ライフサイエンスコーパス: PSD

1 PSD activity can easily be quantified by sequential reag

2 PSD activity has typically been quantified using radioac

3 PSD ultrastructural features are also conserved.

4 PSD-95 disruption has recently been associated with neur

5 PSD-95 is a member of the membrane-associated guanylate

6 PSD-95 is a scaffolding protein that regulates the synap

7 PSD-95 is directly implicated in modulating the electric

8 PSD-95 MAGUK family scaffold proteins are multi-domain o

9 PSD-95 was reduced in the brainstem, basal ganglia, neoc

10 PSD-95, a membrane-associated guanylate kinase, is the m

11 PSDs receiving VGLUT1 inputs also show enhanced nanostru

12 significant correlation with MD (P = 0.007), PSD (P = 0.02), VFI (P = 0.03), and average RNFL thickne

13 The 115 PSD(C24-2) and PSD(10-2) values were significantly corre

14 which generally show reductions in SNAP-25, PSD-95, synapsin and rab3A protein levels in the hippoca

15 mporal cortices, and no changes for SNAP-25, PSD-95, VAMP, and syntaxin in frontal cortex.

16 Therefore, the Kv1.3/PSD-95 association fine-tunes the anti-inflammatory resp

17 28% underwent pancreaticoduodenectomy, 61% PSD, and 11% segmental duodenectomy.

18 find that the postsynaptic proteins PSD-93, PSD-95, and SAP102 differentially regulate excitatory sy

19 Postsynaptic density 95 (PSD-95) is a major synaptic scaffolding protein that pla

20 olfactory cortex, post synaptic density-95 (PSD-95) (p < 0.05), growth associated protein 43 (GAP43)

21 subunit 2B (NR2B), postsynaptic density-95 (PSD-95) and microtubule-associated protein 1A (MAP1A) in

22 is associated with postsynaptic density-95 (PSD-95)-positive synaptosomes, indicating that remaining

23 increase in postsynaptic density protein 95 (PSD-95) by overexpression caused correlated increases in

24 ing protein postsynaptic density protein 95 (PSD-95) stabilizes the surface expression of NMDARs.

25 Postsynaptic density protein 95 (PSD-95), a member of the MAGUK family, recruits Kv1.3 in

26 ld protein, postsynaptic density protein 95 (PSD-95), a process that is deficient in the mouse model

27 Postsynaptic density protein-95 (PSD-95) is a major regulator in the maturation of excita

28 Postsynaptic density protein-95 (PSD-95) localizes AMPA-type glutamate receptors (AMPARs)

29 e heterotrimeric G protein subunit Gnb5 as a PSD-95 complex partner at dendritic spines of rat hippoc

30 dixin-moesin-binding phosphoprotein 50) is a PSD-95, disc large, zona occludens-1 adapter that acts a

31 Using a PSD-95 knockout mouse model (PSD-95(-/-)), we examined h

32 ynapse and illustrate a mechanism by which a PSD-associated K63-linkage-specific ubiquitin machinery

33 y risk factors at embryonic day 14 and adult PSD in mice.

34 b polyps were large (>20 mm) and found after PSD.

35 tified as inhibiting both native C. albicans PSD mitochondrial activity and C. albicans growth, with

36 5) in the cerebellum, and SYP (p < 0.05) and PSD-95 (p < 0.05) in the brainstem.

37 The 115 PSD(C24-2) and PSD(10-2) values were significantly correlated (Spearman

38 oteins (viz., GluR1, GluR4, NR1, PSD-95, and PSD-93), that TH cell somata and tapering neurites are a

39 many synaptic proteins, including AMPARs and PSD-95.

40 creases both pyramidal cell arborization and PSD-95 expression in the cortex of WT but not MMP-9-null

41 ad VF defects with MD -13.7 (+/-10.4) dB and PSD 7.2 (+/-3.6) dB (group II).

42 a significant reduction in spine density and PSD-95-positive synaptic puncta, a reduction of persiste

43 declines in synaptophysin, synapsin II, and PSD-95, whereas reduction in GluR1 was slower and NeuN a

44 effect of unreliable responses on the MD and PSD in SAP.

45 molecular mechanism that regulates NLGN1 and PSD-95 binding and provides insights into excitatory syn

46 We now show that disruption of the NLGN1 and PSD-95 interaction decreases surface expression of NLGN1

47 l-d-aspartate receptor subunit 2B (NR2B) and PSD-95.

48 the PDZ domain scaffold proteins, PICK1 and PSD-95, and their cognate transmembrane binding partners

49 d synaptic levels of glutamate receptors and PSD-95.

50 Using stargazin and PSD-95 as the representatives, we discover that the enti

51 excitatory synapse markers synaptophysin and PSD-95, and significant maturation of AMPA receptor syna

52 and synaptic accumulation of Mdm2 as well as PSD-95 degradation and synapse elimination.

53 that influence the size of their associated PSDs.

54 Behaviorally, PSD-95(-/-) mice exhibit a lack of sociability, as well

55 mutation facilitates the interaction between PSD-95 and its binding partners.

56 forms the next step before going to bimodal PSD estimates.

57 n contrast, SynGAP-beta, which does not bind PSD-95 PDZ domains, is less synaptically targeted and pr

58 e levels of other key PSD proteins that bind PSD-95, although the level of PSD-95 remains constant (W

59 Pin1 recruitment by PSD-95 occurs at specific serine-threonine/proline conse

60 tivity decreases SH3-GK interaction, causing PSD-95 to adopt an open conformation.

61 ived, elongated, and associated with complex PSDs.

62 Long-lived spinules often contained PSD fragments, contacted distal presynaptic terminals, a

63 By interacting with PSD-95, Pin1 dampens PSD-95 ability to complex with NMDARs, thus negatively a

64 Phosphatidylserine decarboxylases (PSDs) are central enzymes in phospholipid metabolism tha

65 Phosphatidylserine decarboxylases (PSDs) catalyze the conversion of phosphatidylserine (PS)

66 Phosphatidylserine decarboxylases (PSDs) catalyze the decarboxylation of phosphatidylserine

67 ry, the estimation routine proved to deliver PSD estimates in line with the reference measurements fo

68 0 accumulates at the postsynaptic densities (PSDs) and causes excessive cleavage of the synaptic prot

69 major constituent of postsynaptic densities (PSDs) from mammalian forebrain.

70 n aggregates such as postsynaptic densities (PSDs) in excitatory synapses and in other dense protein

71 visualise excitatory postsynaptic densities (PSDs) using high-resolution and super-resolution microsc

72 osed by one to three postsynaptic densities (PSDs).

73 ide of, and within, post-synaptic densities (PSDs) from rats.

74 r genes located to the postsynaptic density (PSD) (all Bonferroni corrected p < 0.05).

75 ergic signaling in the postsynaptic density (PSD) as a pathophysiologic mechanism in schizophrenia.

76 The postsynaptic density (PSD) contains a collection of scaffold proteins used for

77 el mRNA and protein in postsynaptic density (PSD) fractions of the hippocampus, a brain region involv

78 of Bbs proteins in the postsynaptic density (PSD) of hippocampal neurons.

79 SynGAP is a postsynaptic density (PSD) protein that binds to PDZ domains of the scaffold p

80 Postsynaptic density (PSD) proteins have been implicated in the pathophysiolog

81 es encoding inhibitory postsynaptic density (PSD) proteins, but not for genes implicated in monogenet

82 oteome complexity, the postsynaptic density (PSD) proteome of zebrafish has lower complexity than mam

83 les concentrate at the postsynaptic density (PSD) to regulate synaptic strength.

84 n to be present at the postsynaptic density (PSD) within excitatory glutamatergic neurons and regulat

85 enesis along with thin postsynaptic density (PSD), and reduced synaptic transmission of pyramidal neu

86 al organization of the postsynaptic density (PSD), deletion of both CAMK2 isoforms did not affect the

87 phosphorylation in the postsynaptic density (PSD).

88 ta-to-gamma relative power spectral density (PSD) ratio to the history of concussion in 81 youth athl

89 At the post-synaptic density (PSD), large protein complexes dynamically form and disso

90 e WAVE complex to the post-synaptic density (PSD), which is critical for synapse and dendritic spine

91 ization of CARM1 with post-synaptic density (PSD)-95 protein, a post-synaptic marker.

92 5 deubiquitination, mobilizing and depleting PSD-95 from synapses.

93 yielded premature habituation and depressed PSD-LTM.

94 fective for treating post-stroke depression (PSD).

95 ysis and applying phase-sensitive detection (PSD), which suppresses the features of inactive surface

96 gm and exploiting phase sensitive detection (PSD).

97 (+/-1.2) dB and pattern standard deviation (PSD) 1.6 (+/-0.3) dB (group I), and 36 eyes had VF defec

98 viation (MD) and pattern standard deviation (PSD) between the two groups (p >/= 0.05).

99 ecently proposed pattern standard deviation (PSD) metric, based upon the 24-2 visual field (VF) test,

100 deviation (MD), pattern standard deviation (PSD), and mean VF sectoral pattern deviation (PD) from S

101 deviation (MD), pattern standard deviation (PSD), and visual field index (VFI)).

102 deviation (MD), pattern standard deviation (PSD), and visual field index (VFI).

103 deviation (MD), pattern standard deviation (PSD), and visual field index (VFI).

104 viation (MD) and pattern standard deviation (PSD), were analyzed with multivariable regression models

105 (MD, r = 0.79), pattern standard deviation (PSD, r = 0.60), and number of locations that were worse

106 ) module, a polarization selective diffuser (PSD), and a slanted projection system.

107 The particle size distribution (PSD) and the stability of nanoparticles enabled medicina

108 A particle size distribution (PSD) estimation method based on light-scattering propert

109 he time-resolved particle size distribution (PSD) in a typical room environment could be predicted we

110 nformation-laden particle-size distribution (PSD) including its shape.

111 of the model are particle size distribution (PSD), bulk density, and residual water content at water

112 s were dominated by SD/pseudo-single-domain (PSD) particles.

113 g approach of pancreas-sparing duodenectomy (PSD) is preferred.

114 Post stroke dysphagia (PSD) is common and associated with poor outcome.

115 The four other subfamilies (EFA6/PSD, IQSEC7/BRAG, FBX8, and TBS) are opisthokont, holozo

116 nced the consolidation of ARM, it eliminated PSD-LTM.

117 oreover, molecular replacement of endogenous PSD-95 with the S561A mutant blocks dendritic spine stru

118 by phosphatidylserine decarboxylase enzymes (PSD) as a suitable target for development of antimicrobi

119 discriminating power, resulting in erroneous PSD estimates.

120 brain disorders or genes encoding excitatory PSD proteins.

121 For PSD, the median was 10.5 years (95% CI 9.3-11.7 years),

122 eyes, vs 104 for VFI (P = .0013) and 107 for PSD (P = .029).

123 that expression of Dlg4 (the gene coding for PSD-95) was strongly reduced after two days of forced sw

124 We used immunostaining for PSD-95 and gephyrin postsynaptic scaffolding proteins as

125 undwork for screening chemical libraries for PSD inhibitors.

126 minute-2 (Mdm2), the ubiquitin E3 ligase for PSD-95, which results in nuclear export and synaptic acc

127 AF6) is identified as a direct E3 ligase for PSD-95, which, together with the E2 complex Ubc13/Uev1a,

128 es straightforward large-scale screening for PSD inhibitors against pathogenic fungi, antibiotic-resi

129 nt readouts in high-throughput screening for PSD inhibitors.

130 y adaptable to high-throughput screening for PSD inhibitors.

131 luorescence-based assay that is specific for PSD and in which the presence of PS causes only negligib

132 tsynaptic densities, cleaves K63-chains from PSD-95.

133 double integrating sphere measurements, good PSD estimates were obtained for particles >=1 mum.

134 extinction-dependent changes in hippocampal PSD CaMKII expression and S831 GluA1 phosphorylation.

135 rotein kinase II (CaMKII) to the hippocampal PSD.

136 t mouse model (PSD-95(-/-)), we examined how PSD-95 deficiency affects NMDAR and AMPAR expression and

137 We identify PSD-95 interactors that differentially bind to the SH3-G

138 under the P rofile of S hannon D ifference (PSD).

139 tively active ROCK enhanced ARM and impaired PSD-LTM, while decreasing ROCK activity rescued the enha

140 Raf enhanced ARM consolidation and impaired PSD-LTM.

141 ctural findings of conformational changes in PSD-95 and demonstrate how conformational transitions in

142 erlying structural and functional changes in PSD-95 that mediate its role in plasticity remain unclea

143 tributable to decreased GluN2B expression in PSD compartment and disruption of the Lnx1-NMDAR-EphB2 c

144 How MEF2 activation results in PSD-95 degradation and why this is defective in Fmr1 KO

145 Ds were diffusing in confined nanodomains in PSDs, which were stable for 15 min or longer.

146 AMPARs rapidly enter stable 'nanodomains' in PSDs with lifetime >15 min, and do not accumulate in ext

147 In contrast, 5-10% of bQD-AMPARs were in PSDs and 90-95% were extrasynaptic as previously observe

148 the phosphomimetic S561D mutation increases PSD-95 dynamics at the synapse.

149 The formation of ARM inhibits PSD-LTM but the underlying molecular processes that medi

150 h increased steady-state levels of other key PSD proteins that bind PSD-95, although the level of PSD

151 ding protein fusion with Plasmodium knowlesi PSD (MBP-His6-Delta34PkPSD) as the enzyme.

152 ching and transgenic mice expressing labeled PSD-95, we comparatively analyzed electrical and Ca(2+)

153 rkers in vivo reveal that 20% of spines lack PSD-95 and are short lived.

154 Like PSD-95, activity blockade in a rat hippocampal slice cul

155 aster store protein synthesis-dependent LTM (PSD-LTM) as well as protein synthesis-independent, anest

156 er measurements could not represent the main PSD characteristics (e.g., particle diameter mode).

157 Clusters of synaptic markers, PSD-95 and synaptophysin, were also recovered in 5xF:pGB

158 For predicting MD, PSD, and mean sectoral PD, models were evaluated using R

159 enzene-bis-aldehyde (DSB-3) assay to measure PSD activity in vitro have laid the groundwork for scree

160 NMDA receptors, drives rapid, CYLD-mediated PSD-95 deubiquitination, mobilizing and depleting PSD-95

161 rotein synthesis-dependent long-term memory (PSD-LTM), but not anesthesia-resistant memory.

162 Using a PSD-95 knockout mouse model (PSD-95(-/-)), we examined how PSD-95 deficiency affects

163 polyubiquitination, which markedly modifies PSD-95's scaffolding potentials, enables its synaptic ta

164 equired to produce narrow, near-monodisperse PSDs.

165 Most PSDs are membrane-bound, and classical radioisotope-base

166 RBC dendrites expand, they form fewer multi-PSD contacts with rods.

167 hose protein product interacts with multiple PSD proteins.

168 Single RBCs often form multiple PSDs with one rod; and neighboring RBCs share 13% of the

169 organised into single and multi-nanocluster PSDs.

170 Instead, narrow PSDs can be and are achieved despite continuous nucleati

171 Nevertheless, PSD occurs in a significant number of patients and const

172 Impaired NLGN1/PSD-95 binding diminished synaptic NLGN1 expression and

173 Functional analysis of PSD and non-PSD interactomes illustrates both common and unique func

174 te central damage (CD) in G eyes with normal PSD(C24-2) values, a post hoc analysis was combined with

175 c density proteins (viz., GluR1, GluR4, NR1, PSD-95, and PSD-93), that TH cell somata and tapering ne

176 nd that inhibition of the impairment of NR2B/PSD-95/MAP1A pathway, may be a novel and preferential op

177 Functional analysis of PSD and non-PSD interactomes illustrates both common and

178 uld improve the depression-like behaviors of PSD mice and upregulate the expression of BDNF in the hi

179 PSDs, allowing an accelerated destruction of PSD-localized fragments by the ubiquitin/proteasome syst

180 arly loss of GluN1, prolonged development of PSD-95 and GluA2 into late childhood, protracted develop

181 ed PDZ(3) ligands to the third PDZ domain of PSD-95 induces functional changes in the intramolecular

182 ) ligands binding to the third PDZ domain of PSD-95, unraveling a hierarchical binding mechanism of P

183 /disks large/zona occludens (PDZ) domains of PSD-95 have been shown to be the key component in the fo

184 for scaffold formation by the PDZ domains of PSD-95.

185 However, the effects of PSD-95 deficiency on the prefrontal cortex (PFC)-associa

186 ARM consolidation, allowing the formation of PSD-LTM.

187 ation of ARM, which permits the formation of PSD-LTM.

188 orm the basis of the scaffolding function of PSD-95 and provide a detailed model for scaffold formati

189 2) of Bdnf promoter IV in the hippocampus of PSD mice.

190 This study highlights the importance of PSD-95 during neurodevelopment in the mPFC and its poten

191 Inhibition of PSD-95 induction following learning impairs both AMPA re

192 high-throughput screening for inhibitors of PSD enzymes across diverse phyla.

193 eins that bind PSD-95, although the level of PSD-95 remains constant (Walkup et al., 2016).

194 e serine 295 residue, increase the levels of PSD-95, and enhance its membrane localization.

195 inus of PSD-95 mediates postsynaptic loss of PSD-95 and AMPARs during homeostatic scaling down.

196 raveling a hierarchical binding mechanism of PSD-95 complex formation.

197 Here we show that phosphorylation of PSD-95 at Ser-561 in its guanylate kinase (GK) domain, w

198 r and bryostatin 1 induce phosphorylation of PSD-95 at the serine 295 residue, increase the levels of

199 clonal resolution using the change point of PSD detected by multivariate adaptive regression splines

200 Bassoon puncta, together with a reduction of PSD-95 levels at dendritic spines, suggesting a reduced

201 l mechanistic insight into the regulation of PSD-95 in dendritic spine structural plasticity through

202 size and number of NR2B and cluster size of PSD-95.

203 in (Ca(2+)/CaM) binding to the N-terminus of PSD-95 mediates postsynaptic loss of PSD-95 and AMPARs d

204 gephyrin puncta increasing to match that of PSD-95 puncta at the larval stage.

205 Expansion of PSDs would alter electrochemistry of synapses, thereby c

206 volves a partial and reversible expansion of PSDs, allowing an accelerated destruction of PSD-localiz

207 y prevented the effects of PKC activators on PSD-95 phosphorylation.

208 complex Ubc13/Uev1a, assembles K63-chains on PSD-95.

209 The effect of FPs on PSD was observed only when FP rate was <15% (beta = -0.2

210 conserved in TARPs bind to multiple sites on PSD-95, thus resulting in a highly specific and multival

211 AR entry is limited by the occupancy of open PSD 'slots', our findings suggest that AMPARs rapidly en

212 Stargazin in complex with PSD-95 or PSD-95-assembled postsynaptic complexes form highly conc

213 significant deterioration sooner than VFI or PSD.

214 esection, including pancreaticoduodenectomy, PSD, or segmental duodenectomy, at Cleveland Clinic.

215 PKC directly phosphorylated PSD-95 and JNK1 in vitro Inhibiting PKC, JNK, or calcium

216 alyses to identify more selective and potent PSD inhibitors with antimicrobial or antitumor activitie

217 epresent a potential strategy for preventing PSD.

218 The postsynaptic density protein PSD-95 contains a three-domain supramodule, denoted PSG,

219 t GluN1 and the postsynaptic density protein PSD-95 in knockouts.

220 oylation of the immobilized scaffold protein PSD-95 nucleates domains at the postsynaptic plasma memb

221 binds to PDZ domains of the scaffold protein PSD-95.

222 ressing the postsynaptic scaffolding protein PSD-95, which increased receptor clustering.

223 ptic marker postsynaptic density 95 protein (PSD-95).

224 Here, we find that the postsynaptic proteins PSD-93, PSD-95, and SAP102 differentially regulate excit

225 d upregulation of the post-synaptic proteins PSD-95, SHANK3 and Homer-1b/c, as well as increased corr

226 set of postsynaptic glutamatergic proteins (PSD-95, GluA2, GluN1, GluN2A, GluN2B), calculated indice

227 mutation of NLGN1 S839 significantly reduced PSD-95 binding.

228 ar the PDZ ligand, and dynamically regulates PSD-95 binding.

229 ptic density and reduction of autism-related PSD-95 and Homer-1 in the hippocampus, which were missin

230 ults showed that the theta-to-gamma relative PSD ratio was significantly lower in the concussion hist

231 ession of a dephosphomimetic of Mdm2 rescues PSD-95 ubiquitination, degradation and synapse eliminati

232 We found that the postsynaptic scaffold PSD-95 (postsynaptic density protein 95) undergoes K63 p

233 mic, exploratory, and originated near simple PSDs, whereas a subset was long-lived, elongated, and as

234 protein) binding to alpha-actinin-stabilized PSD-95, and extracellular interactions through the recep

235 At both stages, PSD-95 puncta are enriched in the most lateral neuropil

236 a highly specific and multivalent stargazin/PSD-95 complex.

237 a phase separation, reminiscent of stargazin/PSD-95-mediated AMPAR synaptic clustering and trapping.

238 nd quantified viral (SIV gag RNA), synaptic (PSD-95; synaptophysin), axonal (neurofilament/neurofilam

239 The TARP_CT/PSD-95 interaction mode may have implications for unders

240 bulk density and residual water content than PSD parameters.

241 At the embryonic stage, we found that PSD-95 puncta outnumber gephyrin puncta, with the number

242 Together, our data indicate that PSD-95 deficiency disrupts mPFC synaptic function and re

243 It is known that PSD-95 shows increased dynamics upon induction of plasti

244 We report that PSDs are nanostructurally distinct between spinal lamina

245 Finally, we show that PSDs exhibit greater nanostructural complexity when part

246 The PSD(C24-2) missed 27 (61%) of these 44 eyes, and the PSD

247 The PSD(C24-2), based upon the central 12 points of the 24-2

248 The PSD-95 GK domain binds to Gnb5, and this interaction is

249 ncreased, vesicles were also larger, and the PSD of endbulb synapses was larger and thicker.

250 2) missed 27 (61%) of these 44 eyes, and the PSD(10-2) missed 23 (52%) of these eyes.

251 ical configuration of the PSL module and the PSD.

252 24-2 visual field (VF) test, as well as the PSD of the 10-2 VF, will miss central glaucomatous damag

253 ampal GluA1 levels remained unaltered at the PSD, but were reduced near the PSD and at perisynaptic s

254 of three interacting GAP/GEF proteins at the PSD, including the RasGAP Syngap1, the ArfGAP Agap2, and

255 erent from the number (22) identified by the PSD(10-2) (P = .15).

256 of G eyes (19) identified as abnormal by the PSD(C24-2) was not significantly different from the numb

257 esent study, we successfully established the PSD model using male C57BL/6 J mice by photothrombosis o

258 mber of AMPA-type glutamate receptors in the PSD and synaptic strength.

259 e the abundance of specific molecules in the PSD.

260 rate was <15%, higher FN rate increased the PSD (beta = 0.51 dB; P < 0.001), and the effect was slig

261 The use of detergents to isolate the PSD and release its membrane-associated proteins complic

262 a fluorescence-based assay that measures the PSD reaction using distyrylbenzene-bis-aldehyde (DSB-3),

263 ltered at the PSD, but were reduced near the PSD and at perisynaptic sites of dendritic spines in ext

264 Neither the PSD(C24-2) nor the PSD(10-2) metric is good measure of e

265 Neither the PSD(C24-2) nor the PSD(10-2) metric is good measure of early CD.

266 al a sex difference in the adaptation of the PSD scaffold to synGAP haploinsufficiency.

267 a unique cluster mainly at the center of the PSD, while AMPARs segregate in clusters surrounding the

268 elopment that promotes the clustering of the PSD-95 (postsynaptic density protein 95).

269 SAP102 is the main representative of the PSD-95 family of postsynaptic MAGUK proteins during earl

270 nds to PSD-95, although the relevance of the PSD-95 interaction is not clear.

271 Genetic deletion of the PSD-95 or P2X4 receptors obliterated ATP-mediated down-r

272 ot affect the biochemical composition of the PSD.

273 interactions involving Agap2 outside of the PSD.

274 with the MD, and had minimal effects on the PSD.

275 SAP97 oriented parallel to the PSD membrane, likely as a dimer through interactions of

276 levels and developmental integration to the PSD.

277 lution to the "inverse problem" in which the PSD informs one as to the correct particle formation mec

278 12 points of the 24-2, was compared with the PSD(10-2).

279 nstrained genes, as well as genes within the PSD and PI pathway harbor rare variation associated with

280 AP and GEF proteins are organized within the PSD signaling machinery, if they have overlapping intera

281 tructural analysis identified E17 within the PSD-95 N-terminus as important for binding to Ca(2+)/CaM

282 ease in TARP and a decrease in synGAP in the PSDs of Syngap1(+/-)rodents.

283 Here, we used the Tiam2 PSD-95/Dlg/ZO-1 (PDZ) domain and a quadruple mutant (QM)

284 receptors, but we found that its binding to PSD-95 was very weak, and deleting the PDZ-binding motif

285 targazin (Stg_CT) is required for binding to PSD-95.

286 ed reduced surface expression and binding to PSD-95.

287 ic cell adhesion molecule, and also binds to PSD-95, although the relevance of the PSD-95 interaction

288 ordingly, increased binding of Ca(2+)/CaM to PSD-95 induced by a chronic increase in Ca(2+) influx is

289 Integral to PSD glutamatergic signaling is reciprocal interplay betw

290 For example, the ratio to PSD-95 of Transmembrane AMPA-Receptor-associated Protein

291 binding of AMPA-type glutamate receptors to PSD-95, was increased in young Syngap1(+/-)mice.

292 CaMKII site, along with an increase in total PSD GluA1.

293 lating the catalytic activity of Pin1 toward PSD-95, facilitates NMDAR synaptic expression and functi

294 The first two PSD-95/disks large/zona occludens (PDZ) domains of PSD-9

295 Stargazin in complex with PSD-95 or PSD-95-assembled postsynaptic complexes form h

296 differential participation in complexes with PSD-95 and gephyrin, which may underlie its role in main

297 rich motif weakened TARP's condensation with PSD-95 and impaired TARP-mediated AMPAR synaptic transmi

298 By interacting with PSD-95, Pin1 dampens PSD-95 ability to complex with NMDA

299 is not widely available and also reacts with PSD's substrate, PS, producing an adduct with lower fluo

300 ndergoes liquid-liquid phase separation with PSD-95, is highly enriched in synapses and is required f