ライフサイエンスコーパス: synaptosomal

1 ugmentation of GABA responding, (3) striatal synaptosomal 45Ca2+ clearance, (4) carbachol-stimulated

2 Evaluation in a synaptosomal 45Ca2+ influx assay showed that 9b did not

3 Ex vivo synaptosomal 5-HT transport studies revealed reduced upt

4 increased UBE2N plays a critical role in the synaptosomal accumulation of mutant huntingtin with age.

5 PrPC was solubilized from purified synaptosomal and microsomal membranes by the nonionic de

6 erved effects of KA appear to be the same in synaptosomal and slice preparations.

7 An early signal of synaptosomal apoptosis is the loss of phospholipid asymm

8 armacological properties similar to those of synaptosomal aspartate release and may therefore be medi

9 to selectively proteolyze the 25,000-dalton synaptosomal associated protein (SNAP-25), a protein fou

10 s known intracellular target protein, 25 kDa synaptosomal associated protein (SNAP-25).

11 ) such as syntaxins 2, 4, and 7 and SNAP-23 (synaptosomal associated protein 23).

12 hey must recruit the proteins syntaxin-1 and synaptosomal associated protein 25 (SNAP-25) in the plas

13 Synaptosomal associated protein of 25 kDa (SNAP-25) is a

14 action of synaptic proteins syntaxin and the synaptosomal associated protein of 25 kDa (SNAP-25) was

15 ein; VAMP) and plasma membrane (syntaxin and synaptosomal associated protein of 25 kDa (SNAP-25)) alo

16 eptor complex (SNARE) with syntaxin 1a and a synaptosomal associated protein of 25 kDa (SNAP-25).

17 expression of a dominant negative mutant of synaptosomal associated protein of 25 kDa molelcular mas

18 The role of SNAP-25 (synaptosomal associated protein of 25 kDa) isotypes in t

19 gainst its intracellular substrate, SNAP-25 (synaptosomal associated protein of 25 kDa).

20 pe E, which is known to cleave the 25,000 Da synaptosomal associated protein, inhibited both transcyt

21 ty, and elicits dose-dependent protection of synaptosomal-associated protein (of 25 kDa) in a primary

22 otype of blind-drunk (Bdr), a mouse model of synaptosomal-associated protein (Snap)-25 exocytotic dis

23 otransmitter release by cleavage of a 25-kDa synaptosomal-associated protein (SNAP-25) and synaptobre

24 wo recently identified isoforms of the 25-kD synaptosomal-associated protein (SNAP-25a and SNAP-25b)

25 ant mouse lacking one copy of the gene for a synaptosomal-associated protein (SNAP25) that interacts

26 as also associated to the phosphorylation of synaptosomal-associated protein 23 (SNAP-23), which was

27 oalescence of VAMP3 and its interaction with synaptosomal-associated protein 23; those events were in

28 omolar concentrations of the cleaved form of synaptosomal-associated protein 25 (cSNAP-25) to be dete

29 nylated peptide substrates designed to mimic synaptosomal-associated protein 25 (SNAP-25) are utilize

30 ions causing flaccid paralysis, specifically synaptosomal-associated protein 25 (SNAP-25) for botulin

31 we showed that in Tg2576 mouse hippocampus, synaptosomal-associated protein 25 (SNAP-25) immunoreact

32 e neurotransmitter acetylcholine by cleaving synaptosomal-associated protein 25 (SNAP-25) within pres

33 mplexes by SNARE proteins syntaxin-1 (Stx1), synaptosomal-associated protein 25 (SNAP-25), and synapt

34 vesicles contain reconstituted syntaxin and synaptosomal-associated protein 25 (SNAP-25), and they a

35 icle-associated membrane protein 2 (VAMP-2), synaptosomal-associated protein 25 (SNAP-25), syntaxin,

36 ortical and hippocampal neurons, and cleaves Synaptosomal-Associated Protein 25 (SNAP-25), the substr

37 eolysis of the endogenous protein substrate, synaptosomal-associated protein 25 (SNAP-25).

38 an essential taste transduction effector) or synaptosomal-associated protein 25 (SNAP25) (a key compo

39 zDHHC AR-binding motif (zDABM) sequences of synaptosomal-associated protein 25 (SNAP25) and cysteine

40 gi zDHHC enzymes and two S-acylated proteins-synaptosomal-associated protein 25 (SNAP25) and cysteine

41 hree proteins synaptobrevin-2, syntaxin, and synaptosomal-associated protein 25 (SNAP25) and is thoug

42 T/E), which shares the same synaptic target, synaptosomal-associated protein 25 (SNAP25), last only s

43 protein receptor (SNARE) proteins (syntaxin, synaptosomal-associated protein 25 [SNAP25], vesicle-ass

44 Snapin binds to synaptosomal-associated protein 25 kDa (SNAP-25) and enh

45 Synaptosomal-associated protein 25 kDa (SNAP-25) is a co

46 ntaxin-3 and its functional association with synaptosomal-associated protein 25 was increased.

47 dentified synaptic binding partners, such as synaptosomal-associated protein 25, as well as voltage-d

48 and a reduced density of synaptic proteins (synaptosomal-associated protein 25, syntaxin, and vesicu

49 eins (dihydropyrimidinase-related protein 1, synaptosomal-associated protein 29, glutamate decarboxyl

50 c complexes (between Munc18b and Syntaxin-2, synaptosomal-associated protein of 23 kilodaltons [SNAP2

51 rnary assemblies of syntaxin, SNAP23/SNAP25 (synaptosomal-associated protein of 23 or 25 kDa), and sy

52 necessary for BoNT/A activity as measured by synaptosomal-associated protein of 25 kDa (SNAP-25) clea

53 utamine (Q) residues in syntaxin and the two synaptosomal-associated protein of 25 kDa (SNAP-25) fami

54 Synaptosomal-associated protein of 25 kDa (SNAP-25) is a

55 Synaptosomal-associated protein of 25 kDa (SNAP-25) is a

56 Synaptosomal-associated protein of 25 kDa (SNAP-25) is a

57 Similarly, the carboxyl terminus of the synaptosomal-associated protein of 25 kDa (SNAP-25) is n

58 tein 2 (SV2), synaptophysin, synapsin I, and synaptosomal-associated protein of 25 kDa (SNAP-25) was

59 n receptor (tSNARE) proteins syntaxin 1A and synaptosomal-associated protein of 25 kDa (SNAP-25) were

60 Here we show that synaptosomal-associated protein of 25 kDa (SNAP-25), a S

61 nces of Hirudo medicinalis synaptobrevin and synaptosomal-associated protein of 25 kDa (SNAP-25), ded

62 C) inhibition or intracellular dialysis with synaptosomal-associated protein of 25 kDa (SNAP-25)-bloc

63 -associated membrane protein (VAMP), and the synaptosomal-associated protein of 25 kDa (SNAP-25).

64 t a presynaptic terminal-associated protein, synaptosomal-associated protein of 25 kDa (SNAP-25).

65 s (PNS) on two mouse lines with mutations in synaptosomal-associated protein of 25 kDa (Snap-25): the

66 The synaptosomal-associated protein of 25 kDa (SNAP25) is a

67 t occurs downstream of the TATA boxes of the synaptosomal-associated protein of 25 kDa and neuronal n

68 sion molecule, protein gene product 9.5, and synaptosomal-associated protein of 25 kDa that collectiv

69 ir serotype A (BoNT/A) that cleaves SNAP-25 (synaptosomal-associated protein of 25 kDa) has also been

70 peptidase which selectively cleaves SNAP-25 (synaptosomal-associated protein of 25 kDa), a critical c

71 s, we investigated the expression of SNAP25 (synaptosomal-associated protein of 25 kDa), a key SNARE

72 lying that syntaxin, synaptobrevin, SNAP-25 (synaptosomal-associated protein of 25 kDa), and CAPS are

73 1), Rab11-interacting proteins, and SNAP25 (synaptosomal-associated protein of 25 kDa)-like protein]

74 ns with hypomorphic lesions in the syntaxin, synaptosomal-associated protein of 25 kDa, and synaptobr

75 ng single mutations I67T/N in neuronal SNARE synaptosomal-associated protein of 25kDa (SNAP-25B), whi

76 ht to be the sole substrate for BoNT/C1, and synaptosomal-associated protein of Mr = 25 000 (SNAP-25)

77 The synaptosomal-associated protein SNAP25 is a key player i

78 nce also supports associations with SNAP-25 (synaptosomal-associated protein, 25 kDa) and SLC6A4 (ser

79 dies SP6 and SP14, which detect syntaxin and synaptosomal-associated protein-25-kd immunoreactivities

80 iously characterized as a binding partner of synaptosomal-associated proteins 25 and 23 and implicate

81 by inhibition of [3H] clonidine binding and synaptosomal biogenic amine uptake, and in vivo by rever

82 nucleotides and Mg2+,Ca2+-induced PTP in non-synaptosomal brain mitochondria exhibits a unique patter

83 Thus, synaptosomal Ca(2+)-stimulated release of FM1-43 dye was

84 ate formation correlated positively with the synaptosomal content of [ATP].

85 in microsomal, synaptic vesicle-enriched and synaptosomal cytosolic fractions from rat brain, as well

86 alpha6-GFP transgenic mice, alpha6-dependent synaptosomal DA release and radioligand binding experime

87 s thought to involve exchange diffusion with synaptosomal dopamine through the dopamine transporter.

88 These results suggest that synaptosomal dopamine transport activity is regulated by

89 ificantly increased the level of hippocampal synaptosomal epsilonPKC to 152% of sham-operated animals

90 omoted significant increases in the level of synaptosomal epsilonPKC.

91 F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-a

92 Loss of synaptosomal F-actin in human postmortem tissue correlat

93 Further, we observed decreased synaptosomal F-actin levels in postmortem brain from mil

94 g glia, whereas mitochondria enriched from a synaptosomal fraction are predominantly neuronal and pre

95 on, protein levels of mGluR1 in the enriched synaptosomal fraction from both the striatum and the med

96 Reduced ATP level was also found in the synaptosomal fraction isolated from Hdh(CAG)150 knock-in

97 nous mouse ASIC1a and was distributed to the synaptosomal fraction of brain.

98 AG1 also reduces the levels of mutant htt in synaptosomal fraction of male HD mice.

99 perform quantitative MudPIT analysis on the synaptosomal fraction of the cerebellum during post-nata

100 ynaptic to a postsynaptic location that uses synaptosomal fractionation after introduction of radiola

101 Synaptosomal fractionation and immunocytochemical staini

102 We used synaptosomal fractionation with Western blotting and imm

103 at striatal neurons in vivo, native ERK from synaptosomal fractions also associated with PSD-93.

104 metry analysis of rat cortical mitochondrial/synaptosomal fractions demonstrated the presence of high

105 Synaptosomal fractions from aged monkey brain increase i

106 increases of GluR2/3-containing receptors in synaptosomal fractions from tetanized slices.

107 eins involved in PD progression, we prepared synaptosomal fractions from the frontal cortices of path

108 ic glutamate transporter 1 (GLT1) from crude synaptosomal fractions in which astrocytic processes are

109 Analysis of synaptosomal fractions revealed that NgR1 is enriched sy

110 Co-immunoprecipitation of synaptosomal fractions showed that GluN2A, 5HT2C recepto

111 recipitate from mouse brain extract and from synaptosomal fractions, consistent with an endogenous in

112 the greatest loss of ubiquitin was found in synaptosomal fractions, suggesting that the endplate swe

113 sferases, respectively, in the golgi and the synaptosomal fractions; (3) a 70.1% (p<0.05) and 42.6% (

114 nd implicate FGF14 in axonal trafficking and synaptosomal function.

115 uN2B Ser(1480) phosphorylation level and the synaptosomal GluN2A protein level in the PVN were signif

116 of lithium or valproate reduced hippocampal synaptosomal GluR1 levels.

117 We characterized synaptosomal glutamate transport activity in a recently

118 However, the synaptosomal glutamate uptake capacity (Vmax) was reduce

119 ALS, produced an enhancement of spinal cord synaptosomal glutamate uptake in control animals and ear

120 d, and the contribution of neuronal GLT-1 to synaptosomal glutamate uptake is greater than expected b

121 late act as substrates for the rat forebrain synaptosomal glutamate uptake system.

122 sine phosphorylation of NR2A and NR2B in the synaptosomal membrane compartment.

123 rease in NR1, NR2A, and NR2B proteins in the synaptosomal membrane fraction; (2) a decrease in NR1, N

124 showing the presence of CASK in soluble and synaptosomal membrane fractions and its enrichment in po

125 as evaluated under equilibrium conditions in synaptosomal membrane fractions subjected to either basa

126 Synaptosomal membrane fractions were tested for CaM kina

127 y the addition of exogenous CaM kinase II to synaptosomal membrane fractions.

128 ormance increased the density of CHTs in the synaptosomal membrane in the right frontal cortex.

129 ecreased the surface/intracellular ratio and synaptosomal membrane levels of NAc GluA1 in morphine-de

130 Using a cell-free, lysed synaptosomal membrane preparation, we show that Ca2+ alo

131 ctive in preventing the oxidative changes in synaptosomal membrane protein conformation and crosslink

132 bonyls revealed direct evidence of increased synaptosomal membrane protein oxidation (248% of control

133 dicated high-affinity interaction of LK with synaptosomal membrane protein(s), but neither LK binding

134 Brain synaptosomal membrane proteins from rats injected with 3

135 ot induce conformational changes in cortical synaptosomal membrane proteins.

136 one (PBN), on the physical state of cortical synaptosomal membrane proteins.

137 al tissues the NR2A and NR2B subunits in the synaptosomal membrane, and not those in the light membra

138 ficantly reduced the 50 kDa DAT isoform in a synaptosomal membrane-associated fraction, but not in a

139 a single class of sites present in rat brain synaptosomal membranes (K(d) = 6.1 nM), and in membranes

140 H]BNZA binds with high affinity to rat brain synaptosomal membranes (Kd = 1.5 nM) and to membranes pr

141 from vesicular compartments (P3 and LP2) to synaptosomal membranes (LP1).

142 ve restored levels of glutamate receptors on synaptosomal membranes and improved cognitive function,

143 fications to lipid and protein components of synaptosomal membranes as determined by electron paramag

144 ADDLs that were bound to detergent-extracted synaptosomal membranes co-immunoprecipitated with NMDA-R

145 ses and ten (45 days, n = 4; 60 days, n = 6) synaptosomal membranes constituted the hypoxic (experime

146 d in eleven (45 days, n = 5; 60 days, n = 6) synaptosomal membranes from normoxic (control) fetuses a

147 eins or protein carbonyl content of cortical synaptosomal membranes from the PBN-injected and saline-

148 cteristic of less oxidized systems, cortical synaptosomal membranes from the PBN-injected SAMP8 mouse

149 ly sensitive enzyme) to report that cortical synaptosomal membranes from the senescence accelerated-p

150 alpha-syn exhibited similar ability to bind synaptosomal membranes in vitro and in HeLa cells, where

151 Exposure of isolated synaptosomal membranes to "apoptotic" cytosolic extracts

152 for 4 days) and subsequently isolated brain synaptosomal membranes were examined for evidence of oxi

153 Synaptosomal membranes were prepared and strychnine-inse

154 Treatment of cells and synaptosomal membranes with the caspase inhibitors preve

155 were evaluated in solution, red blood cells, synaptosomal membranes, and cultured hippocampal neurona

156 mpound blocked [3H]glutamic acid uptake into synaptosomal membranes, and neither compound was able to

157 In experiments with purified rat synaptosomal membranes, both kinetic and equilibrium dat

158 rity of Kalirin-7 protein is associated with synaptosomal membranes, but a fraction is cytosolic.

159 ace [(125)I]dendrotoxin binding to rat brain synaptosomal membranes.

160 ganglia, and shows a strong localization in synaptosomal membranes.

161 r rotenone toxicity, due to reduced striatal synaptosomal mitochondria and synaptic vesicular proton

162 Activation of epsilonPKC increased synaptosomal mitochondrial respiration and phosphorylati

163 ese are distinct from subtypes that modulate synaptosomal norepinephrine release in the rat hippocamp

164 Synaptosomal phosphorylation of NSF is stimulated by pho

165 se findings, the density of CHTs in cortical synaptosomal plasma membrane-enriched fractions from uns

166 levels in a confined biochemical fraction of synaptosomal plasma membranes enriched from the striatum

167 When tested in a nucleus accumbens (NAcs) synaptosomal preparation, AT-1001 inhibits nicotine-indu

168 In a synaptosomal preparation, brain-derived neurotrophic fac

169 in brain synaptosomal preparation, GAD(67) is cleaved to its trun

170 ssessed by measuring the amount remaining in synaptosomal preparations after treatment of whole tecta

171 s was further supported by its enrichment in synaptosomal preparations as detected by immunoblotting.

172 in three independent developing neocortical synaptosomal preparations identified putative interactin

173 d that it associated with Rab3A in rat brain synaptosomal preparations in vitro and the association w

174 ignificant differences in the quality of the synaptosomal preparations or the mitochondrial volume fr

175 Ng present in the rat brain synaptosomal preparations was also oxidized by DEANO in

176 tions were performed from isolated rat brain synaptosomal preparations.

177 AP1B expression is also found in presynaptic synaptosomal preparations.

178 92 kDa protein bands in both rat and chicken synaptosomal preparations.

179 ncreases in pp60c-src protein in hippocampal synaptosomal preparations.

180 ing [3H]-serotonin accumulation in rat brain synaptosomal preparations.

181 actor receptor (SNARE) proteins syntaxin and synaptosomal protein of 25 kDa (SNAP-25), and this assoc

182 results indicate that AH9 antigen is a novel synaptosomal protein that is relatively specific to the

183 enes from different NDD datasets that encode synaptosomal proteins were analyzed for being enriched i

184 PP strategy captured approximately 4% of the synaptosomal proteome, including the unbiased capture of

185 Synaptosomal Rab3A was retained on recombinant GST-tagge

186 s Ca2+-induced Ca2+ release in isolated, non-synaptosomal rat brain mitochondria in the presence of p

187 s confirmed by co-fractionation of FMRP with synaptosomal ribosomes, suggests a possible role of FMRP

188 Using a synaptosomal secretion assay, we found that while K(+)-e

189 To circumvent damage induced by synaptosomal separation, we monitored membrane potential

190 Reduced BoNT/A and BoNT/E cleaved synaptosomal SNAP-25 by 20% and 15%, respectively.

191 latable" surface TCRs that might reside in a synaptosomal structure.

192 ound that the pharmacological profile of the synaptosomal system exhibited the greatest similarity wi

193 istribution of NETs has been defined through synaptosomal transport and autoradiographic approaches,

194 though EAAC1-mediated transport and cortical synaptosomal transport have similar pharmacological prof

195 his, IL15Ralpha knock-out mice had increased synaptosomal uptake of (3)H-GABA.

196 on the low side of therapeutic, up-regulated synaptosomal uptake of glutamate.

197 ve and nontoxic dose was further used in the synaptosomal uptake studies.

198 comparison of the pharmacological profile of synaptosomal uptake with those of the individual EAAT cl

199 ssing glutamate uptake capacity by measuring synaptosomal uptake.