ライフサイエンスコーパス: PSD95

1 SAP102) and postsynaptic density protein 95 (PSD95).

2 DZ protein, postsynaptic density protein 95 (PSD95).

3 disrupt the association of KV1 channels with PSD95.

4 including synaptophysin, NMDAR1, CaMKII, and PSD95.

5 plex, decreased soluble Abeta, and increased PSD95.

6 AP25 and the post-synaptic proteins NR2b and PSD95.

7 lg family, including Dlg1/SAP97, SAP102, and PSD95.

8 rane protein complex that includes Veli3 and PSD95.

9 d not interact with the other PDZ domains of PSD95.

10 tein complex with NMDA receptor subunits and PSD95.

11 idual spines where it colocalized with SAP90/PSD95.

12 icroglia as well as the postsynaptic protein PSD95.

13 icroglia as well as the postsynaptic protein PSD95.

14 ceptors, soluble guanylyl cyclase (sGC), and PSD95.

15 oted in the postsynaptic scaffolding protein PSD95.

16 ompetitive inhibition of binding of ErbB4 to PSD95.

17 guanylyl cyclase (sGC, the NO receptor), and PSD95 (a protein that anchors receptors and enzymes at t

18 MTAP1A to postsynaptic density molecule 95 (PSD95), a core component in the cytoarchitecture of syna

19 ncodes for post-synaptic density protein 95 (PSD95), a major synaptic protein that clusters glutamate

20 investigated expression and localization of PSD95, a dendritic post-synaptic protein, within oligode

21 h increased the colocalization of GIRK2 with PSD95, a dendritic spine marker.

22 e hippocampal neurons and codistributes with PSD95, a major scaffolding protein of the excitatory pos

23 We also found that the PDZ1 domain of PSD95, a postsynaptic scaffolding protein, interacted wi

24 of transfected neurons expressing GFP-tagged PSD95, a prominent PSD protein, revealed that up to 40%

25 response element binding protein (CREB) and PSD95 after TBI.

26 and KA1-2 subunits of the kainate receptor; PSD95), all but two (GluR4 and KA1) were expressed at qu

27 Loss of PSD95 also depolarized cVSMCs in pressurized cerebral ar

28 naptic proteins (synaptophysin, synapsin and PSD95), AMPA and NMDA receptor subunits found no signifi

29 hanging PSD95 palmitoylation in PSDs altered PSD95 and AMPAR levels but did not affect NMDAR levels.

30 Here, we demonstrate that HCN1, Kv1.1, PSD95 and GAD67 unexpectedly mark patterns of basket cel

31 LBP is colocalized with the synaptic marker PSD95 and is found in close proximity to processes of mi

32 ue-Dawley rats were isolated for analysis of PSD95 and K(V)1 channel proteins.

33 lored whether a specific interaction between PSD95 and KV1 channels enables protein kinase A phosphor

34 nded to reduced coimmunoprecipitation of the PSD95 and KV1 proteins without altering surface expressi

35 ohistochemistry and had higher expression of PSD95 and mGluR6 and less GFAP expression compared with

36 The subsequent decline in PSD95 and mGluR6 between 1 and 12 months in Rs1-KO retin

37 PSD95 and mGluR6 levels were normal at 1 month on Wester

38 1, the OPL was disrupted in Rs1-KO, and some PSD95 and mGluR6 was mislocalized in the outer nuclear l

39 Levels of PSD95 and mGluR6 were determined by quantitative Western

40 PSD95 and mGluR6 were juxtaposed in the OPL of the Rs1-K

41 nfluences the association between GluN2A and PSD95 and modulates GluN2A enrichment into LR.

42 tatory synapses that lack SHANK3 but contain PSD95 and N-methyl-D-aspartate (NMDA) receptors with fas

43 roteins can accelerate palmitate turnover on PSD95 and N-Ras.

44 a unique PDZ-PDZ domain interaction between PSD95 and nNOS.

45 ing from a protein complex of NMDA receptor, PSD95 and nNOS.

46 The synaptic proteins PSD95 and NR2B were reduced in dendritic fields and redi

47 Synaptic changes in NMDAR, AMPAR, PSD95 and phosphorylated CaMKIIalpha became apparent in

48 doxorubicin-induced loss of synaptic protein PSD95 and restored microglial morphology in the hippocam

49 d genetic labeling of two of these proteins (PSD95 and SAP102), and Spinning Disc confocal Microscopy

50 Here, we measured PSD95 and SAP97 conformation in vitro and in postsynapti

51 Within PSDs, PSD95 and SAP97 were largely in the extended conformatio

52 he immunoreactivity of postsynaptic markers (PSD95 and spinophilin) and a presynaptic marker (syntaxi

53 hippocampus and amygdala and were limited to PSD95 and SV2A.

54 pression in microglia partially reduced both PSD95 and synaptic densities.

55 red microglia increased post-synaptic marker PSD95 and synaptic density as determined by the co-local

56 he neuronal marker MAP2 and synaptic markers PSD95 and synaptophysin in AD mice was significantly rev

57 O neurons, including the scaffolding protein PSD95 and the NMDA receptors along with the known CPEB3

58 reases in the levels of post-synaptic marker PSD95 and the pre-synaptic marker synaptophysin.

59 Other palmitoylated proteins (e.g. PSD95 and Wnt) are not substrates for Hhat, and Porcupin

60 ynthase (nNOS) from postsynaptic density 95 (PSD95) and a reduced production of the potent vasodilato

61 ecting the post-synaptic density protein 95 (PSD95) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepro

62 ound higher postsynaptic density protein 95 (PSD95) and lower glutamate decarboxylase 67 (GAD67) expr

63 Postsynaptic density protein 95 (PSD95) and synapse-associated protein 97 (SAP97) are hom

64 s an increase in postsynaptic density GluR1, PSD95, and actin proteins; while postsynaptic density mG

65 oteins, including GCAP1 and 2, PDE6b, AIPL1, PSD95, and CTBP1 indicates dysregulation of calcium home

66 to a critical synaptic scaffolding molecule, PSD95, and leads it to degradation via ubiquitination.

67 sociated postsynaptic density proteins NF-L, PSD95, and SAP102 was also detected in the thalamus of s

68 d postsynaptic density proteins NF-L, PSD93, PSD95, and SAP102.

69 ronal plasticity markers such as synapsin I, PSD95, and synaptophysin, and a decrease of spontaneous

70 PSD95 appears to function as a critical 'dilator' scaffo

71 ating that the genes encoding neuroligin and PSD95 are altered in autism patients, suggest that a mol

72 We show that EO and PSD95 are necessary for SC NMDA receptor (NMDAR)-depende

73 Therefore, our study suggests that CREB and PSD95 are novel substrates of PERK, so inhibition of PER

74 reveals that copies of the synaptic protein PSD95 are synthesized in response to local activation of

75 Conclusively, this work validates PSD95 as a key player in memory and establishes epigenet

76 explored the possibility that cVSMCs express PSD95 as a scaffold to promote K(V)1 channel expression

77 the third PDZ domains of DLG1/SAP97 and DLG4/PSD95 as interaction partners for the PDZ binding motif

78 In general, the spine head geometry and PSD95 assemblies were highly dynamic, their changes depe

79 PSD95 associated with AMPARs (via transmembrane AMPAR re

80 P4 (SAPAP4), a key post-synaptic density 95 (PSD95) associated gene, truncated by the chromosome tran

81 SAP90/PSD95-associated protein 3 (SAPAP3; also known as DLGAP3

82 g phenotype caused by dysregulation of Sap90/Psd95-associated protein 3 (Sapap3; also known as Dlgap3

83 Loss of CD3zeta in brain decreased GluN2A-PSD95 association and GluN2A synaptic localization.

84 a photo-oxidizing TimeSTAMP tag reveals new PSD95 at developing dendritic structures of immature neu

85 These scaffold proteins, such as PSD95, bind to Kir2.1 channels via a PDZ-binding motif (

86 KO male mice, GluN2A is less associated with PSD95 both in ex vivo synaptosomes and in cultured hippo

87 uA1 and GluA2 subunits were colocalized with PSD95 but not synapsin I, suggesting a postsynaptic loca

88 vel of the postsynaptic scaffolding protein, PSD95, but not of PSD93, overcomes the refractory period

89 the scaffolding postsynaptic density protein PSD95, but the mode of control appears to be different f

90 young brain, and that even though SAP102 and PSD95 can bind the same NMDARs, only PSD95 enables SC sy

91 Palmitoylation of PSD95 changed its conformation from a compact to an exte

92 Treatment increased PSD95 co-immunoprecipitating with NR2B and, independent

93 mice, which coincided with a greater vGlut1/PSD95 colocalization, higher dendritic spine density, an

94 pression in KO neurons can rescue GluN2A and PSD95 colocalization.

95 The AKAP79/150-PSD95 complex is disrupted in hippocampal neurons during

96 lar and functional heterogeneity in synaptic PSD95 complexes and reveal critical roles for L27 domain

97 ophysin-tagged fluorescent proteins, but not PSD95, consistent with their output function.

98 ns can induce the assembly and clustering of PSD95-containing postsynaptic complexes, displaying a no

99 The expression of PSD95 correlated with the expression of NR1, NR2A, NR2B,

100 Also, PSD95 dendrite labeling reveals that larger motor units

101 th augmented association of the 5-HT2AR with PSD95 differentiated HI from LI rats.

102 response element binding protein (CREB) and PSD95 directly at the S129 and T19 residues, respectivel

103 The mechanism by which SNX27 and PSD95 discriminate these channels was previously unclear

104 his study, we report that the conserved PDZ (PSD95, Discs large, ZO-1) domain-containing protein PATJ

105 1 (NHERF-1) by binding the first of two PDZ (psd95, discs-large, ZO-1) domains.

106 ite by binding of the AQP4 C terminus to the PSD95-Discs large-ZO1 (PDZ) domain of syntrophin, a comp

107 PDZ (PSD95/Discs large/ZO-1) domains are ubiquitous protein i

108 pical transmembrane protein, Crumbs, and two PSD95/discs large/zonula occludens domain proteins, prot

109 nduction of the wild-type protein but not of PSD95, Dlg, ZO-1 (PDZ), or leucine rich repeat domain mu

110 HtrA1 is localized to microtubules in a PDZ (PSD95, Dlg, ZO1) domain-dependent, nocodazole-sensitive

111 at contains leucine-rich repeats (LRR) and a PSD95-Dlg-Zol (PDZ) domain and that interacts specifical

112 To date, Mpdz, which encodes the multiple PSD95/DLG/ZO-1 (PDZ) domain protein (MPDZ), is the only

113 y terminus, which contains a C-terminal PDZ (PSD95/Dlg/ZO-1) binding motif; 2) blocking PDZ binding b

114 fic sequence motifs of PLC-beta and the PDZ (PSD95/Dlg/ZO-1) domains of Par proteins.

115 f the "b" splice type contain predicted PDZ (PSD95/Dlg/ZO-1) interaction domains.

116 with mutations that ablate a potential PDZ (PSD95/dlg/ZO-1) interaction motif and a putative tyrosin

117 and contains a single consensus sequence in PSD95/DLG/zo-1, which implies cross-linking of PP1 to tr

118 anger regulatory factor-2 and CFTR through a PSD95/Dlg/ZO-1-based interaction.

119 NAD is a scaffolding protein containing five PSD95/dlg/zonular occludens-1 (PDZ) domains that tether

120 tween aa 475-589, which is separate from the PSD95/dlg/zonular occludens-1 (PDZ) interacting domain.

121 PSD95, Dlg1, ZO-1 (PDZ) domain in NHERF4 inhibited GCC c

122 ly distinct class of ligand specificity in a PSD95, DLG1, ZO-1 (PDZ) domain preferentially occurs thr

123 cling of transmembrane cargos that contain a PSD95, Dlg1, zo-1 (PDZ)-binding motif.

124 MPDZ is a multi-PDZ (PSD95/DLG1/ZO-1) domain scaffold present at apical cell

125 gh-risk alpha types target a select group of PSD95/DLG1/ZO1 (PDZ) domain-containing proteins by using

126 se findings show a coordinated regulation of PSD95/Dlg4 mRNA by FMRP and FXR2P that ultimately affect

127 e of FXR2P leads to decreased translation of PSD95/Dlg4 mRNA in the hippocampus, implying a role for

128 with FMRP in binding to the 3'-UTR of mouse PSD95/Dlg4 mRNA.

129 teins, such as postsynaptic density protein (PSD95), Drosophila disc large tumor suppressor (Dlg1), z

130 We used PSD95-eGFP mice, to visualise excitatory postsynaptic de

131 102 and PSD95 can bind the same NMDARs, only PSD95 enables SC synaptic maturation.

132 We analysed the Dlg4/PSD95 epigenetic landscape in hippocampal tissue and des

133 but not ventral, striatum, cocaine decreases PSD95 expression and phosphorylation of cortactin, a cyt

134 ore, DNMT3L overexpression increased APP and PSD95 expression in differentiating neurons, whereas DNM

135 PSD95 expression level regulates AMPAR nanodomain size a

136 critical histone marks and subsequently Dlg4/PSD95 expression, which, importantly, impacted several h

137 evidence that astrocytic activation enhances PSD95 expression.

138 th specificity with different members of the PSD95 family of SAPs.

139 of SGN fibers with ectopic overexpression of PSD95 far outside the synaptic region.

140 CAPON competes with PSD95 for interaction with nNOS, and overexpression of C

141 50 (AKAP79/150) and postsynaptic density 95 (PSD95) form a complex that controls the opposing actions

142 Ribbons and PSD95-FP clusters were more stable when these components

143 olar cells (BCs) and postsynaptic densities (PSD95-FP) of retinal ganglion cells (RGCs).

144 Coimmunoprecipitation of Ggamma13 and PSD95 from brain and of Ggamma13 and SAP97 from taste ti

145 notypes of which are consistent with loss of PSD95 function.

146 ters of the scaffolding proteins gephyrin or PSD95 fused to GFP.

147 to express Post Synaptic Density 95 protein (PSD95) fused to either eGFP or mEos2 and imaged with two

148 ere transfected with a vector encoding a GFP-PSD95 fusion protein.

149 tripartite requirement of GluN2B, PSD93 and PSD95 gate the incorporation of receptors into approxima

150 pe in hippocampal tissue and designed a Dlg4/PSD95 gene-targeting strategy: a Dlg4/PSD95 zinc finger

151 port that N-terminal alternative splicing of PSD95 generates an isoform, PSD95beta that contains an a

152 PSD95-GFP fluorescent puncta represented functional syna

153 Immunoelectron microscopy confirmed that PSD95-GFP predominantly localized to ultrastructurally i

154 ment with gp120 IIIB decreased the number of PSD95-GFP puncta by 37 +/- 4%.

155 Tat (24 h) decreased the number of PSD95-GFP puncta by 50 +/- 7%.

156 -gephyrin puncta and decreased the number of PSD95-GFP puncta.

157 ed the Tat-induced decrease in the number of PSD95-GFP puncta.

158 PSD95-GFP was confirmed as a marker of excitatory input

159 otein 95 fused to green fluorescent protein (PSD95-GFP) enabled visualization of synaptic sites.

160 d a GFP-tagged postsynaptic density protein (PSD95-GFP) to visualize dendritic morphology and postsyn

161 otein 95 fused to green fluorescent protein (PSD95-GFP).

162 naptic density 95-green fluorescent protein (PSD95-GFP).

163 nsity 95 fused to green fluorescent protein (PSD95-GFP).

164 plasmid coding for the postsynaptic protein PSD95-GFP.

165 In addition, retroviruses that encode either PSD95:GFP or Syn:GFP revealed striking alterations in th

166 o increased levels of the synaptic proteins, PSD95, GluA1, and Synapsin 1 and enhanced synaptic funct

167 postsynaptic density (PSD) scaffold protein, PSD95, identified large (>1 microm) and irregularly shap

168 However, PSD95 immunolabeling intensities were substantially lowe

169 ying dendrites express postsynaptic density (PSD95) immunoreactive puncta suggesting that they receiv

170 opic glutamate receptor (iGluR) subunits and PSD95 in 5 precisely defined and dissected thalamic subd

171 urons, with loss of the postsynaptic protein PSD95 in a p75NTR-dependent manner.

172 ere no significant effects of PSIL or PME on PSD95 in any brain area when these were analyzed separat

173 ivo microglia and colocalization of Iba1 and PSD95 in brain cryosection.

174 Moreover, decrease in the loss of PSD95 in cbs(+/-) mice results in improvement of IL-1bet

175 els is enabled by a dynamic association with PSD95 in cerebral arteries and suggest that a disruption

176 t labeled presynaptic VAMP2 and postsynaptic PSD95 in long-term cultured live primary neurons in 96 w

177 However, the physiological role of PSD95 in mediating molecular signaling in cVSMCs is unkn

178 This interaction between ApoEr2 and PSD95 in neurons was modulated by NMDA receptor activati

179 The physical interaction of Ggamma13 with PSD95 in the cellular milieu was confirmed in pull-down

180 n of the synaptic proteins synaptophysin and PSD95 in the hippocampus, and prevented BCCAO-induced lo

181 of Ggamma13 abolished its interactions with PSD95 in two-hybrid and pull-down assays.

182 ts (GluR1, GluR2), or PSD protein of 95 kDa (PSD95) in either brain region.

183 Full-length PSD95 increased cell surface levels of ApoEr2 and its cl

184 all visual brain regions examined, synaptic PSD95 increases rapidly following simultaneous eyelid op

185 We also found that the PDZ2 domain of PSD95 interacted with the NR2A and NR2B subunits of NMDA

186 AMPAR subunit delivery again through a SAP97-PSD95 interaction.

187 y of GluA1-containing AMPARs through a SAP97-PSD95 interaction.

188 licated by the GPER agonist G1: G1 increased PSD95-IR in strata oriens, lucidum, and radiatum of CA3

189 Our findings provide initial evidence that PSD95 is expressed in cVSMCs, and the K(V)1 channel is o

190 Finally, we provide evidence that PSD95 is one of the substrates of ZDHHC8.

191 Postsynaptic density-95 (PSD95) is a 95 kDa scaffolding molecule in the brain tha

192 Postsynaptic density-95 (PSD95) is a scaffolding protein that associates with vol

193 Furthermore, miniature NMDAR currents after PSD95 KD show an activity-triggered calcineurin sensitiv

194 PSD95 knockdown (KD) in vivo blocks this LTP, but not lo

195 Conversely, phosphorylation of PSD95 leads to its downregulation in pericontusional cor

196 PLC is also necessary for decreases in spine PSD95 levels and AMPAR internalization.

197 PSD95 levels are diminished in ageing and neurodegenerat

198 The variability of VGlut1 and PSD95 levels at excitatory inputs across PVIs was larger

199 mutant of PERK (PERK-K618A) rescues BDNF and PSD95 levels in the pericontusional cortex by reducing p

200 with internalization of AMPARs, decreases in PSD95 levels, and loss of AKAP79/150 and PKA from spines

201 Excitatory synapses have a wide range of PSD95 lifetimes extending from hours to several months,

202 tamatergic synapses, the scaffolding protein PSD95 links the neuronal isoform of nitric-oxide synthas

203 aging in two color channels allowed to probe PSD95 localization relative to the spine head morphology

204 n interactions (eg, postsynaptic density 95 (PSD95)), may drive the predisposition to inherent impuls

205 While PSD95-mediated clustering was subunit independent, selec

206 These data identify PSD95 nanoclusters as a basic structural unit, or buildi

207 sub-regions revealed they comprised discrete PSD95 nanoclusters that were spatially organised into si

208 The topography of the PSD95 nanoorganization was more dynamic after environmen

209 pathway of PDZ3, the third PDZ domain of the PSD95 neuronal protein, is populated by a trimeric beta-

210 ting the interaction of tau with Fyn and the PSD95-NMDA receptor complex.

211 stsynaptic sites where it interacts with the PSD95-NMDA receptor complex.

212 by regulating its ability to associate with PSD95/NMDA receptor complexes.

213 overexpression of CAPON results in a loss of PSD95/nNOS complexes in transfected cells.

214 , APP, apolipoprotein E, the synaptic marker PSD95 (now known as DLG4), the astrocyte marker GFAP, ot

215 usly superresolve the dynamics of endogenous PSD95 of the post-synaptic density and spine geometry in

216 out mice, with no change in GluA2/3, VGluT1, PSD95 or synaptophysin.

217 either the postsynaptic density (PSD) marker PSD95 or the presynaptic protein synaptophysin, as contr

218 ns, possessing either a palmitoylation site (PSD95) or an L27 domain (SAP97).

219 turnover on postsynaptic density protein 95 (PSD95) or N-Ras.

220 sms that (dys)regulate transcription of Dlg4/PSD95, or other plasticity genes, are largely unknown, l

221 PSD95 oriented perpendicular to the PSD membrane, with i

222 relatively conserved across all sub-regions, PSD95 packing into nanoclusters also varied between sub-

223 Changing PSD95 palmitoylation in PSDs altered PSD95 and AMPAR lev

224 e consistent with differential regulation of PSD95 palmitoylation in PSDs resulting from the clusteri

225 These results indicate that in PSDs, PSD95 palmitoylation, conformation, and its interactions

226 ino acids in the Kir2.1 tail associated with PSD95 PDZ1,2 by NMR spectroscopy, revealing that a stret

227 Delta414-424, completely disrupts binding to PSD95 PDZ1,2.

228 uffices to switch the binding specificity of PSD95(pdz3) quantitatively towards a class-switching lig

229 Using a PDZ domain (PSD95(pdz3)) model system, we show that sector positions

230 comprising postsynaptic density protein 95 (PSD95), PKA and its anchor AKAP150, and protein phosphot

231 structures was accompanied by appearance of PSD95-positive debris that colocalized with the processe

232 unofluorescent staining showed a 28% loss of PSD95-positive excitatory postsynaptic puncta in hippoca

233 der neurons as well as increased VGlut2- and PSD95-positive puncta, indicative of increased excitator

234 tment with PAFR antagonist BN52021 prevented PSD95-positive synapse loss in hippocampi of mice with E

235 receptor subunits GluR2 or GluR2/3 or of the PSD95 (postsynaptic density 95) family scaffolding prote

236 PSD95 (postsynaptic density protein), mGluR6 (metabotrop

237 Antisense-mediated knockdown of PSD95 profoundly reduced K(V)1 channel expression and su

238 with and stabilizes the scaffolding protein PSD95, promoting dendritic spine maturation.

239 in, TCF1, LEF1, Cyclin D1, c-myc, Wnt7a, and PSD95 protein levels 4 h later.

240 evidenced by augmented spine density, higher PSD95 protein levels, and larger miniature EPSCs.

241 replacement was slowest in the cortex, where PSD95 protein lifetime is longest.

242 We show that DLG4 (PSD95) protein is synthesised by microglia in immature m

243 DLG4 encodes postsynaptic density-95 (PSD95) protein, which plays critical roles in the format

244 DLG4, encoding the postsynaptic density-95 (PSD95) protein.

245 n conjunction with decreased neurite number, PSD95-protein levels and glutamate receptor expression.

246 rtex by reducing phosphorylation of CREB and PSD95 proteins after TBI.

247 Expression of Gad67, Nmdar1 and Psd95 proteins are also reduced.

248 In contrast, puncta levels of VGlut1 and PSD95 proteins were higher in postpubertal monkeys and p

249 rter 1 (VGlut1) and postsynaptic density 95 (PSD95) proteins were quantified to assess variability in

250 or the NMDA receptor associated PSD proteins PSD95, PSD93, NF-L, and SAP102 in subjects with schizoph

251 The related MAGUKs SAP90/PSD95, PSD93/chapsyn-110, SAP97, and SAP102 all bound to

252 nrandom interval consistent with that of the PSD95 puncta on ganglion cells.

253 inor-to-major variant ratios predicted lower PSD95+ puncta density on PV interneurons.

254 Mean density of VGlut1+/PSD95+ puncta on PV+ neurons predicted the activity-depe

255 Mean density of VGlut1+/PSD95+ puncta on PV+ neurons was 18% lower in schizophre

256 lut1+) and postsynaptic density 95-positive (PSD95+) puncta, on PV interneurons was lower in postpube

257 nd postsynaptic density protein 95-positive [PSD95+] puncta) per surface area of parvalbumin-positive

258 Thus, the presence of a PSD95 punctum creates a nearby zone from which other inp

259 Veli-2, and the third PDZ domain of SAP97, a PSD95-related protein.

260 PSD95 remained tethered to presynaptic terminals in Veza

261 taining for the postsynaptic density protein PSD95 revealed that spines with high pPAK or pCofilin le

262 on; the most well-characterized being PSD93, PSD95, SAP102, and NF-L.

263 o the intercellular junction proteins dlg-A, PSD95/SAP90, SAP97, Z01, and Z02 and that contains DHR-,

264 s of mature spines and postsynaptic proteins PSD95, SAP97, GluA1, AMPAR-mediated basal synaptic trans

265 K(V)1) channel is one key binding partner of PSD95 scaffolds in neurons.

266 GluR2 and the postsynaptic protein PSD95 show progressive colocalization in tissue from P10

267 s: 1) the linear density of synaptic inputs (PSD95 sites/linear mum) varied surprisingly little and s

268 Analysis of >14,000 synapses (represented by PSD95-stained excitatory synapses) shows that there is a

269 eta metabolism, the regional distribution of PSD95 strongly correlated with the regional pattern of a

270 of PSD95 subunits in vivo revealed that each PSD95 subunit was sequentially replaced over days and we

271 Time-stamping of PSD95 subunits in vivo revealed that each PSD95 subunit

272 Members of the postsynaptic density-95 (PSD95)/synapse-associated protein-90 (SAP90) family of s

273 C1alpha and TFAM and synaptic-synaptophysin, PSD95, synapsin 1, synaptobrevin 1, neurogranin, GAP43 a

274 1alpha, TFAM (biogenesis) and synaptophysin, PSD95, synapsin 1, synaptobrevin 1, neurogranin, GAP43 a

275 re assayed for the synaptic proteins, GAP43, PSD95, synaptophysin and SV2A, using western blots.

276 Remarkably, mGluR-dependent increase of PSD95 synthesis is abolished in neurons lacking Fxr2.

277 sociation with BACE1 and neprilysin, but not PSD95 that regionally associated with full-length amyloi

278 ed specifically with the third PDZ domain of PSD95, the sole PDZ domain of Veli-2, and the third PDZ

279 e enzyme by an intermediary adaptor protein, PSD95, through a unique PDZ-PDZ domain interaction betwe

280 rols the selective recruitment of GluN2A and PSD95 to this specific compartment.

281 data indicate that young SC LTP arises from PSD95 unsilencing of silent synapses, that unsilencing i

282 MT3LshRNA could partially rescue the APP and PSD95 up-regulation in DS cells.

283 We identified PSD95, Veli-2, and other PDZ domain-containing proteins

284 ed for immunostaining or Western blotting of PSD95, vGLUT1, vGAT, gephyrin, PV, and SST.

285 ction of the artificial transcription factor PSD95-VP64 rescued memory deficits in aged and Alzheimer

286 PSD95 was detected in cVSMCs and it co-immunoprecipitate

287 ither CBS or IL-1R, IL-1beta-induced loss of PSD95 was rescued along with a decrease in the level of

288 teraction of Ggamma13 with the PDZ domain of PSD95 was via the C-terminal CAAX tail of Ggamma13 (wher

289 ErbB4 with postsynaptic density protein 95 (PSD95) was significantly reduced in the brains of BACE1(

290 Since alpha1.2 contains a binding motif for PSD95, we explored the possibility that cVSMCs express P

291 eir associated postsynaptic membrane protein PSD95 were both increased in schizophrenia in CA3 tissue

292 The synaptic genes synaptophysin and PSD95 were up-regulated, and mitochondrial function was

293 ies but reduced immunolabeling intensity for PSD95) were found in the somatosensory cortex.

294 F1, LEF1, Cyclin D1, c-myc, Wnt7a, Wnt1, and PSD95) were measured in the dorsal hippocampus 5 min or

295 DA receptor subunits NR2A and -B, as well as PSD95, were tethered to the complex.

296 alized with clusters of the scaffold protein PSD95, which are generally of larger size than AMPAR nan

297 iated guanylate kinases (MAGUKs), SAP102 and PSD95, which form a scaffold for the ion-passing glutama

298 ariable patterning and most sheaths localize PSD95 with patterning similar to exocytosis site locatio

299 sity as determined by the co-localization of PSD95 with pre-synaptic marker VGLUT2 in vitro.

300 a Dlg4/PSD95 gene-targeting strategy: a Dlg4/PSD95 zinc finger DNA-binding domain was engineered and