ライフサイエンスコーパス: flip-flop

1 interleaflet transport of lipid molecules ("flip-flop").

2 ependence generated the enthalpic barrier to flip-flop.

3 ith bidirectional, transbilayer phospholipid flip-flop.

4 re not, as previously interpreted, represent flip-flop.

5 yers by promoting transmembrane diffusion or flip-flop.

6 r non-bilayer arrangements of lipids support flip-flop.

7 flippases, are responsible for phospholipid flip-flop.

8 holipid translocase activity or phospholipid flip-flop.

9 hospholipids) are used as tracers to monitor flip-flop.

10 was accompanied by nonspecific phospholipid flip-flop.

11 ng of the mechanism of ATP-independent lipid flip-flop.

12 y-ions, ion pairs, charged lipids, and lipid flip-flop.

13 ic molecules that undergo rapid transbilayer flip-flop.

14 ced bending stress is mediated by fatty acid flip-flop.

15 at demonstrate deformation-induced molecular flip-flop.

16 concluded that dissociation was slower than flip-flop.

17 - or ADIFAB-containing vesicles, we assessed flip-flop.

18 on, which were 3-10-fold faster than that of flip-flop.

19 teral diffusion followed by membrane bilayer flip-flop.

20 donor into the aqueous phase rather than by flip-flop.

21 ids move across the membrane only by passive flip-flop.

22 We therefore, therefore, developed Flip-Flop, a flippase-dependent in vivo cassette-inversi

23 rate bubble logic AND/OR/NOT gates, a toggle flip-flop, a ripple counter, timing restoration, a ring

24 hbour distances result in fewer nuclear spin flip-flops, a less fluctuating intra-crystalline magneti

25 translocases facilitate phosphatidylcholine flip-flop across erythrocyte membranes.

26 ime for FFA binding to the outer surface and flip-flop across the bilayer, it was concluded that diss

27 ardiac myocytes, raises the possibility that flip-flop across the lipid phase alone may not be able t

28 ther the rate-limiting step for transport is flip-flop across the membrane or dissociation into the a

29 The upper limit of the rate of flip-flop across the membrane was independent of tempera

30 t, and entrapped pyranine was used to detect flip-flop across the membrane.

31 ris(aminoethyl)amine facilitate phospholipid flip-flop across vesicle membranes; that is, they act as

32 of single molecules, we found that alphatoc flip-flops across the SDPC bilayer on a submicrosecond t

33 Phospholipid translocation (flip-flop) across membrane bilayers is typically assesse

34 We propose a model for the flip-flop action of this enzyme through a concerted appr

35 he calcium binding motif abolishes the lipid flip-flop activity of PLS3.

36 by DFMO, restored both enhanced phospholipid flip-flop and appearance of PS during apoptosis.

37 Rate constants for both flip-flop and dissociation decreased exponentially with

38 We determined the rate constants for flip-flop and dissociation for small (SUV), large (LUV),

39 embranes is rate-limited by a combination of flip-flop and dissociation rates.

40 was faster than flip-flop, and for all FFA, flip-flop and dissociation were faster in SUV than in LU

41 Changes in internal pH caused by flip-flop and metabolism were measured by trapping a flu

42 nsport of the AOFA is limited by the rate of flip-flop and that this rate is a sensitive function of

43 e the net rate of M-C6-NBD-PE translocation (flip-flop) and the steady-state distribution of endogeno

44 vesicle types, dissociation was faster than flip-flop, and for all FFA, flip-flop and dissociation w

45 f the technique to the study of phospholipid flip-flop are discussed.

46 ids and cholesterol exhibit rapid diffusion (flip-flop), as fast as milliseconds, across both protein

47 PLS3 activity, determined by a lipid flip-flop assay, was activated by calcium and tBid but i

48 sed theoretical modeling to demonstrate that flip-flop associations can occur when the investigated v

49 e findings could explain previous reports of flip-flop associations.

50 Do such "flip-flop" associations confirm or refute the previous a

51 , both components exhibited similar rates of flip-flop at a given mole fraction of DSPE.

52 To better understand the nature of the flip-flop barrier, we measured the temperature dependenc

53 Neuronal activity can rapidly flip-flop between stable states.

54 n are dispensable for Wt1-mediated chromatin flip-flop but essential for maintaining the insulating b

55 flippases, are proposed to facilitate lipid flip-flop, but no ER flippase has been biochemically ide

56 somata, we found that the H-cell somata can "flip-flop" by 180 degrees between an anterior and poster

57 cts of exchanging amino acid residues in the flip-flop cassette of GluR2i and GluR2o were investigate

58 Moreover, alternative splicing of the flip/flop cassette downstream of the R/G site is closely

59 onstrating that both PLSCR1 and phospholipid flip-flop characterize this specialized domain of polari

60 ans can be understood in terms of a neuronal flip-flop circuit involving reciprocal inhibition betwee

61 ds bistable pH modulation from an "enzymatic flip-flop" circuit that comprises glucose dehydrogenase

62 mpetition (r-K selection), facilitation, and flip-flop competition (where the competitive hierarchy a

63 For compound 7b, a flip-flop coordination of the phosphorus atoms was propo

64 Alternatively, the flip-flop could represent part of an on-off switch for r

65 to create precise switched states, molecular flip-flops could be used as the basis of a novel molecul

66 ions; we term this mode of action "chromatin flip-flop." Ctcf and cohesin are dispensable for Wt1-med

67 direction of contralateral BF shifts shows a flip-flop, depending on the spatial relationship between

68 -labeled annexin V and enhanced phospholipid flip-flop detected by the uptake of 1-palmitoyl-1-[6-[(7

69 ants for the two lipid systems, while NBD-PS flip-flop did not occur.

70 microM); similar affinities but with smaller flip-flop differences were obtained for GluR1 through 3.

71 We also establish that flip-flop does not occur in synthetic phospholipid vesic

72 ling suggesting that stimulated phospholipid flip-flop does not require additional mobilization of PL

73 AMPA receptors, implicating residues in the flip-flop domain as critical determinants of splice vari

74 Site-directed mutagenesis of residues in the flip-flop domain of GluR2 revealed that, although exchan

75 n to anchor to the membrane because of these flip-flop dynamics, which occur in the mus-ms time range

76 this evolution and determined that the lipid flip-flop event happens most frequently at the interface

77 Once a flip-flop event is triggered, a CHOL molecule takes an a

78 CHOL flip-flop events are observed with a rate constant of 3

79 R mRNA indeed exhibited reprogramming of the flip/flop exons for GluA1 and GluA2 subunits in response

80 associated with splicing of the alternative flip/flop exons.

81 -10 times faster than the rate constants for flip-flop, flip-flop must be the rate-limiting step for

82 used to measure the intrinsic rate of lipid flip-flop for 1,2-dimyristoyl-sn-glycero-3-phosphocholin

83 We further demonstrated that (i) flip-flop for FA with 14-22 carbons is much faster than

84 d headgroup, we have studied the kinetics of flip-flop for single-lipid and mixed-lipid bilayers cons

85 o play a key role in determining the rate of flip-flop for these two species.

86 nonlinear-enhanced rotation sensing, optical flip-flops for photonic memories as well as exceptionall

87 The flip/flop H-bond of Ser219 may play a dual role first in

88 < linoleate (18:2), and (3) the barrier for flip-flop has a significant enthalpic component.

89 the methods used in studies reporting rapid flip-flop have not been interpreted correctly.

90 polarity affect the pathway and the rate of flip-flop in a liquid crystalline 1,2-dipalmitoyl-sn-gly

91 e area of activation for native phospholipid flip-flop in a protein-free DPPC planar-supported lipid

92 Using the assay we show that phospholipid flip-flop in Bacillus vesicles occurs rapidly (half-time

93 nterestingly, melittin did not induce lysoMC flip-flop in POPG vesicles and was found to remain stabl

94 , biochemical fractionation, and analyses of flip-flop in proteoliposomes reconstituted with ER membr

95 at specific proteins facilitate phospholipid flip-flop in the ER, we reconstituted transport-active p

96 The kinetics and thermodynamics of flip-flop in the mixtures did not vary uniformly with ch

97 The kinetics of lipid flip-flop in these membranes was measured by sum-frequen

98 istical mechanics and operational amplifiers/flip-flops in cybernetics.

99 an undergo reversible topological inversion (flip flop) in the membrane until they are trapped in a f

100 the process of CHOL interleaflet transport (flip-flop) in a dipalmitoylphosphatidycholine (DPPC)-CHO

101 y acids (FA) from and transbilayer movement (flip-flop) in small unilamellar phosphatidylcholine vesi

102 The rate of "flip-flop" increases with increases in intramembrane bil

103 o stabilize this network by participating in flip-flop interactions with the hydroxyl groups.

104 to the passive diffusion of un-ionized FFA (flip-flop) into and out of the cell and in response to t

105 f its slow rate on the molecular time scale, flip-flop is challenging also for computational techniqu

106 results, in contrast to those reporting that flip-flop is extremely fast, indicate that the lipid bil

107 pany PEG-mediated SUV fusion, but that lipid flip-flop is not mechanistically related to the fusion p

108 rate limiting, while other studies find that flip-flop is rate limiting and on the order of seconds.

109 We conclude that flip-flop is rate limiting for transport of FFA across l

110 hase transition, and one occurrence of lipid flip-flop is seen at this concentration.

111 In all instances, the rate constant for flip-flop is smaller than koff, and because the rate of

112 data strongly suggest that while nonspecific flip-flop is the driving event for PS appearance in the

113 We have demonstrated recently that flip-flop is the rate-limiting step for transport of ole

114 than the rate of transport, we conclude that flip-flop is the rate-limiting step for transport.

115 eir trans-bilayer movement, commonly denoted flip-flop, is very slow.

116 re > or = 100 s, yielding rate constants for flip-flop (k(ff)) that were < or = 0.01 s(-1).

117 ion of the rate constants for binding (kon), flip-flop (kff), and dissociation (koff) for the transpo

118 ion of the rate constants for binding (kon), flip-flop (kff), and dissociation (koff) for the transpo

119 palmitoyl-sn-glycero-3-phosphocholine (DPPC) flip-flop kinetics on the lateral membrane pressure in a

120 ator, NAND gates, and cascade the gates into Flip-Flop latch.

121 ted in a substantial increase in the rate of flip-flop manifested as an increase in the Arrhenius pre

122 ranslocation across the lipid bilayer by the flip-flop mechanism (<5 s).

123 d rapidly crosses the plasma membrane by the flip-flop mechanism (both events occur within 5 s); and

124 els which incorporate a half-of-the-sites or flip-flop mechanism do not apply to this enzyme.

125 consistent with the half-the-sites activity, flip-flop mechanism proposed for this and other similar

126 ld have to compete with the highly effective flip-flop mechanism.

127 iaceae, and Metschnikowiaceae families, as a flip/flop mechanism that inverted a section of chromosom

128 Therefore, the rmPFC seems to act as a "flip-flop" mechanism in controlling behavior.

129 We propose a lipid "flip-flop" mechanism in which the sugar groups are seque

130 tter elucidate the structural basis for the "flip-flop" mechanism of substrate movement across the li

131 cell membrane bilayers occurs by a passive "flip-flop" mechanism of the drug between two membrane le

132 strate both a flux stabilizer and a bistable flip-flop memory.

133 The Flip-Flop method is efficient and reliable, and permits

134 The flip-flop mode of drug binding correlates with the struc

135 We validated quantitative predictions of our flip-flop model by measuring the number of H(+) delivere

136 he hemiacetal intermediate in support of the flip-flop model for GAP binding.

137 n of the C3 phosphate is consistent with the flip-flop model proposed for the enzyme mechanism.

138 A prominent hypothesis, the "flip-flop" model, predicts that increased and sustained

139 ed to the popularity of half-of-the-sites or flip-flop models for the enzyme reaction mechanism.

140 nine trapped within lipid vesicles to detect flip-flop more directly, have reported that flip-flop ra

141 (SCR) catalyzes phospholipid transmembrane (flip-flop) motion.

142 ow equilibrated release of the hormones by a flip-flop movement of the intact reactive loop into and

143 aster than the rate constants for flip-flop, flip-flop must be the rate-limiting step for the transpo

144 Dye efflux and lipid flip-flop occur concomitantly with the transient peptide

145 Carboxyfluorescein efflux and lipid flip-flop occur with essentially identical rate constant

146 pid vesicles; most investigators report that flip-flop occurs within the resolution time of the metho

147 own to strongly promote the translocation or flip-flop of a fluorescent, C(6)NBD-labeled phosphatidyl

148 fter internalization by endocytosis, induces flip-flop of anionic lipids from the cytoplasmic facing

149 Destabilization induces flip-flop of anionic lipids from the cytoplasmic-facing

150 In contrast, there is no demonstrable flip-flop of bilirubin diglucuronide or bilirubin ditaur

151 lower kinetics could represent either slower flip-flop of FA across highly organized, rigid regions o

152 Membrane partitioning and trans-membrane flip-flop of Fe-Af have also been studied via fluorescen

153 In addition, trans-membrane flip-flop of Fe-Af occurs with a rate constant, k(p) = 1

154 , but its initiation can be as simple as the flip-flop of glutamatergic receptor subtypes triggered b

155 we showed by stopped flow measurements that flip-flop of long chain (14-18 carbons) FA is very fast.

156 re-forming peptides, there was no measurable flip-flop of lysoMC, indicating that asymmetric distribu

157 d not be determined because it induced rapid flip-flop of lysoMC.

158 ate rapid (t((1/2)) < 20 s), ATP-independent flip-flop of N-(6-((7-nitro-2-1,3-benzoxadiazol-4-yl)ami

159 ate PS appearance resulting from nonspecific flip-flop of phospholipids across the plasma membrane du

160 ng of the outer monolayer lipids but without flip-flop of phospholipids and without mixing or leakage

161 We investigated the transbilayer movement or flip-flop of phospholipids in vesicles derived from the

162 holipid translocase activity and nonspecific flip-flop of phospholipids of various classes.

163 ranslocase and calcium-mediated, nonspecific flip-flop of phospholipids play a role.

164 e ghost have shown that polyamines can alter flip-flop of phospholipids, we asked whether alterations

165 flip-flop of pure DSPE to be slower than the flip-flop of pure DSPC by nearly 2 orders of magnitude.

166 Using this approach, we have found the flip-flop of pure DSPE to be slower than the flip-flop o

167 osed upon SUV preloaded with FA, the rate of flip-flop of saturated very long chain FA (C20:0, C:22:0

168 fatty acid and the subsequent transmembrane flip-flop of the fatty acid-cation complex.

169 in agreement with our previous results, that flip-flop of the long chain AOFA is slow relative to eit

170 ansported electroneutrally in the bilayer by flip-flop of the protonated fatty acid.

171 FAs through membranes could occur rapidly by flip-flop of the un-ionized form of the FFA.

172 It is possible that the flip-flopping of the carrier lipid is mediated by a flip

173 The other is to measure spontaneous flip-flops of charges across the membrane under voltage-

174 heir putative role in mediating transbilayer flip/flop of membrane lipids, the PLSCRs may also functi

175 bility by catalyzing transbilayer movement ("flip-flop") of anionic forms of fatty acids, so allowing

176 s, we infer that the transbilayer diffusion (flip-flop) of cholesterol must have proceeded faster tha

177 ntaneous transfer and transbilayer movement (flip-flop) of lipid analogs labeled with the fluorescent

178 ssessing the rate of transbilayer diffusion (flip-flop) of lysoMC.

179 vesicle contents, or transbilayer movement (flip-flop) of the phospholipid probes, or fusion of vesi

180 Transbilayer movement, or flip-flop, of lipids across the endoplasmic reticulum (E

181 egistration observed was not caused by lipid flip-flop or by lateral rearrangement of preexisting lar

182 es from the release of DOX into the water to flip-flop over the membrane center.

183 n interlocus correlations contribute to this flip-flop phenomenon.

184 Mechanistic understanding of the flip-flop process is weak at the molecular level.

185 We investigate the effect of the flip-flop process on mechanical stress across the bilaye

186 In a presumed lipid flip-flop process similar to Ostwald ripening, the small

187 onolayer surface imbalance, namely inward PG flip-flop promoted by the local transmembrane pH gradien

188 We introduce the flip-flop qubit, a combination of the electron-nuclear s

189 Polar lipids must flip-flop rapidly across biological membranes to sustain

190 Such web of "flip-flops" rapidly converged to a stereotyped distribut

191 Fatty acids (FA) are known to diffuse (flip-flop) rapidly across protein-free phospholipid bila

192 better characterize the dependence of lipid flip-flop rate and thermodynamics on the nature of the l

193 However, only the flip-flop rate constants increased significantly with te

194 The flip-flop rate is independent of membrane cholesterol co

195 central ion and the bath spins suppress the flip-flop rate of the neighbour bath spins and yield a s

196 s relatively hydrophilic, and had a very low flip-flop rate, making it an ideal transport substrate.

197 e partitioned position controls the membrane flip-flop rate, whereas membrane partitioning determines

198 The flip-flop rates are determined by solving the Master Equ

199 Comparison of the flip-flop rates determined for GUV with values estimated

200 by using stopped-flow fluorometry to resolve flip-flop rates of both short and long chain AOFA in ves

201 flip-flop more directly, have reported that flip-flop rates of long chain AOFA are extremely rapid (

202 Three amino acid residues in the flip-flop region (Thr765, Pro766, and Ser775 in flip and

203 lta739-784) by deleting the splice-variable "flip/flop" region of the L3 domain in the wild-type rece

204 due substitution within the splice-variable "flip/flop" region.

205 leaflet to the other of a lipid bilayer, or flip-flop, represents a putative mechanism for their tra

206 e therefore propose that the function of the flip-flop sequence module in the channel opening process

207 is of these results, we hypothesize that the flip/flop sequence cassette of AMPA receptors, in a sequ

208 at both proteins catalyzed Ca2+-dependent PL flip-flop similar to that observed for the action of Ca2

209 m analysis of the responses of AMPA receptor flip/flop splice variants, which, despite differences in

210 uncovering an additional regulatory role for flip/flop splicing in excitatory signaling.

211 different arginine/glycine (R/G) editing and flip/flop status.

212 The other motif peptides do not induce lipid flip-flop, suggesting an alternate mechanism.

213 In this flip-flop switch arrangement, GABAergic REM-on neurons (

214 on recent data in rat regarding the putative flip-flop switch for REM sleep control.

215 s of the REM-on and REM-off areas may form a flip-flop switch that sharpens state transitions and mak

216 This further supports the sleep-wake "flip-flop switch" hypothesis and a role for histamine in

217 nding arousal system and may form part of a "flip-flop switch" hypothesized to regulate sleep and wak

218 tal structure for implementing memory is the flip-flop switch, a circuit that can be triggered to fli

219 Here we propose a brainstem flip-flop switch, consisting of mutually inhibitory REM-

220 resembling what electrical engineers call a "flip-flop switch." This switch may help produce sharp tr

221 ry model that is analogous to an electronic 'flip-flop' switch.

222 s at a time, so the structure is a molecular flip-flop that could direct alternative firing of replic

223 lization, and at longer times, trans-bilayer flip-flop that opposes asymmetric lateral segregation an

224 volume (V(f)) model revealed V(f) values for flip-flop that ranged between approximately 12 and 15 An

225 However, whether flip-flop through the hydrophobic core of the bilayer or

226 e lipids, and/or a slower rate of diffusion (flip-flop) through the lipid domains compared to the rat

227 ter and inner leaflets of the bilayer allows flip-flop to be separated from the time course of AOFA b

228 nitored the time course of transbilayer AOFA flip-flop using carboxyfluorescein (CF) trapped within t

229 phospholipids (as a measure of transbilayer flip-flop) using NBD-labeled phosphatidylcholine, and (i

230 e rate of bilirubin transmembrane diffusion (flip-flop) using stopped-flow fluorescence techniques.

231 The rate of TEMPO-DPPC flip-flop was an order-of-magnitude slower compared to D

232 In addition, peptide-induced lipid flip-flop was directly measured using fluorescence energ

233 Under these conditions, NBD-PE flip-flop was proportional to the amount of fusion, but

234 Previously, we found that transbilayer flip-flop was the rate-limiting step for transport of lo

235 gnificantly with temperature; the barrier to flip-flop was virtually entirely due to an enthalpic act

236 ipid redistribution (presumably due to lipid flip-flop) was indicated by a loss of fluorescence inten

237 The important step of transbilayer movement (flip-flop) was not measured directly as a consequence of

238 id scramblase 1 (PLSCR1) is controversial in flip-flop, we sought evidence for its role in enhanced p

239 ayers and that the times for long chain AOFA flip-flop were > or = 100 s, yielding rate constants for

240 the lower limits established for the rate of flip-flop, with t1/2 of dissociation ranging from 20 ms

241 catalyzes trans-bilayer lipid movement (i.e. flip-flop) within the inner membrane.

242 w SFVS can be used to directly measure lipid flip-flop without the need for a fluorescent or spin-lab