ライフサイエンスコーパス: PSD

1 PSD ultrastructural features are also conserved.

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

3 PSDs are unusual decarboxylase containing a pyruvoyl pro

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

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

6 wn approach to simultaneously remove PSD-93, PSD-95, and SAP102, the MAGUKs previously shown to be re

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

8 based inhibitors of postsynaptic density-95 (PSD-95) can reduce ischemic brain damage and inflammator

9 cumbens for postsynaptic density protein 95 (PSD-95) and SAP90/PSD-95-associated protein 3, as well a

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

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

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

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

14 of synaptic postsynaptic density protein 95 (PSD-95).

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

16 ecifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent

17 teract with postsynaptic density protein-95 (PSD-95), a key scaffold protein that anchors NMDA recept

18 cking the guanylate kinase domain of PSD-95 (PSD-95(GK)), we analyzed the contribution of PSD-95 to f

19 d in cultured hippocampal cells expressing a PSD-95 mutant unable to undergo prolyl-isomerization, th

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

21 scover that SynGAP, one of the most abundant PSD proteins and a Ras/Rap GTPase activator, forms a hom

22 at PKC promotes synaptogenesis by activating PSD-95 phosphorylation directly through JNK1 and calcium

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

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

25 opment to regulate AMPA receptor (AMPAR) and PSD-95 content at excitatory synapses.

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

27 creased overlap between immunostained AZ and PSD markers; in contrast, the SVZ-AZ spatial coupling is

28 tor dependent persistent changes of CDK5 and PSD-95 protein levels specifically within the stimulated

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

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

31 ive rpS6 phosphorylation, spine density, and PSD-95 expression.

32 th postsynaptic glutamate receptor GluA4 and PSD-95 clusters was significantly impaired in du/du mice

33 conclusion, Rph3A interacts with GluN2A and PSD-95 forming a complex that regulates NMDARs stabiliza

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

35 The MD and PSD.

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

37 nvestigated the relationship between PKC and PSD-95.

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

39 nt effects (p<0.05) on the particle size and PSD.

40 tial functional interaction between STEP and PSD-95.

41 (APP) metabolism, synaptic markers (SV2 and PSD-95), and targets of Fyn (Pyk2 and Tau) were studied

42 king of the synaptic proteins Syntaxin1a and PSD-95 and the TrkB and DCC receptors in Munc18-1(-/-) n

43 tic tectal neurons coexpressing tdTomato and PSD-95-GFP revealed that neurons were morphologically si

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

45 d depletes the number of membrane-associated PSD-95-like vertical filaments and transmembrane structu

46 that influence the size of their associated PSDs.

47 ion reveals that the distance between the AZ-PSD distance is decreased by 30 nm, while electron micro

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

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

50 ibit reduced protein levels of the canonical PSD component PSD-95 in the brain, which stems from prot

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

52 rotein levels of the canonical PSD component PSD-95 in the brain, which stems from protein destabiliz

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

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

55 Activation of the Mdm2 pathway degrades PSD-95, a scaffolding protein that clusters NMDARs at th

56 Postsynaptic densities (PSDs) are membrane semi-enclosed, submicron protein-enri

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

58 EphA7 essentially in postsynaptic densities (PSDs) of dendritic spines and shafts, and on some astroc

59 ciated with isolated postsynaptic densities (PSDs) suggests the PSD-associated postsynaptic plasma me

60 tion in vitro and in postsynaptic densities (PSDs) using FRET and EM, and examined how conformation r

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

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

63 and a thinning of the postsynaptic density (PSD) at hippocampal synapses.

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

65 e receptors within the postsynaptic density (PSD) determine excitatory synaptic strength.

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

67 ation of PSD-95 to the postsynaptic density (PSD) is known to lead to synaptic maturation and strengt

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

69 ere was an increase in postsynaptic density (PSD) thickness and an upregulation of GluA3 AMPA recepto

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

71 receptor complexes in postsynaptic density (PSD) were in fact increased in schizophrenia cases.

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

73 ed GluA1 levels at the postsynaptic density (PSD), but did not affect extrasynaptic sites.

74 itic spine density and postsynaptic density (PSD)-95 and spinophilin-positive clusters in the cortex

75 , active zone (AZ) and postsynaptic density (PSD).

76 those involved in the postsynaptic density (PSD).

77 Power spectral density (PSD) analysis reveals chaotic oscillations that are cons

78 The slope of the power spectral density (PSD) of the optical fluctuations was calculated to deter

79 ine head diameter and post synaptic density (PSD) area, as well as an increase in overall synapse den

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

81 5 deubiquitination, mobilizing and depleting PSD-95 from synapses.

82 Poststroke depression (PSD) has been recognized by psychiatrists for more than

83 Post stroke depression (PSD) is one of the most common complications of ischemic

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

85 gm and exploiting phase sensitive detection (PSD).

86 (+/-1.2) dB and pattern standard deviation (PSD) 1.6 (+/-0.3) dB (group I), and 36 eyes had VF defec

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

88 nges in mean and pattern standard deviation (PSD) from the mean baseline fields were compared between

89 as defined by VF pattern standard deviation (PSD) or glaucoma hemifield test (GHT) outside normal lim

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

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

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

93 Herein, the particle size distribution (PSD) of aluminium oxyhydroxide and aluminium hydroxyphos

94 article size and particle size distribution (PSD) of the nanodispersions were investigated.

95 Particle size distributions (PSDs) of the expectorated boluses were measured by using

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

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

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

99 We show that the Plasmodium falciparum PSD can restore the essential function of the yeast gene

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

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

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

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

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

105 Our findings support a dual role for PSD-95 in stabilizing synaptic NMDARs by binding directl

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

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

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

109 Collectively, these data identify PSD-95 in the IL as a critical mechanism supporting the

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

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

112 binding, Pin1 triggers structural changes in PSD-95, thus negatively affecting its ability to interac

113 nockdown of PSD-95 or in vivo as detected in PSD-95-KO mice, demonstrating that PSD-95 excludes STEP6

114 inally, the experience-dependent increase in PSD-95 is prevented by antagonism of the mGluR5 receptor

115 tein that anchors NMDA receptors (NMDARs) in PSD via GluN2-type receptor subunits.

116 Elimination of the serine 295 residue in PSD-95 abolished PKC-induced membrane accumulation.

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

118 bumin-positive interneurons was unaltered in PSD-95 KO mice.

119 SD-95 are present in higher concentration in PSDs isolated from mice with a heterozygous deletion of

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

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

122 Changing PSD95 palmitoylation in PSDs altered PSD95 and AMPAR levels but did not affect N

123 ential regulation of PSD95 palmitoylation in PSDs resulting from the clustering of palmitoylating and

124 calization of EphA7, being preferentially in PSDs, and in perisynaptic astrocytic leaflets, provides

125 These results indicate that in PSDs, PSD95 palmitoylation, conformation, and its intera

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

127 variations (n = 15; 2 subjects withdrew) in PSDs of both NA and RA samples were small (e.g., laser d

128 aptic vesicle density, and greatly increased PSD-95 clustering.

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

130 weeks from the fourth day after MCAO induced PSD-like depressive phenotypes in mice.

131 ocampal primary neurons blocks NMDAR-induced PSD-95 down-regulation and AMPAR endocytosis.

132 ked dimeric ligands, which potently inhibits PSD-95 and shows improved in vitro blood plasma stabilit

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

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

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

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

137 ether with increases in the synaptic markers PSD-95 and Vglut1.

138 c cleavage reaction to give rise to a mature PSD harboring a pyruvoyl prosthetic group.

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

140 PSD-associated postsynaptic plasma membrane (PSD-PM) as one specific location of synaptic remodeling.

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

142 ion of BAI1 with MDM2 in the brain modulates PSD-95 levels and thereby regulates synaptic plasticity.

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

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

145 organised into single and multi-nanocluster PSDs.

146 l particle sizes (72.88-142.85nm) and narrow PSDs (polydispersity index<0.40).

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

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

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

150 Therefore, it is possible that the NR2A/PSD-95 signaling complex has a role in adolescent MS eff

151 Accumulation of PSD-95 to the postsynaptic density (PSD) is known to lea

152 activator-mediated membrane accumulation of PSD-95.

153 complex in part via the anchoring action of PSD-95, in which they constitutively affect each other's

154 The activity of PSD-95 is tightly controlled by several post-translation

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

156 , and sought to identify the neural basis of PSD-95-mediated memory maintenance using ex vivo immedia

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

158 Comparison of PSD sequences across multiple phyla reveals a uniquely c

159 PSD-95(GK)), we analyzed the contribution of PSD-95 to fear memory formation and retrieval, and sough

160 homo-trimer and binds to multiple copies of PSD-95.

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

162 mouse lacking the guanylate kinase domain of PSD-95 (PSD-95(GK)), we analyzed the contribution of PSD

163 ing proteins that bind to the PDZ domains of PSD-95 are present in higher concentration in PSDs isola

164 e PDZ (PSD-95, Discs-large, ZO-1) domains of PSD-95, the principal PSD scaffold, and can occupy as ma

165 by restricting binding to the PDZ domains of PSD-95.

166 PSD-95 inhibitors and further exploration of PSD-95 as a drug target.

167 kinase II and also by inducing expression of PSD-95 and synaptophysin.

168 The failure of PSD-95(GK) mice to retrieve remote cued fear memory was

169 l for phase-transition-mediated formation of PSD.

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

171 ants significantly decrease the incidence of PSD compared with placebo.

172 developmental maturation was independent of PSD-95.

173 geting membrane biogenesis via inhibition of PSD activity.

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

175 rovides a new model for the investigation of PSD.

176 on in the PSD is increased upon knockdown of PSD-95 or in vivo as detected in PSD-95-KO mice, demonst

177 oth the neuronal MT network and the level of PSD-93 in neurons of the mammalian brain.

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

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

180 Loss of PSD-95 in the visual cortex after the closure of the cri

181 Further elucidation of the mechanism of PSD may ultimately lead to specific targeted treatments.

182 ress in understanding the pathophysiology of PSD.

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

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

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

186 e length but positively with the presence of PSD-95.

187 ndomized controlled trials for prevention of PSD have shown that antidepressants significantly decrea

188 have been in the treatment and prevention of PSD.

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

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

191 Restoration of PSD-95 expression in hippocampal neurons in BAI1-deficie

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

193 s the synaptic localization and stability of PSD-95 and links these events to changes in neuronal act

194 ockdown of PKC also reduced the synthesis of PSD-95 and the presynaptic protein synaptophysin by 30 a

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

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

197 nd miR-125a in regulating the translation of PSD-95 mRNA.

198 Early antidepressant treatment of PSD appears to enhance both physical and cognitive recov

199 mized controlled trials for the treatment of PSD have demonstrated the efficacy of antidepressants.

200 s can facilitate new pharmacological uses of PSD-95 inhibitors and further exploration of PSD-95 as a

201 roximately 10-40 times higher frequencies of PSDs, on their shafts and spines.

202 rmation and activity-dependent modulation of PSDs is considered as one of the most basic molecular ev

203 r of silent synapses, diminishes the size of PSDs without changes in pre- or postsynaptic membrane, a

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

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

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

207 , thus indicating that the action of Pin1 on PSD-95 is critical for this effect.

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

209 significant deterioration sooner than VFI or PSD.

210 that STEP61 binds to PSD-95 but not to other PSD-95 family members.

211 ed increased levels of serum cortisol in our PSD mice.

212 ture that are similar to mice overexpressing PSD-95, a major scaffolding protein of postsynaptic dens

213 mulation of PKC and phosphorylated PSD-95 (p-PSD-95(S295)) coincided with an increased number of syna

214 and inducible counterparts, displays a PDZ (PSD-95/Dlg/ZO-1) domain located at its N terminus involv

215 Its alpha1 isoform binds to all three PDZ (PSD-95, Discs-large, ZO-1) domains of PSD-95, the princi

216 brane accumulation of PKC and phosphorylated PSD-95 (p-PSD-95(S295)) coincided with an increased numb

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

218 We used the essential role of Plasmodium PSD in yeast as a tool for screening a library of anti-m

219 epresent a potential strategy for preventing PSD.

220 We determined that BAI1 prevents PSD-95 polyubiquitination and degradation through an int

221 arge, ZO-1) domains of PSD-95, the principal PSD scaffold, and can occupy as many as 15% of these PDZ

222 or association with the postsynaptic protein PSD-95.

223 ts association with the postsynaptic protein PSD-95.

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

225 tner of the postsynaptic scaffolding protein PSD-95 and AMPA glutamate receptors (AMPARs).

226 o impaired synthesis of the synaptic protein PSD-95, suggesting that this phenomenon contributes to s

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

228 ression of the synaptic scaffolding proteins PSD-95 and SAP90/PSD-95-associated protein 3.

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

230 DM2), the E3 ubiquitin ligase that regulates PSD-95 stability.

231 knockdown approach to simultaneously remove PSD-93, PSD-95, and SAP102, the MAGUKs previously shown

232 IgSF11 required PSD-95 binding for its excitatory synaptic localization.

233 ction of the yeast gene in strains requiring PSD for growth.

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

235 naptic density protein 95 (PSD-95) and SAP90/PSD-95-associated protein 3, as well as the levels of ph

236 naptic scaffolding proteins PSD-95 and SAP90/PSD-95-associated protein 3.

237 n of the plasma membrane-associated scaffold PSD-95, which allows for transport of receptors to the p

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

239 and interacted directly with and stabilized PSD-95 at synapses.

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

241 The multivalent nature of the SynGAP/PSD-95 complex is critical for the phase separation to o

242 tected in PSD-95-KO mice, demonstrating that PSD-95 excludes STEP61 from the PSD.

243 We find that PSD-95 expression destabilizes STEP61 via ubiquitination

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

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

246 These findings reveal not only that PSD-95-dependent silent synapse maturation in visual cor

247 We show that PSD-95 is dispensable for the formation and expression o

248 idue within a GS(S/T) motif, suggesting that PSDs belong to the D-H-S serine protease family.

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

250 ing both types of glutamate receptors at the PSD and are consistent with a structural model where MAG

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

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

253 dynamic anchoring mechanism of SynGAP at the PSD, our results also suggest a model for phase-transiti

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

255 trating that PSD-95 excludes STEP61 from the PSD.

256 tivity-dependent SynGAP dispersions from the PSD.

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

258 Scaffold proteins in the PSD are abundant receptor binding partners, yet electron

259 phosphorylated at Ser-773 and Ser-802 in the PSD fraction, and its phosphorylation by CDK5 and CaMKII

260 tion, we detect low amounts of STEP61 in the PSD fraction.

261 that dysregulation of genes involved in the PSD is a key factor in the pathogenesis of BD.

262 However, STEP61 expression in the PSD is increased upon knockdown of PSD-95 or in vivo as

263 rinergic modulation of NMDA receptors in the PSD-95 mutants dramatically decreased the threshold of L

264 nsistent with low STEP61 localization in the PSD.

265 e the abundance of specific molecules in the PSD.

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

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

268 nGAP-alpha1 regulates the composition of the PSD by restricting binding to the PDZ domains of PSD-95.

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

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

271 at Egr-1 is a transcription repressor of the PSD-95 gene and is recruited to the PSD-95 promoter in r

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

273 ated liquid-like droplets reminiscent of the PSD.

274 rn the overall molecular organization of the PSD.

275 interactions involving Agap2 outside of the PSD.

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

277 d postsynaptic densities (PSDs) suggests the PSD-associated postsynaptic plasma membrane (PSD-PM) as

278 s, yet electron microscopy suggests that the PSD is highly crowded, potentially restricting the diffu

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

280 PSD95 oriented perpendicular to the PSD membrane, with its palmitoylated, N-terminal domain

281 r of the PSD-95 gene and is recruited to the PSD-95 promoter in response to NMDAR activation.

282 levels and developmental integration to the PSD.

283 y is formed in a concerted reaction when the PSD proenzyme undergoes an endoproteolytic cleavage into

284 Moreover, tight protein packing within the PSD may modulate the synaptic dwell time of many TM prot

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

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

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

288 We now report that STEP61 binds to PSD-95 but not to other PSD-95 family members.

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

290 Binding of SynGAP to PSD-95 induces phase separation of the complex, forming

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

292 inferior NFL quadrant thickness, age, and VF PSD.

293 Pin1 controls synaptic content of NMDARs via PSD-95 prolyl-isomerization and the expression of dendri

294 These results define the mechanism whereby PSDs begin their biochemical existence as proteases that

295 racts with GluN2A(1349-1389) as well as with PSD-95(PDZ3) domains, creating a ternary complex.

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

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

298 dent de-phosphorylation and interaction with PSD-95 multi-protein complex.

299 ity through its tripartite interactions with PSD-95 and AMPARs.

300 Finally, we found that mice with PSD were responsive to the tri-cyclic antidepressant imi

301 Within PSDs, PSD95 and SAP97 were largely in the extended confo