ライフサイエンスコーパス: homer

1 anslation of the synaptic proteins GluA1 and Homer.

2 1128R; mGlu5(R/R)) that abrogates binding to Homer.

3 AR subunit GluA1 and the scaffolding protein Homer.

4 eptides targeting the Shank interaction with Homer.

5 renin-1 and the postsynaptic adaptor protein Homer.

6 , we report that Shank proteins also bind to Homer.

7 tome, CTD, PharmGKB, DrugBank, PharmGKB, and HOMER.

8 ed with the postsynaptic scaffolding protein Homer.

9 a model to show that IP(3) and the scaffold Homer 1 (H1) regulate the rate of translocation and retr

10 Mice lacking Homer 1 exhibited a myopathy characterized by decreased

11 Moreover, diminished Homer 1 expression in mouse models of Duchenne's muscula

12 These findings provide direct evidence that Homer 1 functions as an important scaffold for TRP chann

13 Because the scaffolding protein Homer 1 has been implicated in TRP channel regulation, w

14 tion, a strong gene-gene interaction between homer 1 homolog (Drosophila) (HOMER1) and DRD1 was predi

15 Homer 1 knockout myotubes displayed increased basal curr

16 This spontaneous cation influx in Homer 1 knockout myotubes was blocked by reexpression of

17 e's muscular dystrophy suggests that loss of Homer 1 scaffolding of TRP channels may contribute to th

18 otagmin, glutamate receptors -1, -4, and -5, homer-1 and -2, and tenascin-R.

19 Expression of the Homer-1 mRNAs reaches 66% of the brain total Homer mRNAs

20 levels of the constitutive expression of the Homer-1, -2 and -3 mRNAs across mouse tissues.

21 that the molecular profile of expression of Homer-1, -2 and -3 mRNAs in muscle containing tissues re

22 constitutively expresses high levels of the Homer-1, -2 and -3 mRNAs.

23 e long and the short variants of each of the Homer-1, Homer-2 and Homer-3 proteins reflects the funda

24 Expression of the homer 1a (H1a) immediate-early gene produces a short hom

25 ription of the immediate-early genes Arc and Homer 1a (H1a) is dynamically regulated in response to s

26 rms of Homer, which cannot self-multimerize (Homer 1a and a Homer 2 C-terminal deletion), did not alt

27 ed expression of Group 1 mGluR-related genes Homer 1a and Arc.

28 In both cases, RNA silencing of Homer 1a but not control RNA interference treatment prev

29 These data demonstrate that Homer 1a can reduce mGluR5 coupling to postsynaptic effe

30 n of somatic calcium channels was altered by Homer 1a expression.

31 activating peptide (PACAP) to induce native Homer 1a expression.

32 ng that it resulted specifically from native Homer 1a expression.

33 mediate early genes (IEGs) c-Fos, Egr-1, and Homer 1a in the amygdala and the nucleus accumbens (NAc)

34 In vivo, the immediate early Homer 1a is anticipated to enhance ion channel modulatio

35 In sympathetic neurons, both Homer 1a overexpression and PACAP treatment reversed the

36 om EPSC inhibition, similar to the effect of Homer 1a overexpression.

37 ast, mGluR5 alone or mGluR5 coexpressed with Homer 1a successfully travels through the secretory path

38 I examined the ability of endogenous Homer 1a to alter mGluR signaling in rat sympathetic neu

39 We found that, by changing the ratios of Homer 1a to Homer 1b in vivo, by either induction of end

40 neurons were reduced compared with those in Homer 1a W24A-expressing cells.

41 mediate early gene product Homer (now termed Homer 1a) regulates the trafficking and surface expressi

42 xpression of the short Homer protein isoform Homer 1a, and an increased coupling of mGlu5 receptors t

43 blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRPC1.

44 ant negative, immediate early form of Homer, Homer 1a, strongly reduced EPSC modulation, but the W24A

45 uced EPSC modulation, but the W24A mutant of Homer 1a, which cannot bind mGluRs, had no effect.

46 llular calcium responses in the processes of Homer 1a-expressing neurons were reduced compared with t

47 activity-regulated cytoskeletal protein) and Homer 1a.

48 receptor mGluR1alpha, the plasticity factor Homer-1A, and the scaffolding postsynaptic density prote

49 memory formation (Arc, Zif268, NR2B, GluR1, Homer-1a, Nur77/TR3).

50 In the present study, we demonstrate that Homer 1b (H1b), a constitutively expressed splice form o

51 that, by changing the ratios of Homer 1a to Homer 1b in vivo, by either induction of endogenous Home

52 ion of cross-linking-capable forms of Homer (Homer 1b, 1c, 2, and 3, termed long forms) occluded grou

53 kout myotubes was blocked by reexpression of Homer 1b, but not Homer 1a, and by gene silencing of TRP

54 an increased coupling of mGlu5 receptors to Homer 1b/c proteins in the hippocampus.

55 in, with the coiled-coil (CC)-Homer proteins Homer-1b and Homer-2, two components of the molecular sc

56 Staining of Vesl-1L/Homer 1c (V-1L) immunoreactivity and TUNEL cytochemistry

57 heterodimers exhibit altered trafficking via Homer 1c when compared with CaR:CaR homodimers.

58 increased transcription of H1a and uncoupled homer 1c-GFP (green fluorescent protein) clusters.

59 hich cannot self-multimerize (Homer 1a and a Homer 2 C-terminal deletion), did not alter mGluR-ion ch

60 d the short variants of each of the Homer-1, Homer-2 and Homer-3 proteins reflects the fundamental pr

61 pression, followed by Homer-3 mRNA (22%) and Homer-2 mRNAs (12%).

62 rmone-releasing hormone receptor (GHRHR) and Homer-2 were underexpressed.

63 coiled-coil (CC)-Homer proteins Homer-1b and Homer-2, two components of the molecular scaffold that e

64 d calcium current modulation associated with Homer 2b expression.

65 Homer 2b induced cell surface clusters of mGluR5 in SCG

66 etabotropic glutamate receptor 5a (mGluR5a), Homer 2b, diacylglycerol lipase alpha, and CB(1)R.

67 Moreover, Homer-3 and its EVH1 domain fragment reduced transcripti

68 ibe the second patient with cerebellitis and Homer-3 antibodies and report a novel, highly specific i

69 ient and a previously described patient with Homer-3 antibodies are similar to those of patients with

70 Homer-3 antibodies were demonstrated by immunoblot of re

71 autoimmune cerebellar ataxia associated with Homer-3 antibodies.

72 The presence of Homer-3 autoantibodies should be considered in the diffe

73 Homer-3 colocalizes and modulates the activity of group

74 Homer-3 coprecipitated with CCAAT/enhancer binding prote

75 Consistent with these results, knockdown of Homer-3 increased SRE activation.

76 These findings suggest that Homer-3 may be involved in the regulation of SRE activat

77 in total Homer mRNAs expression, followed by Homer-3 mRNA (22%) and Homer-2 mRNAs (12%).

78 variants of each of the Homer-1, Homer-2 and Homer-3 proteins reflects the fundamental principles of

79 Overexpression of Homer-3 reduced transcriptional activation via the serum

80 Upon T-cell receptor (TCR) engagement, Homer-3 was recruited to the contact area of Jurkat cell

81 Homer-3, a member of the EVH1 family, is expressed in th

82 re demonstrated by immunoblot of recombinant Homer-3.

83 is less associated with its binding partner Homer, a scaffolding protein that regulates mGlu5 locali

84 One novel finding with each Homer agonist (H1c and H1-EVH1) was that in combination

85 additive, an effect also observed for these Homer agonists in the Ca2+ spark studies.

86 demonstrate physiologic binding of PIKE-L to Homer, an adaptor protein known to link metabotropic glu

87 Here we show that Homer and Bifocal act redundantly to promote posterior a

88 atory and inhibitory postsynaptic scaffolds, Homer and Gephyrin.

89 not the observed cocaine-induced changes in Homer and glutamate receptor expression generalized acro

90 rsal striatum, NR2a levels were elevated but Homer and Group1 mGluR levels were unchanged.

91 mode rationalizes conserved features of both Homer and Homer ligands that are not shared by other EVH

92 The EVH1 domain mediates these actions of Homer and is selectively blocked by a peptide that mimic

93 uR5 in heterologous cells in the presence of Homer and mediates the coclustering of Homer with PSD-95

94 biochemically isolated complex comprised of Homer and metabotropic glutamate receptors.

95 r respective interacting/clustering proteins Homer and PICK1.

96 affolding protein, Preso1, that binds mGluR, Homer and proline-directed kinases and that is required

97 Thus, Shank may cross-link Homer and PSD-95 complexes in the PSD and play a role in

98 e important in other cell types that express Homer and RyR1.

99 Homer and Shank are among the most abundant scaffolding

100 Here, we demonstrate that Homer and Shank, together, form a mesh-like matrix struc

101 We have created a mutation of homer and show that flies homozygous for this mutation a

102 mponents of the postsynaptic density--Shank, Homer and SPAR--have been found to regulate the structur

103 tic proteins neuronal nitric oxide synthase, Homer, and beta-catenin.

104 ate the binding site for the adaptor protein Homer, and thereby enhance mGluR-Homer binding to reduce

105 analysis and the Western blotting using pan-Homer antibody revealed that mouse heart, skeletal muscl

106 Using anti-Homer antibody we show that Homer is expressed in a broa

107 The scaffolding protein Homer assembles SOC complexes, but its role in VSMCs is

108 mer oligomerization, enabling it to uncouple homer assemblies.

109 in mice that deletes exon 21, including the Homer binding domain.

110 int mutation in mGluR5 that markedly reduces Homer binding exhibited a 50% reduction in binge alcohol

111 /2 activation, whereas a mutation within the Homer binding region in the carboxyl-terminal tail (P114

112 ed for their phosphorylation of mGluR at the Homer binding site.

113 tor protein Homer, and thereby enhance mGluR-Homer binding to reduce signaling.

114 ing RyR1 with a point mutation of a putative Homer-binding domain exhibit significantly reduced (appr

115 A single Homer-binding site is identified in Shank, and Shank and

116 F-actin cytoskeleton and a second requiring Homer but independent of intact F-actin, may act redunda

117 nality, we engineered dimeric and tetrameric Homer by deleting a part of coiled-coil domain or replac

118 omer-dependent interactions, indicating that Homer can facilitate the integration of Ca(2+)-dependent

119 g site is identified in Shank, and Shank and Homer coimmunoprecipitate from brain and colocalize at p

120 tudies indicate that long and short forms of Homer compete for binding to mGluRs and regulate their c

121 Recent observations indicate a role for Homer complexes in signal transduction, synaptogenesis a

122 lecule linking NMDA receptor-PSD-95 to Shank-Homer complexes, acts in these processes.

123 l domain, present in long but not short form Homer, confers an increase in agonist potential apparent

124 All Homers contain the N-terminal sequence responsible for t

125 The underlying mechanism relies on a Homer-containing protein scaffold, but not GPCR- or Ca(2

126 Shank and Homer cooperate to induce accumulation of IP3 receptors

127 Long forms of Homer decreased modulation of N- and M-type currents but

128 ase in effector-memory T cell populations in Homer-deficient mice, which also developed autoimmune-li

129 its subsynaptic distribution in response to Homer deletion and MPTP lesion.

130 Thus, nigrostriatal dopaminergic lesion and Homer deletion lead to changes in the trafficking of gro

131 These data show that Homer deletion mimics the behavioral and neurochemical p

132 Furthermore, these Homer-dependent effects on mGluR signaling may mechanist

133 nvolves metabotropic glutamate receptors and Homer-dependent interactions, indicating that Homer can

134 Homer did not significantly alter the spatio-temporal pr

135 sent work reveals a novel mechanism by which Homer directly modulates the function of its target prot

136 disrupts mGluR5 interactions with long-form Homers enhanced mGluR-induced epileptiform burst firing

137 Reporting recently in Cell Host & Microbe, Homer et al. (2016) characterize an elegant eukaryotic q

138 Homer EVH1 (Ena/VASP Homology 1) domains interact with p

139 have determined the crystal structure of the Homer EVH1 domain complexed with a peptide from mGluR (T

140 demonstrate that the adaptor protein, termed Homer, facilitates a physical association between TRPC1

141 The proteins of the Homer family bind to proline-rich sequences in group I m

142 signals from mGluR5 to ERK1/2, the member of Homer family Homer1b/c forms a central signaling pathway

143 found that Homer2 and Homer3, members of the Homer family of cytoplasmic scaffolding proteins, are ne

144 The homer family of molecular scaffolds provides spatial org

145 Members of the Homer family of proteins are known to form multimeric co

146 proline motif that mediates interaction with Homer family proteins is critical for the synaptic clust

147 study, we investigated the responsiveness of Homer family proteins to dopamine stimulation with the p

148 s tuned to identify broad regions (SICER and HOMER) favorably supports our approach on existing GRO-s

149 CC-Homers form natural complexes that cross-link mGluRs and

150 riments that provide the first evidence that Homer forms a tetramer via its coiled-coil domain, in wh

151 ich causes delocalization of Bifocal but not Homer from the oocyte cortex, severely disrupts anchorin

152 In contrast to the prevailing notion of Homer function, Homer1c (long form) and Homer1-EVH1 (sho

153 teins reflects the fundamental principles of Homer functions.

154 Members of the Homer gene family are regulated by acute and chronic coc

155 We now show that long and short forms of Homer H1 (H1c and H1-EVH1) are potent activators of Ca2+

156 ic deletion of a short, dominant negative of Homer, H1a, rescues many phenotypes of Fmr1 KO mice.

157 Expression of cross-linking-capable forms of Homer (Homer 1b, 1c, 2, and 3, termed long forms) occlud

158 e dominant negative, immediate early form of Homer, Homer 1a, strongly reduced EPSC modulation, but t

159 s are rescued by the expression of wild-type homer in a subset of neurons that include the ellipsoid

160 ate a function for scaffold proteins such as Homer in axon guidance.

161 less associated with its scaffolding protein Homer in Fmr1 KO mice, and restoration of mGlu5-Homer in

162 Our results find specific roles for Homer in mGluR signaling and plasticity and suggest that

163 ock-out mice were used to assess the role of Homer in MPTP-induced redistribution of group I mGluRs.

164 ed by expressing mGluRs and various forms of Homer in rat superior cervical ganglion (SCG) sympatheti

165 epeated cocaine administration and implicate Homer in regulating addiction to cocaine.

166 In addition, overexpression of Homer in the developing Xenopus retinotectal system resu

167 essing both wild-type and mutant isoforms of Homer in Xenopus optic tectal neurons.

168 In order to characterize expression of Homers in mouse brain and peripheral tissues we have dev

169 properties of the sparks, demonstrating that Homer increases the rate of opening of RyRs, with no cha

170 ect of intense study, direct measurements of Homer-induced changes in postsynaptic mGluR-effector cou

171 e, mGluR-LTD is insensitive to disruption of Homer interactions and mGluR activation of PI3K-mTOR is

172 er in Fmr1 KO mice, and restoration of mGlu5-Homer interactions by genetic deletion of a short, domin

173 nd plasticity and suggest that reduced mGluR-Homer interactions in Fmr1 KO mice lead to a deficit in

174 Here, we examined the role of Homer interactions in mGluR-LTD and mGluR signaling to p

175 Our findings reveal new functions for mGluR5-Homer interactions in the brain and delineate distinct m

176 Disruption of mGluR-Homer interactions selectively blocks mGluR activation o

177 luR5 (mGluR5ct), shown previously to disrupt Homer interactions with mGluRs, blocks mGluR-LTD and mGl

178 The TRPC1-Homer-IP(3)R complex is dynamic and its disassembly para

179 Homer is a crucial postsynaptic scaffolding protein invo

180 ion to its known role as an adapter protein, Homer is a direct modulator of Ca(2+) release gain.

181 The glutamate receptor adaptor protein Homer is concentrated in the postsynaptic density of exc

182 Using anti-Homer antibody we show that Homer is expressed in a broad range of tissues but is hi

183 show coordinated locomotion, suggesting that Homer is not essential for basic neurotransmission.

184 xpressing a mutant mGlu5 that cannot bind to Homer is sufficient to mimic many of the biochemical, ne

185 Homer is the first example of an "adapter" that also mod

186 potential role for both immediate early gene Homer isoforms and constitutively expressed Homer isofor

187 repeated cocaine alters the expression of CC-Homer isoforms and their associated glutamate receptors

188 ) mice, mGluR5 was less associated with long Homer isoforms but more associated with the short Homer1

189 The presence of different Homer isoforms can act as a switch to reprioritize mGluR

190 Homer isoforms and constitutively expressed Homer isoforms in behavioral pathologies associated with

191 e spatial and temporal distributions of both Homer isoforms were similar in the neuropil and cell bod

192 GluR1a were found in MPTP-treated normal and Homer knock-out mice.

193 The scaffolding protein Homer, known to interact with both IP3R and RYR, is expr

194 e results suggested that disruption of mGlu5-Homer leads to phenotypes of FXS.

195 the nucleus accumbens (NAC), and the reduced Homer levels were accompanied by decreases in mGluR1a, N

196 rently through the multimeric association of Homer ligand.

197 ctively blocked by a peptide that mimics the Homer ligand.

198 r understanding the biological properties of Homer-ligand complexes.

199 nalizes conserved features of both Homer and Homer ligands that are not shared by other EVH1 domains.

200 to its mammalian counterpart, the Drosophila Homer localizes to the dendrites and the endoplasmic ret

201 DGL-alpha mutants that do not bind Homer maintained their ability to generate 2-AG in intac

202 Homer may facilitate signal transduction from cell-surfa

203 Thus, Homer may regulate the magnitude and predominate signali

204 This work provides strong evidence that Homer-mGlu5 binding contributes to symptoms associated w

205 Homer-1 mRNAs reaches 66% of the brain total Homer mRNAs expression, followed by Homer-3 mRNA (22%) a

206 bled/Vasp homology 1 domain, suggesting that Homer must bind to one or more of its partners for prope

207 We show that null homer mutant flies exhibit both increased sensitivity to

208 tivity and rapid tolerance phenotypes of the homer mutants are rescued by the expression of wild-type

209 However, we found that homer mutants display defects in behavioral plasticity a

210 Homer-NFAT binding was also antagonized by active serine

211 thesis that cocaine-induced changes in mGluR-Homer-NMDA signaling pathways may be important neuroadap

212 pts anchoring of osk gene products only when Homer (not Bifocal) is absent.

213 ice form of the immediate early gene product Homer (now termed Homer 1a) regulates the trafficking an

214 r protein that lacks the domain required for homer oligomerization, enabling it to uncouple homer ass

215 pathways (a conventional IP3/Ca2+ vs a novel Homer pathway) that differentially mediate the mGluR5-ER

216 Consistent with the hypothesis that mGluR5-Homer-PI3K signaling may be a mechanism governing excess

217 mGluRI agonists enhanced mGluRI-Homer-PIKE-L complex formation, leading to activation of

218 rs (mGluRIs) enhances formation of an mGluRI-Homer-PIKE-L complex, leading to activation of PI3 kinas

219 naptic dynamin and, like its binding partner Homer, plays a significant role in dendritic spine morph

220 tween dynamin-3 and the postsynaptic adaptor Homer positions the EZ near the PSD.

221 ng PRG5 in mature neurons not only increased Homer-positive spine numbers but also augmented spine he

222 Homer postsynaptic scaffolding proteins regulate forebra

223 e first insight into the structure of native Homer protein as a tetramer and the functional significa

224 neuronal function associated with changes in Homer protein expression described in the recent literat

225 alteration of mGluR signaling by changes in Homer protein expression may represent a viable mechanis

226 in expression of Homer2a/b with a related CC-Homer protein Homer1b/c, as well as their associated glu

227 The constitutively expressed (CC) Homer protein Homer2a/b actively regulates behavioral an

228 ice showed a reduced expression of the short Homer protein isoform Homer 1a, and an increased couplin

229 (H1a) immediate-early gene produces a short homer protein that lacks the domain required for homer o

230 competed with the cross-linking isoforms of Homer proteins (Homer1b/c and Homer2a/b) to uncouple the

231 Here, we demonstrate that Homer proteins also physically associate with ryanodine

232 Homer proteins also self associate and function as adapt

233 These findings support the link between Homer proteins and monogenic autism, and lay the groundw

234 However, although Homer proteins and their interaction with mGluRs have be

235 gm constitutively express high levels of the Homer proteins and their mRNAs.

236 f group I mGluR localization and function by Homer proteins appears to be a viable means for neurons

237 Homer proteins are a family of multidomain cytosolic pro

238 Homer proteins are a family of scaffolding proteins of t

239 Homer proteins are integral components of the postsynapt

240 Homer proteins are integral to the assembly of proteins

241 We tested whether Homer proteins are involved in axon pathfinding in vivo,

242 Homer proteins bind specifically to the C termini of the

243 The selective expression of Homer proteins contributes to these differentiation-depe

244 Homer proteins form an adapter system that regulates cou

245 Homer proteins form multivalent complexes that bind prol

246 R1/5 signal regulation by natively expressed Homer proteins has been elusive.

247 Homer proteins have been proposed to play a role in syna

248 Moreover, Homer proteins have been shown to modulate RyR-dependent

249 ia a PPxxF domain, with the coiled-coil (CC)-Homer proteins Homer-1b and Homer-2, two components of t

250 The role of Homer proteins in channel modulation was investigated by

251 nt on the distribution of group I mGluRs and Homer proteins in GP and STN, specific changes in the ul

252 the expression levels of group I mGluRs and Homer proteins in GP and striatum.

253 portance of the IP3/Ca2+ signaling and novel Homer proteins in group I mGluR-mediated activation of e

254 2b was used to demonstrate the importance of Homer proteins in neuroplasticity produced by repeated e

255 ges in AMPA transmission can be regulated by Homer proteins in response to physiologically relevant s

256 VSMCs and are the first to show the role of Homer proteins in VSMCs and its importance in neointima

257 TRP channel regulation, we hypothesized that Homer proteins play a significant role in skeletal muscl

258 etabotropic glutamate receptors (mGluRs) and Homer proteins play critical roles in neuronal functions

259 Furthermore, Homer proteins regulate mGluR1/5 function by acting as a

260 Homer proteins regulate signal transduction, synaptogene

261 most studies focusing on mGluR regulation by Homer proteins used relatively long-term overexpression.

262 work has demonstrated direct interaction of Homer proteins with type 1 and type 2 ryanodine receptor

263 lu receptors (mGluRI) to PI 3-kinase through Homer proteins, adaptors that bind mGluRI.

264 ugh group I mGluRs is regulated, in part, by Homer proteins, and it was found that the blunting of gr

265 As CC-Homer proteins, Group1 mGluRs and NMDA receptors activel

266 lternative splicing generates a family of 17 Homer proteins.

267 ion of the Drosophila gene homer, the single Homer-related gene in fly.

268 Our results argue that in the CNS, Homer-related proteins operate in the ER and in dendrite

269 In this issue of Developmental Cell, Gui and Homer report that the proper execution of meiosis I in m

270 agenesis confirms the importance of specific Homer residues for ligand binding.

271 Homer's action depends on its ability to crosslink and i

272 group I mGluRs are organized with members of Homer scaffold proteins into multiprotein complexes invo

273 that deficiency of Shank3 can impair mGluR5-Homer scaffolding, resulting in cortico-striatal circuit

274 tic deletion of Homer1a restored mGluR5-long Homer scaffolds and corrected several phenotypes in Fmr1

275 Both mGluR5-Homer scaffolds and mGluR5-mediated signalling are selec

276 Here we provide evidence that altered mGluR5-Homer scaffolds contribute to mGluR5 dysfunction and phe

277 These results reveal new roles for the Homer scaffolds in regulation of mGlu5 function and impl

278 Acute, peptide-mediated disruption of mGluR5-Homer scaffolds in wild-type mice mimicked many Fmr1(-/y

279 We suggest that integrity of Homer scaffolds is essential for normal mGluR-eCB functi

280 We propose that the Homer-Shank complex serves as a structural framework and

281 s links between the GTPase dynamin-3 and the Homer/Shank complex.

282 rved when mGluR5 was expressed alone or with Homer short forms.

283 When coexpressed with long forms of Homer, short forms restored the mGluR1a-mediated calcium

284 ent in Vienna, when I became acquainted with Homer Smith's essays on kidney function.

285 he Ser-Pro tandem are oriented away from the Homer surface, and the Phe forms a unique contact.

286 alcium pools by a family of proteins, termed Homer, that cross-link the receptor to inositol trisphos

287 and characterization of the Drosophila gene homer, the single Homer-related gene in fly.

288 mature PSD, PSD-95, SAPAP1/GKAP, Shank, and Homer to dendritic spine synapses.

289 t interfering with the ability of endogenous Homer to form protein-protein interactions resulted in a

290 nt of spine heads via its ability to recruit Homer to postsynaptic sites.

291 t the protein expression levels of GluR1 and Homer, two synaptic proteins whose translation has been

292 ruption of dynamin-3 or its interaction with Homer uncouples the PSD from the EZ, resulting in synaps

293 Short forms of Homer, which cannot self-multimerize (Homer 1a and a Hom

294 tion of mGlu5 with scaffold protein effector Homer, which regulates mechanistic target of rapamycin (

295 e fall into two distinct groups of 12 "long" Homers, which all have a coiled-coil domain at their C t

296 domain at their C termini, and five "short" Homers, which lack such a domain.

297 y further suggest that the interaction of CC-Homer with DGL-alpha is necessary for appropriate functi

298 in this motif, which prevents the binding of Homer with mGluR1a, reduced its colocalization with a po

299 ce of Homer and mediates the coclustering of Homer with PSD-95/GKAP.

300 to the surgical pathology files of the James Homer Wright Pathology Laboratories, Massachusetts Gener