ライフサイエンスコーパス: SUR

1 SUR contains three hydrophobic domains, TM(0), TM(1), an

2 SUR fragments, lacking TMD0, fail to modulate KIR.

3 SUR is indispensable for normal channel function, and mu

4 SUR is involved in nucleotide regulation of the channel

5 SUR measurements were summarized for each brain region.

6 SUR values were computed as the ratio of tumor SUV and b

7 SUR, an ATP-binding cassette protein, associates with Ki

8 SUR-5 also has some sequence similarity to acetyl coenzy

9 SUR-6 and KSR (kinase suppressor of Ras) function at a s

10 SURs calculated with weight versus lean body mass versus

11 SURs determined by using average pixel values provide st

12 SURs were computed as the ratio of tumor SUV to blood SU

13 ively, were used to probe gating of K(IR)6.0/SUR K(ATP) channels.

14 ensitive K+ channels (KATP channels) (KIR6.0/SUR)4.

15 s demonstrated that sulfonylurea receptor 1 (SUR 1) regulated nonselective cation channel, the NC(Ca-

16 KSR (kinase suppressor of Ras), SUR-8/SOC-2, SUR-6/PP2A-B and CDF-1.

17 Because these neurons express the Kir6.2/SUR-1 isoform of the K(ATP) channel, we sought to examin

18 dent models that systemic delivery of Kir6.2/SUR-1-selective KCOs enhance the glucose counterregulato

19 quitous adenine nucleotide-gated K(IR)6.0(4)/SUR(4) channels link membrane excitability with cellular

20 demonstrate that human adipocytes express a SUR that regulates [Ca2+]i and, consequently, exerts coo

21 otassium channel subunits (K(IR)6.x) with a (SUR-K(IR)6.x)4 stoichiometry.

22 than acute DIE mice, but identical to acute SUR.

23 uated the direct role of the human adipocyte SUR in regulating adipocyte metabolism.

24 effects of these compounds on the adipocyte SUR and its associated K(ATP) channel.

25 t to DM revealed smoking state, MTV, and all SUR-based parameters as significant prognostic factors.

26 Although SUR is an important regulator of Kir6, the specific SUR

27 TMD0 is thus the domain that anchors SUR to the KIR pore.

28 es via two types of channels, with SUR 1 and SUR 2, probably SUR2B, sulfonylurea receptors.

29 assium (K(ATP)) channels comprise Kir6.2 and SUR subunits.

30 hannel (composed of two subunits: Kir6.2 and SUR-1) are responsible for the most common and severe fo

31 structurally unrelated subunits, Kir6.2 and SUR.

32 ucleotide sequences predicted that III-A and SUR-III can form looped hairpins.

33 sequences composing the predicted III-A and SUR-III hairpin-loops are crucial for optimal RNA accumu

34 Interaction between aldolase and SUR was confirmed using GST pulldown assays and coimmuno

35 Uptake-time-corrected SUV (cSUV) and SUR (cSUR) have been proposed as uptake-time-independent

36 ons suggest that static (18)F-FDG PET/CT and SUR(stat) analysis provides an alternative to dynamic (1

37 e time dependence compared with SUV(max) and SUR(max) The K(i) (,max) can be predicted from cSUR(max)

38 stage, N stage, and smoking state, MTV- and SUR-based parameters were significant prognostic factors

39 PET/CT and used for calculations of SUV and SUR(stat) Mean K(i) values of the whole imaged field of

40 ons were compared with corresponding SUV and SUR(stat) values, respectively, by means of linear regre

41 the fractional paired differences in SUV and SUR.

42 ences in accuracy among the visual, SUV, and SUR analyses.

43 When coexpressed with any SUR subtype, the activated-currents were increased by 2-

44 Average SUR images were displayed as 2-dimensional and 3-dimensi

45 Removal of PP2A-B55/SUR-6 and the nuclear lamina simultaneously further disr

46 Here, we uncover a role for PP2A-B55/SUR-6 in regulating centrosome separation.

47 Mechanistically, PP2A-B55/SUR-6 regulates nuclear size before mitotic entry, in tu

48 ations predicted the requirement of PP2A-B55/SUR-6 regulation of nuclear size and nuclear-envelope dy

49 , including protein phosphatase 2A (PP2A-B55/SUR-6), biophysical regulators, including dynein, and th

50 ned through the concerted action of PP2A-B55/SUR-6-regulated nuclear envelope-based dynein pulling fo

51 (50(ATP)) values argue the regulatory "beta" SUR subunits play a preeminent role in coupling excitati

52 urfaces when the alleged interaction between SUR-III and III-A is disturbed.

53 Differences in sequence between SUR and between SUR2 isoforms may underlie the tissue-sp

54 n area reduction of contact surfaces between SUR and Kir.

55 on via its effects on low-affinity cell body SUR.

56 upon high- and low-affinity binding to brain SUR.

57 insic gating of Kir6.2 is greatly altered by SUR.

58 uptake can be improved when characterized by SUR instead of SUV.

59 is, however, more efficiently stimulated by SUR than K(IR)6.2, thus providing a mechanism for differ

60 Chimeric SURs were coexpressed with Kir6.2 in Xenopus oocytes, an

61 espective of the identity of the coassembled SUR subunit.

62 og UNC-62 and the Mediator complex component SUR-2.

63 ce were injected with a construct containing SUR cDNA and a calcium-calmodulin kinase IIalpha promote

64 MD0/Kir6.2Delta26 than for the corresponding SUR channels.

65 ual ratios of paired SUVs into corresponding SURs.

66 intrascan repeatability of K(i) , SUV, cSUV, SUR, and cSUR among malignant lesions on PET/CT.

67 Different SUR subtypes (SUR1, SUR2A, SUR2B) largely determine the

68 t in these tissues are composed of different SUR subunits that confer different drug sensitivities.

69 eted) to examine the coassembly of different SUR.

70 by 2- to 13-fold, indicating that different SUR can coassemble.

71 Therefore, different SUR subtypes can coassemble into K(ATP) channels with di

72 h Kir6.1 or Kir6.2 coassemble with different SUR isoforms to form heteromultimeric functional K(ATP)

73 ure and function of ABC proteins and discuss SUR, its regulation of the K(ATP) channel, and its role

74 ssed in mouse myocardium and is the dominant SUR isoform in the atrium.

75 he human homologue of Caenorhabditis elegans SUR-2, a protein required for many developmental process

76 we describe the isolation of cDNAs encoding SUR-like proteins from mouse, SUR2A and SUR2B.

77 el function, and mutations in genes encoding SURs increase the susceptibility to diabetes, myocardial

78 of Mg2+, ATP inhibition of all Kir6.2-F333I/SUR channel types was reduced, although SUR1-containing

79 tages (p = 0.028) and grades (p = 0.043) for SUR interventions, but not for SRP.

80 at -40 and -100 mV (S is an abbreviation for SUR; TMD0/Kir6.2Delta26, but not TMD0/Kir6.2, can exit t

81 Several competing models for SUR/KIR coupling exist.

82 A structural and functional SUR-8 homolog in humans specifically binds K-Ras and N-R

83 s a substitution at the catalytic glutamate, SUR(1E1507Q), with a significantly increased affinity fo

84 The hamster SUR, containing the analogous mutation, had normal ATP s

85 Compared with K(i), SUR(stat) and SUV tracked the same direction of change i

86 The good K(i)-SUR(stat) correlations suggest that static (18)F-FDG PET

87 Conclusion: The K(i)-SUR(stat) correlations were considerably stronger than t

88 e GLP-1 receptor is constitutively active in SUR-1(-/-) beta-cells.

89 quence of this is a conformational change in SUR to increase the SUR/glybenclamide binding affinity.

90 Conformational changes in SUR are also observed, resulting in an area reduction of

91 Furthermore, cAMP content in SUR-1(-/-) islets was reduced by exendin-(9-39) both bas

92 ting that NBF1-NBF2 heterodimers may form in SUR and other eukaryotic ABC proteins.

93 f exendin-(9-39) on fasting blood glucose in SUR-1(-/-) mice.

94 ihood of a second intervention was higher in SUR patients (p < 0.001).

95 in-(9-39) normalizes fasting hypoglycemia in SUR-1(-/-) mice via a direct effect on insulin secretion

96 cretion and corrects fasting hypoglycemia in SUR-1(-/-) mice.

97 secretion, which is abnormally increased in SUR-1(-/-) islets.

98 Fasting blood glucose levels in SUR-1(-/-) mice treated with exendin-(9-39) were signifi

99 Understanding the mutations in SUR and KIR6.X is allowing insight into how these channe

100 Mutations in SUR have been identified in individuals affected with fa

101 ratio reflecting the reduction in the TRV in SUR relative to SUV.

102 correspond to a reduction of variability in SUR by an RTRV factor of 0.9 in comparison to SUV.

103 rminal bundle of five alpha-helices found in SURs, binds to and activates KIR6.0.

104 he standard intubate-surfactant-extubate (IN-SUR-E) technique without increasing the risk of adverse

105 andomly assigned (1:1) to IN-REC-SUR-E or IN-SUR-E and then followed up.

106 cPNA 2 years, including 64 infants in the IN-SUR-E group and 73 infants in the IN-REC-SUR-E group.

107 the IN-REC-SUR-E group compared with the IN-SUR-E group.

108 arge or major disability at cPNA 2 years (IN-SUR-E: 13 children [20.3%] vs IN-REC-SUR-E: 10 children

109 wo transmembrane domains but some, including SUR and MRP1 (multidrug resistance protein 1), contain a

110 ) subunits that assemble as octamers, (K(IR)/SUR)(4).

111 ating to Kir6.2Delta26 and that swapping L0 (SUR truncated after L0)between SUR1 and SUR2A only parti

112 demonstrated that in isolation even TMD0-L0 (SUR truncated after L0) cannot confer the wild-type intr

113 Mutation of Kir6.2, like SUR, appears to lead to the PHHI phenotype suggesting th

114 Mammalian SUR genes are associated with K(ATP) (ATP-sensitive pota

115 e have also identified a potential mammalian SUR-5 homolog that is about 35% identical to the worm pr

116 The SUV(max), cSUV(max), SUR(max), and cSUR(max) were all strongly correlated wit

117 For both tracers, SUV(max) and maximum SUR (SUR(max)) had large early-to-late increases (i.e.,

118 ) were found for scan-time-corrected maximum SUR (HR = 3.9) and mean SUR (HR = 4.4).

119 me-corrected maximum SUR (HR = 3.9) and mean SUR (HR = 4.4).

120 MgATP-dependent hyper-stimulation of mutant SUR can compromise the ability of K(ATP) channels to fun

121 co-expressed Kir6.2 with wild-type or mutant SUR in Xenopus oocytes and recorded the resulting curren

122 in humans and urge others to (re)test mutant SUR/K(IR)6 channels from probands in physiologic MgATP.

123 ations of channels with more than two mutant SUR can dominate hyperpolarizing currents in heterozygou

124 We have isolated a novel SUR variant (SUR1bDelta33) from a hypothalamic cDNA libr

125 d regulatory element of approximately 30 nt (SUR-III) that is positioned immediately upstream of III-

126 d form of Kir6.2 expressed in the absence of SUR, was unaffected by the mutation.

127 r6.2DeltaC) that expresses in the absence of SUR.

128 f KATP channels results from the assembly of SUR and KIR6.X subtypes KIR6.1-based channels differ fro

129 Block of SUR 1 with sulfonylurea such as glibenclamide has been s

130 We found that glinides, another class of SUR-binding hypoglycemic drugs, also markedly increased

131 ituted in functional form by coexpression of SUR, the sulfonylurea-binding protein, and the inwardly

132 in which TMD0-L0 links the MDR-like core of SUR with the K(IR) pore.

133 TMD0 connects to the core domain of SUR through a cytosolic linker (L0).

134 The separable effects of SUR on ATP inhibition and channel kinetics implies that

135 etermined by the ATPase-driven engagement of SUR into discrete conformations.

136 ted Kir6.2 can form a channel independent of SUR, we deleted 114 nucleotides from the carboxy terminu

137 e and mutant channels and was independent of SUR.

138 Two topological models of SUR have been proposed containing either 13 transmembran

139 ns, the nucleotide binding domains (NBDs) of SUR contain a highly conserved "signature sequence" (the

140 two nucleotide-binding fold (NBF) regions of SUR are known to be critical for normal glucose regulati

141 These findings show the key role of SUR in sensing the metabolic index in humans and urge ot

142 eparable and to identify the two segments of SUR responsible for these isoform differences.

143 unique opportunity for functional studies of SUR using a genetic approach.

144 s implies that the cytoplasmic C terminus of SUR either directly modulates the affinity of a weak ATP

145 ed the B site on the amino-terminal third of SUR and colabeled the associated K(IR).

146 The reduction of SURs was most severe in the contralateral (the brain reg

147 iple tandems, T1 and T2, each containing one SUR (SUR1 or SUR2A) and two Kir6.2Delta26 (last 26 resid

148 e investigated uptake-based parameters, only SUR was an independent prognostic factor for OS and DM.

149 n reaction indicated that SUR2B was the only SUR isoform expressed in SUR2(+/+) mesenteric artery smo

150 Kir6.x or SUR mutations result in KATP channelopathies, which refl

151 tent of the yeast plasma membrane, and other SUR genes suppress rvs167 via effects on sphingolipid sy

152 In PP2A-SUR-6-depleted embryos, the levels of ZYG-1 and SAS-5 ar

153 Together, our findings indicate that PP2A-SUR-6 promotes centriole assembly by protecting ZYG-1 an

154 6.0 pores of KATP channels are ABC proteins, SURs, receptors for channel opening and closing drugs.

155 eins such as KSR (kinase suppressor of Ras), SUR-8/SOC-2, SUR-6/PP2A-B and CDF-1.

156 tigate whether the tumor-to-blood SUV ratio (SUR) can improve TRV in tracer uptake.

157 he tumor-to-blood standardized uptake ratio (SUR) can improve the prognostic value of tracer uptake v

158 PET, the SUV and standardized uptake ratio (SUR) of a viable tumor generally increase during the pos

159 The specific uptake ratio (SUR) of each volume of interest and voxel was calculated

160 ntitatively using the standard uptake ratio (SUR).

161 alysis of SUV or standardized uptake ratios (SUR(stat), uptake time-corrected ratio of (18)F-FDG conc

162 13 reports) and standardized uptake ratios (SURs) for 562 lesions (in eight reports) were performed.

163 The specific uptake ratios (SURs) were calculated according to the formula (specific

164 palsy, or cognitive impairment in the IN-REC-SUR-E group compared with the IN-SUR-E group.

165 IN-SUR-E group and 73 infants in the IN-REC-SUR-E group.

166 fants were randomly assigned (1:1) to IN-REC-SUR-E or IN-SUR-E and then followed up.

167 ars (IN-SUR-E: 13 children [20.3%] vs IN-REC-SUR-E: 10 children [13.7%]; P = .36).

168 intubate-recruit-surfactant-extubate [IN-REC-SUR-E]) improved the efficacy of treatment compared with

169 ng K+ channel, and the sulfonylurea receptor SUR, an ATP binding cassette protein.

170 ming protein, and the sulphonylurea receptor SUR, a regulatory protein.

171 ) from the cells in contrast to SU receptor (SUR)-1 inhibitors, which may modify intermediary and ene

172 annels in beta-cells, sulfonylurea receptor (SUR) 1 and Kir6.2, have operational KATP channels and sh

173 P)) metabolic sensor [sulfonylurea receptor (SUR) 1 and potassium inwardly rectifying channel (Kir) 6

174 channel (Kir) 6.2 and sulfonylurea receptor (SUR) 1 critically regulate pancreatic islet beta-cell me

175 either the Kir6.2 or sulfonylurea receptor (SUR) 1 subunit of the channel have previously been shown

176 The ability of the sulfonylurea receptor (SUR) 1 to suppress seizures and excitotoxic neuron damag

177 -type [SUR2(+/+)] and sulfonylurea receptor (SUR) 2-deficient [SUR2(-/-)] mouse myogenic mesenteric a

178 re heteromultimers of sulfonylurea receptor (SUR) and KIR6.X subunits associated with a 1:1 stoichiom

179 n ion conductor and a sulfonylurea receptor (SUR) ATPase.

180 Using putative sulfonylurea receptor (SUR) coiled-coil domains as baits in a 2-hybrid screen a

181 ed by a member of the sulfonylurea receptor (SUR) family and a member of the inwardly rectifying pota

182 The sulfonylurea receptor (SUR) gene, now known to encode an integral component of

183 899/D11S1324 near the sulfonylurea receptor (SUR) gene.

184 The sulfonylurea receptor (SUR) is a member of the ATP-binding cassette family that

185 The sulfonylurea receptor (SUR) is another atypical ABC protein that regulates acti

186 ng fold (NBF2) of the sulfonylurea receptor (SUR) of an individual diagnosed with persistent hyperins

187 ding cassette family (sulfonylurea receptor (SUR) or cystic fibrosis transmembrane conductance regula

188 d from four each of a sulfonylurea receptor (SUR) regulatory subunit and an inwardly rectifying potas

189 6.2) and a regulatory sulfonylurea receptor (SUR) subunit, an ATP-binding cassette (ABC) transporter

190 rised of K(IR)6.x and sulfonylurea receptor (SUR) subunits that assemble as octamers, (K(IR)/SUR)(4).

191 s and four modulatory sulfonylurea receptor (SUR) subunits.

192 ing on the pancreatic sulfonylurea receptor (SUR) to increase (e.g., glibenclamide) or decrease (e.g.

193 tifier Kir6.2 and the sulfonylurea receptor (SUR), a member of the ATP-binding cassette superfamily.

194 The sulfonylurea receptor (SUR), an ATP-binding cassette (ABC) protein, assembles w

195 nce regulator (CFTR), sulfonylurea receptor (SUR), and heavy metal tolerance factor 1 (HMT1) homologs

196 6.2 (Kir6.2) and the sulfonylurea receptor (SUR), now renamed SUR1, subunits of pancreatic beta-cell

197 action of the ATPase, sulfonylurea receptor (SUR), on K(IR) sufficient to elicit a physiologically si

198 It is comprised of sulfonylurea receptor (SUR)-1 and Kir6.2 proteins.

199 in the high-affinity sulfonylurea receptor (SUR)-1 cause one of the severe recessively inherited dif

200 the MDR-like core of sulfonylurea receptor (SUR)-1.

201 binding sites on the sulfonylurea receptor (SUR).

202 el and its associated sulfonylurea receptor (SUR).

203 ABC transporter-like sulfonylurea receptor (SUR).

204 ATP/ADP-sensing (sulfonylurea receptor (SUR)/K(IR)6)(4) K(ATP) channels regulate the excitabilit

205 the L0 region of the sulfonylurea receptor (SUR)1, the regulatory subunit of the pancreatic ATP-sens

206 P) channel contains a sulfonylurea receptor (SUR)2 regulatory subunit and aimed to identify the molec

207 act by binding to a sulphonylurea receptor (SUR) in the pancreatic beta-cell membrane which inhibits

208 e subunits with four sulphonylurea receptor (SUR) regulatory subunits.

209 high-affinity to the sulphonylurea receptor (SUR) subunit of the ATP-sensitive potassium (K(ATP)) cha

210 ed by the regulatory sulphonylurea receptor (SUR) subunit of the channel may also be modified.

211 and four regulatory sulphonylurea receptor (SUR) subunits.

212 The sulphonylurea receptor (SUR) SUR1 serves as the regulatory subunit of the K(ATP)

213 ulatory subunit, the sulphonylurea receptor (SUR).

214 imers of KIR6.2 and a sulfonylurea receptor, SUR, an ATP binding cassette (ABC) protein with several

215 pes of the regulatory sulfonylurea receptor, SUR, and pore-forming, K(+) inward rectifier subunits, K

216 They comprise four sulfonylurea receptors (SUR) and four potassium channel subunits (Kir6) and are

217 e heteromultimers of sulfonylurea receptors (SUR) and inwardly rectifying potassium channel subunits

218 including regulatory sulfonylurea receptors (SUR) SUR1 and SUR2B but not SUR2A and pore-forming subun

219 Kir6.x) subunits and sulfonylurea receptors (SURs).

220 ted partnership with sulfonylurea-receptors (SURs) makes the TRPM4 channel a promising novel target f

221 onparametric Kruskal-Wallis test on regional SUR was used for group comparison between healthy contro

222 known as the seemingly unrelated regression (SUR) model that allows different genetic models for diff

223 mposed of pore-forming Kir6.2 and regulatory SUR subunits.

224 functional topology model for the regulatory SUR subunits of K(ATP) channels.

225 zoxide-induced vasodilation does not require SURs.

226 In addition to their roles in Ras signaling, SUR-6/PR55 and LET-92/PP2A-C cooperate to control mitoti

227 ng systems defined the lifetimes of specific SUR conformations gating K(ATP) channels.

228 an important regulator of Kir6, the specific SUR domain that associates with Kir6 is still unknown.

229 ubunit PAA-1, and the B55 regulatory subunit SUR-6 function together to positively regulate centriole

230 comprises a sulphonylurea receptor subunit (SUR) and an inwardly rectifying K+ channel subunit (Kir)

231 ferred by the sulfonylurea receptor subunit, SUR.

232 and a cloned KATP composed of two subunits (SUR/Kir6.2) stably expressed in a mammalian cell line.

233 For both tracers, SUV(max) and maximum SUR (SUR(max)) had large early-to-late increases (i.e., poor

234 d scaling and root planing (SRP) or surgery (SUR) were included.

235 0 steps day(-1) to induce an energy surplus (SUR group; n = 14) or to the same regimen but with 45 mi

236 study showed high heritability for survival (SUR) under all three phenotyping conditions.

237 c inflammation in dying (DIE) and surviving (SUR) mice suffering from cecal ligation and puncture sep

238 ated with a 1:1 stoichiometry as a tetramer (SUR/KIR6.X forms the pores, whereas SUR regulates their

239 We show here that SUR itself does not possess intrinsic channel activity b

240 We propose that SUR-dependent, inhibitory ATP-enhanced interactions of t

241 We show that SUR TMD0, the N-terminal bundle of five transmembrane he

242 ses an activated ras allele, and showed that SUR-7 is a divergent member of the cation diffusion faci

243 he Ras(P34G) mutant protein, suggesting that SUR-8 may mediate its effects through Ras binding.

244 The SUR gene region accounted for 44.7% of the phenotypic va

245 The SUR-8 protein interacts directly with Ras but not with t

246 ude or open-channel dwell times; and (4) the SUR activator ("KATP channel opener"), diazoxide, activa

247 nnel can be either Kir6.1 or Kir6.2, and the SUR subunit may be a SUR2 splice variant or a similar pr

248 less likely that SUR1bDelta33 serves as the SUR subunit for the VMH KATP channel.

249 These results suggest that defects at the SUR locus may be a major contributor to the inherited ba

250 Similar to the human condition, the SUR-1(-/-) mouse is hypoglycemic when fasted and hypergl

251 Critically, the SUR+EX group received additional dietary energy intake t

252 A/K(IR)6.2 channels was used to identify the SUR regions that specify the selective response of sarco

253 sed 2-fold from baseline to follow-up in the SUR group (17 +/- 16 nmol (120 min) l(-1); P = 0.002) wh

254 ssue was significantly down-regulated in the SUR group (P = 0.005).

255 tissue were differentially expressed in the SUR group; expression of SREBP-1c, FAS and GLUT4 was sig

256 = 0.002) whereas there was no change in the SUR+EX group (1 +/- 6 nmol (120 min) l(-1)).

257 conformational change in SUR to increase the SUR/glybenclamide binding affinity.

258 body surface area in the denominator of the SUR calculation provide equivalent ROC curve areas and a

259 Capture of the SUR catalytic cycle in prehydrolytic states facilitated

260 aximum pixel value in the calculation of the SUR for any of the three denominators (P < or = .05).

261 quence changes in the two NBF regions of the SUR gene in 35 NIDDM patients.

262 r6.2 locus is within 5 kilobases (kb) of the SUR gene on chromosome 11p15.1 and it is a necessary mem

263 through an intrinsic ATPase activity of the SUR subunit.

264 leotide binding folds (NBF1 and NBF2) of the SUR subunit.

265 to examine the therapeutic potential of the SUR-1-selective potassium channel opener (KCO), NN414, t

266 rich linker connecting the two halves of the SUR-ABC core is observed in a quatrefoil-like conformati

267 el to different sulfonylureas depends on the SUR isoform.

268 etic double mutant analyses suggest that the SUR-7-mediated effect is not a general toxic response.

269 They primarily act by binding to the SUR subunit of the ATP-sensitive potassium (K(ATP)) chan

270 The SURs of bilateral caudate, anterior putamen, posterior p

271 The SURs of bilateral striatal regions exhibited significant

272 haracteristic curve analysis showed that the SURs of the bilateral posterior putamen and contralatera

273 Therefore SUR-6/PR55 and LET-92/PP2A-C probably act together to de

274 Therefore, SUR-6 must influence Raf activity via a different mechan

275 ed KATP channels containing any of the three SUR variants, but in excised patches the extent of block

276 KATP channel openers, which bind to SUR, promoted ATPase activity in purified sarcolemma.

277 This indicates Mg-nucleotide binding to SUR and the transduction of binding into opening of the

278 KCO binding to SUR is Mg-ATP-dependent and antagonizes the inhibition o

279 Thus, by binding to SUR NBF2 and antagonizing ATP inhibition of KATP++ chann

280 ction and show that it acts in opposition to SUR-6 and KSR-1.

281 teins (CBP, SRC-1, PBP, PRIP, PIMT, TRAP100, SUR-2, and PGC-1), other proteins that have not previous

282 Using Xenopus oocytes to coexpress truncated SUR constructs with Kir6, we demonstrated by immunopreci

283 ed patients underwent SRP, and 142 underwent SUR as their APT.

284 ill running at 70% of maximum oxygen uptake (SUR+EX group; n = 12).

285 PET studies were evaluated by using SURs calculated with the average or maximum region-of-in

286 nic death (DIE 80- and 50-fold higher versus SUR).

287 ene that is highly related to the vertebrate SUR family.

288 annel openers regulate arterial diameter via SUR-dependent and -independent pathways.

289 etramer (SUR/KIR6.X forms the pores, whereas SUR regulates their activity.

290 senteric artery smooth muscle cells, whereas SURs were absent in SUR2(-/-) cells.

291 l are the same or separate proteins, whether SUR confers ATP-sensitivity on an ATP-insensitive pore-f

292 There has been much debate as to whether SUR and the K-ATP channel are the same or separate prote

293 mer serves as an ATP-inhibitable pore, while SUR is a regulatory subunit endowing sensitivity to sulp

294 and which are conferred by association with SUR.

295 ir follicles via two types of channels, with SUR 1 and SUR 2, probably SUR2B, sulfonylurea receptors.

296 h before death time points and compared with SUR of the same post-cecal ligation and puncture day.

297 ubregions, K(i) was linearly correlated with SUR(stat) (r (2) >= 0.84), whereas K(i)-SUV correlations

298 than one type of functional interaction with SUR, and that F333 interacts differentially with SUR1 an

299 activated by Mg-nucleotide interactions with SUR.

300 erential interactions of Mg-nucleotides with SUR isoforms.

301 rements can be reduced by replacing SUV with SUR as the uptake measure.