Activated Akt phosphorylates phospholamban, a process that does not require beta-adre

18 fficiency was rescued by a decreased dose of phospholamban, a sarco/endoplasmic reticulum Ca2+-ATPase

19 G myocytes had changes in LTCC, SERCA2a, and phospholamban abundance, which appear to be adaptations

20 tein phosphatase-1 activity, thus modulating phospholamban activity and secondarily, the sarcoplasmic

21 NKA function in a manner similar to the way phospholamban affects the related SR Ca-ATPase (inhibiti

22 We observed that phospholamban altered ATP-dependent calcium translocatio

23 Similarly, selective mutation of phospholamban amino acids critical for enhancing SR Ca(2

24 1 (I-1), a direct calcineurin substrate, and phospholamban, an indirect target, oscillated directly o

25 protein S-nitrosylation, in general, and for phospholamban and cardiac troponin C S-nitrosylation, in

26 cardiac Ca(2+)-handling proteins, including phospholamban and cardiac troponin C, thereby playing an

27 isoproterenol-induced PKA phosphorylation of phospholamban and contractile responses in myocytes.

28 pha (PKCalpha) can both lower phosphorylated phospholamban and depress myocyte calcium cycling.

29 ion was maintained, whereas, oscillations in phospholamban and I-1 phosphorylation were lost.

30 arcoplasmic reticulum for phosphorylation of phospholamban and increases in myocyte contraction.

31 inhibitor-1, promoting dephosphorylation of phospholamban and inhibition of the sarcoplasmic reticul

32 n blot analysis showed an induction of total phospholamban and its phosphorylated form in inguinal fa

33 ding insights into the physiological role of phospholamban and its regulatory effect on SERCA transpo

34 balance and spontaneous SR Ca2+ cycling, ie, phospholamban and L-type Ca2+ channels (and likely other

35 tiple modes of interaction between SERCA and phospholamban and observed that once a particular mode o

36 tudies revealed increased phosphorylation of phospholamban and p70S6K.

37 nificantly attenuates PKA phosphorylation of phospholamban and rapidly reduces contraction rate incre

38 Through simulation of the natural protein phospholamban and redesign of variants, we define a ster

39 ectedly decreased protein kinase A-dependent phospholamban and ryanodine receptor 2 phosphorylation (

40 Phosphorylation of phospholamban and ryanodine receptor was significantly i

41 e present study, we evaluated the effects of phospholamban and sarcolipin on calcium translocation an

42 However, how phospholamban and sarcolipin regulate SERCA is not fully

43 ice demonstrated no changes in expression of phospholamban and sarcoplasmic reticulum Ca(2+) ATPase,

44 ced CaMKIIdelta-dependent phosphorylation of phospholamban and the ryanodine receptor 2.

45 ted validated PKA and CaMKII target sites on phospholamban and the ryanodine receptor using genetical

46 s that regulate Ca(2+) handling in myocytes, phospholamban and the voltage-dependent L-type Ca(2+) ch

47 the SR appear to be due to STIM1 binding to phospholamban and thereby indirectly activating SERCA2a

48 acid further enhances the phosphorylation of phospholamban and TnI as well as contraction responses i

49 key role in limiting PKA phosphorylation of phospholamban and TnI for myocyte contraction responses

50 ation, yields maximal PKA phosphorylation of phospholamban and TnI, and myocyte contraction responses

51 ufficient for maximal PKA phosphorylation of phospholamban and TnI.

52 o a small increase in PKA phosphorylation of phospholamban and troponin I (TnI), and contraction resp

53 monstrated by decrease in phosphorylation of phospholamban and troponin I after beta-adrenergic stimu

54 ion and diffusion for PKA phosphorylation of phospholamban and troponin I, and for myocyte contractio

55 eptor complex but not for phosphorylation of phospholamban and troponin I.

56 reticulum Ca(2+) ATPase, increased levels of phospholamban and troponin T phosphorylation, and reduce

57 of extracellular signal-regulated kinase and phospholamban), and contraction.

58 activities at the SR, PKA phosphorylation of phospholamban, and contractile responses in PGE2-pretrea

59 other Ca2+ handling proteins, in particular phospholamban, and its phosphorylation status.

60 Increased phosphorylation of CaMKII, phospholamban, and ryanodine receptor 2 was detected in

61 oplasmic endoplasmic reticulum Ca(2+)ATPase, phospholamban, and ryanodine receptor proteins, as well

62 )-handling proteins (L-type Ca(2+) channels, phospholamban, and sarcoplasmic/endoplasmic reticulum ca

63 r2808 in ryanodine receptor type-2, Ser16 in phospholamban, and Ser23/24 in troponin-I were hyperphos

64 nalysis showed reduced levels of calmodulin, phospholamban, and SERCA2.

65 activities, promotes PKA phosphorylation of phospholamban, and ultimately enhances myocyte contracti

66 ulum calcium pump (SERCA) and its regulator, phospholamban, are essential components of cardiac contr

67 insight into how four hereditary mutants of phospholamban, Arg(9) to Cys, Arg(9) to Leu, Arg(9) to H

68 ition, the ISO-stimulated phosphorylation of phospholamban at Ser(16) was reduced by 27% in TG hearts

69 hosphorylation of other PKA targets, such as phospholamban at Ser16, phospholemman at Ser68 and cardi

70 rotein kinase A-dependent phosphorylation of phospholamban at Ser16.

71 ta(C) expression, whereas phosphorylation of phospholamban at Thr17, an endogenous indicator of CaMKI

72 se activity (p < 0.0004), phosphorylation of phospholamban (at Ser16 site; p = 0.04) and cardiac trop

73 culum Ca(2+)ATPase showed no recovery, while phospholamban, beta-adrenergic receptor, and the inotrop

74 chieved through increased phosphorylation of phospholamban by protein kinase A and relief of sarco/en

75 e calcium channel, sodium-calcium exchanger, phospholamban, calcineurin, and calcium/calmodulin-depen

76 Our results also indicated that phospholamban can establish an inhibitory interaction wi

77 doplasmic reticulum Ca2+ ATPase 2a (SERCA2a)/phospholamban complex contribute to heart failure.

78 Notably, S-nitrosylation of phospholamban consequent upon betaAR stimulation is nece

79 We conclude that STIM1 binding to phospholamban contributes to the regulation of SERCA2a a

80 Phospholamban deficiency rescued SR Ca(2+) content and S

81 uble-null mice also was partially rescued by phospholamban deletion.

82 ve further validated alpha-actinin isoforms, phospholamban, dystrophin, alphaB-crystallin, and calseq

83 de, and [Ca(2+)] decline rates, with reduced phospholamban expression, all of which were most promine

84 ted that adenylyl cyclase VI reduces cardiac phospholamban expression.

85 ent with a role for PLM analogous to that of phospholamban for SR Ca-ATPase (SERCA): inhibition of Na

86 University of Cincinnati), and Roger Hajjar (Phospholamban Foundation), who have had a long-standing

87 We demonstrate that the role of Arg(9) in phospholamban function is multifaceted: it is important

88 mine the phenotypic spectrum associated with phospholamban gene (PLN) mutations.

89 sarcoplasmic reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine recepto

90 gnaling activation and CaMKII-dependent RyR2/phospholamban hyperphosphorylation in an immortalized mo

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 rol, P <0.05) and reduced phosphorylation of phospholamban in HF (Ser16, 30 +/- 10% and Thr17, 41 +/-

94 eduction in the extent of phosphorylation of phospholamban in the left ventricular myocardium of HF p

95 e of SR markers (calsequestrin, SERCA2a, and phospholamban) in pRHM, suggesting that the mitochondria

96 calcium ATPase SERCA, namely sarcolipin and phospholamban, in explicit lipid bilayers.

97 Because STIM1 binding to phospholamban increases sarcoplasmic reticulum Ca(2+) lo

98 Phospholamban is a small phosphoprotein in the cardiac s

99 These results suggest that phospholamban is an important component of the mechanism

100 tional sampling of monomeric, membrane-bound phospholamban is described from computer simulations.

101 SERCA2a is downregulated and phospholamban is hypophosphorylated in failing hearts, r

102 in saponin-permeabilized wild type (WT) and phospholamban knockout (PLB-KO) mouse ventricular myocyt

103 ent protein kinase (CaMKII) in permeabilized phospholamban knockout (PLN-KO) mouse myocytes phosphory

104 activity was also constitutively elevated in phospholamban-knockout antrum smooth muscle cells relati

105 The resting membrane potential of phospholamban-knockout antrum smooth muscle cells was hy

106 sence of SNP, STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells was in

107 in, inhibited STOC activity in wild-type and phospholamban-knockout antrum smooth muscle cells.

108 wave activity was significantly increased in phospholamban-knockout antrum smooth muscles compared to

109 smooth muscle cells to a greater extent than phospholamban-knockout antrum smooth muscles.

110 cells, but had no effect on STOC activity in phospholamban-knockout cells.

111 cells, but had no effect on STOC activity of phospholamban-knockout cells.

112 evated intracellular Ca(2+) wave activity of phospholamban-knockout cells.

113 ntrum smooth muscle cells from wild-type and phospholamban-knockout mice.

114 mproved cardiac BH(4) stores, phosphorylated phospholamban levels, and diastolic dysfunction.

115 ted) had 3-fold higher SERCA2a and 40% lower phospholamban levels.

116 Phospholamban modulates contractility by inhibiting SERC

117 Mechanistically, HAX-1 promoted formation of phospholamban monomers, the active/inhibitory units of t

118 with this, mice expressing a superinhibitory phospholamban mutant had low SR Ca(2+) content and slow

119 states of SERCA, we found that the effect of phospholamban on SERCA depends on substrate preincubatio

120 ements, proteoliposomes containing SERCA and phospholamban or sarcolipin were adsorbed to a solid-sup

121 handling proteins was not (calsequestrin and phospholamban) or was minimally (SERCA) affected.

122 n phosphorylation of troponin I, troponin T, phospholamban, or myosin light chain-1 or -2.

123 hosphorylation of cardiac troponin I (cTnI), phospholamban, or ryanodine receptor (RyR2).

124 ion of fibronectin, smooth muscle actin, and phospholamban (p < 0.001).

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 sed expression of protein kinase A-dependent phospholamban phosphorylation at Ser16 and CaMKII (Ca(2+

137 ](i) decline (by 28%; n=12, all P<0.05), and phospholamban phosphorylation at Ser16, but Ca current w

138 RCA2a) protein expression and an increase in phospholamban phosphorylation at serine 16, similar to h

139 dulin-dependent protein kinase II)-dependent phospholamban phosphorylation at Thr17.

140 Phospholamban phosphorylation by protein kinase A (PKA)

141 i/o inhibitor pertussis toxin normalized the phospholamban phosphorylation by protein kinase A, rever

142 basal PKA activity, indexed by gradations in phospholamban phosphorylation effected by a specific PKA

143 Elevated Nox2 activity increased phospholamban phosphorylation in both hearts and cardiom

144 ype 2a activity, SR Ca(2+) uptake rates, and phospholamban phosphorylation in SR fractions.

145 Cyclopiazonic acid and graded changes in phospholamban phosphorylation produced by beta-adrenergi

146 n and adrenergic responsiveness by enhancing phospholamban phosphorylation via protein kinase A.

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 function through redox-regulated changes in phospholamban phosphorylation.

159 ATPase (SERCA) pump activity is modulated by phospholamban (PLB) and sarcolipin (SLN) in cardiac and

160 that of known regulators of SERCA activity, phospholamban (PLB) and sarcolipin (SLN).

161 protein binding interactions between native phospholamban (PLB) and SERCA2a in sarcoplasmic reticulu

162 actions between the transmembrane domains of phospholamban (PLB) and the cardiac Ca2+ pump (SERCA2a)

163 or presence of the SERCA regulatory partner, phospholamban (PLB) and were unaltered by PLB phosphoryl

164 mic reticulum (SR) Ca(2+)-ATPase (SERCA) and phospholamban (PLB) are essential for intracellular Ca(2

165 egulatory role of the C-terminal residues of phospholamban (PLB) in the membranes of living cells, we

166 Phospholamban (PLB) inhibits the activity of SERCA2a, th

167 Phospholamban (PLB) is a 52-amino acid integral membrane

168 Phospholamban (PLB) is a pentameric transmembrane protei

169 Phospholamban (PLB) is a small transmembrane protein tha

170 Given that phospholamban (PLB) is robustly present in adult but poo

171 e measured in-gel fluorescence anisotropy of phospholamban (PLB) labeled with the biarsenical fluorop

172 Three cross-linkable phospholamban (PLB) mutants of increasing inhibitory str

173 Phospholamban (PLB) oligomerization, quaternary structur

174 Phospholamban (PLB) or the sarcoplasmic reticulum Ca2+-A

175 oblot method to measure the mole fraction of phospholamban (PLB) phosphorylated at Ser16 (X(p)) in bi

176 We have studied the differential effects of phospholamban (PLB) phosphorylation states on the activi

177 SERCA) Ca2+ reuptake, modulated by increased phospholamban (PLB) phosphorylation, and the decreased t

178 Phospholamban (PLB) physically interacts with Ca(2+)-ATP

179 Phospholamban (PLB) plays a key role as a regulator of s

180 Our model of phospholamban (PLB) regulation of the cardiac Ca(2+)-ATP

181 e kinetic assays to test the hypothesis that phospholamban (PLB) stabilizes the Ca-ATPase in the E2 i

182 loss-of-function mutants, L31A and L31C, of phospholamban (PLB) to bind to and inhibit the Ca(2+) pu

183 A naturally occurring R9C mutation of phospholamban (PLB) triggers cardiomyopathy and prematur

184 e, protein kinase A (PKA) phosphorylation of phospholamban (PLB) was decreased, whereas PKA phosphory

185 sites on the ryanodine receptor (RyR) and on phospholamban (PLB) were increased in CaMKIIdelta(C) TG.

186 e polypeptide chains and their modulation by phospholamban (PLB) were measured in native cardiac sarc

187 ct of phosphorylation on the interactions of phospholamban (PLB) with itself and its regulatory targe

188 performed molecular dynamics simulations of phospholamban (PLB), a 52-residue integral membrane prot

189 on and mutation on the cytoplasmic domain of phospholamban (PLB), a 52-residue protein that regulates

190 In cardiac muscle, SERCA is regulated by phospholamban (PLB), a small inhibitory phosphoprotein t

191 SERCA activity in muscle can be regulated by phospholamban (PLB), an affinity modulator, and sarcolip

192 oplasmic reticulum Ca(2+) ATPase 2 (SERCA2), phospholamban (PLB), and AKAP18 in a multiprotein signal

193 ) uptake adenosine triphosphatase (SERCA2a), phospholamban (PLB), and increased PLB phosphorylation (

194 al dynamics of an integral membrane protein, phospholamban (PLB), and thereby its functional inhibiti

195 al dynamics of an integral membrane protein, phospholamban (PLB), in a lipid bilayer.

196 doplasmic reticulum Ca(2+)-ATPase (SERCA) by phospholamban (PLB), we expressed Cerulean-SERCA and yel

197 ATPase] and SERCA2a calcium pump isoforms by phospholamban (PLB), we quantified PLB-SERCA interaction

198 ce (EPR) to probe the functional dynamics of phospholamban (PLB), which regulates the Ca-ATPase (SERC

199 s cAMP- and PKA-dependent phosphorylation of phospholamban (PLB), which relieves the inhibitory effec

200 eticulum Ca-ATPase (SERCA) and its regulator phospholamban (PLB).

201 coplasmic reticulum Ca-ATPase (SERCA2a), and phospholamban (PLB).

202 erminal membrane-spanning helical domains of phospholamban (PLB).

203 ry interaction with a transmembrane peptide, phospholamban (PLB).

204 culum Ca(2+)-ATPase (SERCA)) in complex with phospholamban (PLB).

205 Hence like phospholamban, PLM exists as a pump-inhibiting monomer a

206 We hypothesized that phospholamban (PLN) ablation would restore SR Ca(2+) loa

207 Phospholamban (PLN) and sarcolipin (SLN) are two single-

208 es structural and functional similarity with phospholamban (PLN) and sarcolipin (SLN), which inhibit

209 protein subunits, the most well-known being phospholamban (PLN) and sarcolipin (SLN).

210 on with the short integral membrane proteins phospholamban (PLN) and sarcolipin (SLN).

211 ated by the small integral membrane proteins phospholamban (PLN) and sarcolipin (SLN).

212 he integral membrane protein complex between phospholamban (PLN) and sarcoplasmic reticulum Ca(2+)-AT

213 um ATPase (SERCA) and its regulatory partner phospholamban (PLN) are essential for myocardial contrac

214 ith specific increases in phosphorylation of phospholamban (PLN) at both Ser16 and Thr17, relieving i

215 ated with decreased (50%) phosphorylation of phospholamban (PLN) at serine 16, whereas phosphorylatio

216 )plasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) complex regulates heart relaxation t

217 oplasmic reticulum Ca(2+)-ATPase (SERCA) and phospholamban (PLN) controls Ca(2+) transport in cardiom

218 A mutation in the coding region of the phospholamban (PLN) gene (R14del) is identified in famil

219 Mutations in the phospholamban (PLN) gene are associated with dilated car

220 14 (PLN-R14Del) in the coding region of the phospholamban (PLN) gene in a large family with heredita

221 ative roles of cardiac troponin I (cTnI) and phospholamban (PLN) in beta-adrenergic-mediated hastenin

222 Phospholamban (PLN) is a type II membrane protein that i

223 Phospholamban (PLN) is an effective inhibitor of the sar

224 Phospholamban (PLN) is an essential regulator of cardiac

225 A 52-residue membrane protein, phospholamban (PLN) is an inhibitor of an adenosine-5'-t

226 Phospholamban (PLN) is an inhibitor of cardiac sarco(end

227 Phospholamban (PLN) is an inhibitor of the Ca2+ affinity

228 The cardiac membrane protein phospholamban (PLN) is targeted by protein kinase A (PKA

229 rogression of LV disease was associated with phospholamban (PLN) mutation (OR, 8.8; 95% CI, 2.1-37.2;

230 decreased cardiac contractility with reduced phospholamban (PLN) phosphorylation at serine-16, the ma

231 Phospholamban (PLN) plays a central role in Ca(2+) homeo

232 Phospholamban (PLN) regulates calcium translocation with

233 The regulatory interaction of phospholamban (PLN) with Ca(2+)-ATPase controls the upta

234 The interaction of phospholamban (PLN) with the sarco-endoplasmic reticulum

235 In cardiomyocytes, PKA targets phospholamban (PLN), a membrane protein that inhibits th

236 expression, phosphorylation, and function of phospholamban (PLN), a sarcoendoplasmic reticulum regula

237 Phospholamban (PLN), a single-pass membrane protein, reg

238 0% identity with the transmembrane domain of phospholamban (PLN), and recent solution NMR studies car

239 ng, the type-2 ryanodine receptor (RyR2) and phospholamban (PLN), enhances the susceptibility to AF,

240 nd interacts with the small membrane protein phospholamban (PLN), inhibiting the cardiac sarco/endopl

241 nd Phd3 dramatically decreased expression of phospholamban (PLN), resulted in sustained activation of

242 hatase 1 modulate the inhibitory activity of phospholamban (PLN), the endogenous regulator of the sar

243 tion with SERCA2a or its regulatory protein, phospholamban (PLN), we measured its effects on SERCA2a

244 in complex formed by Ca2+-ATPase (SERCA) and phospholamban (PLN), which in humans is responsible for

245 We generated phospholamban (PLN)-deficient S2814D(+/+) knock-in mice

246 We generated phospholamban (PLN)-deficient/S2814D(+/+) knock-in mice

247 tic Network of Excellence consortium to cure Phospholamban (PLN)-induced cardiomyopathy (CURE-PLaN) u

248 ), whose activity is reversibly regulated by phospholamban (PLN).

249 ing the L-type Ca(2+) channel (Ca(V)1.2) and phospholamban (PLN).

250 ecreased CaMKII-dependent phosphorylation of phospholamban (PLN).

251 in a manner similar to that of its homologue phospholamban (PLN).

252 phorylation of cardiac troponin I (cTnI) and phospholamban (PLN).

253 Although total phospholamban protein expression was unchanged, there wa

254 asmic endoplasmic reticular calcium ATPase 2/phospholamban protein ratio (45% reduced; P=0.03).

255 r sarcoplasmic reticulum Ca2+ ATPase pump to phospholamban protein ratio in SAN than in right atrium.

256 SERCA2a and phospholamban protein were unchanged in MR versus contro

257 Phospholamban R14del mutation carriers are at high risk

258 ee mortality ratio method in a cohort of 403 phospholamban R14del mutation carriers, we found a stand

259 gnant ventricular arrhythmias in a cohort of phospholamban R14del mutation carriers.

260 The pathogenic phospholamban R14del mutation causes dilated and arrhyth

261 Much like phospholamban regulation of SERCA, phospholemman exists

262 speed of atrial contraction independently of phospholamban regulation.

263 AF caused by TBX5 deficiency were rescued by phospholamban removal, which normalized SERCA function.

264 e redundantly to phosphorylation not only of phospholamban, ryanodine receptor 2, and histone deacety

265 DHF reduced phospholamban, ryanodine receptor, and sarcoplasmic reti

266 e receptor 2 phosphorylation (-42+/-9% for P-phospholamban-S16 and -22+/-7% for P-ryanodine receptor

267 activity by displacing the SERCA inhibitors, phospholamban, sarcolipin, and myoregulin.

268 12), which regulate Na(+) ,K(+) -ATPase, and phospholamban, sarcolipin, myoregulin and DWORF, which r

269 r, HAX-1 sequestered Hsp90 from IRE-1 to the phospholamban-sarcoplasmic/endoplasmic reticulum calcium

270 c hearts showed increased phosphorylation of phospholamban Ser-16 and Thr-17 compared with the alpha-

271 in SERCA2a expression and phosphorylation of phospholamban Ser-16.

272 he kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relax

273 estern blot analyses revealed decreases in p-phospholamban, SERCA2a, p-CX43, p-GSK-3alpha/beta, nucle

274 reticulum Ca(2+) leak/load relationship) and phospholamban Serine16 phosphorylation (Western blot).

275 Phosphorylated phospholamban stabilizes a unique conformation of SERCA

276 way analogous to the regulation of SERCA by phospholamban-that is un-phosphorylated PLM exerts a ton

277 Earlier studies have shown that SLN and phospholamban, the other well studied small SERCA-regula

278 In the case of phospholamban, the restrained ensemble sampled the confo

279 Agonist-evoked phosphorylation by CaMKII at phospholamban (Thr-17), but not of ryanodine2 (Ser-2814)

280 the ryanodine receptor (RyR2) (Ser2815) and phospholamban (Thr17) in a PKC-dependent manner.

281 acetylase 5 phosphorylation (Ser498) but not phospholamban (Thr17), whereas the converse holds for ca

282 memory in the interaction between SERCA and phospholamban, thus providing insights into the physiolo

283 ype Ca(2+) channels, ryanodine receptors and phospholamban to basal levels.

284 estration, since the ratio of phosphorylated phospholamban to total phospholamban was sharply reduced

285 s--glycophorin A, the M2 proton channel, and phospholamban--using only peptide sequence and the nativ

286 eased PKA phosphorylation of cTnI, RyR2, and phospholamban versus controls.

287 The CaMKII target pT17-phospholamban was 5.5-fold increased only in sarcomere-m

288 sphorylation of the SERCA regulatory protein phospholamban was increased in cells cultured under 5% O

289 activation) of the SERCA2a-inhibitor protein phospholamban was increased in pAF.

290 earts of female mice, whereas phosphorylated phospholamban was increased.

291 Although phosphorylation of phospholamban was not altered, miR-1 overexpression incr

292 tio of phosphorylated phospholamban to total phospholamban was sharply reduced in all three mutant he

293 Pase], RyR2 [ryanodine receptor 2], and PLB [phospholamban]) was found in ex vivo perfused adult isol

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