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1 eviated excessive fragmentation of important synaptic proteins.
2 f amyloid precursor protein, amyloid-beta or synaptic proteins.
3 tant for trafficking and function of several synaptic proteins.
4 d glutamatergic marker VGluT1, pre- and post-synaptic proteins.
5 glutamatergic synapses and interact with key synaptic proteins.
6 ion of the Golgi apparatus and missorting of synaptic proteins.
7 synaptic adhesion and recruitment of diverse synaptic proteins.
8 ole in the localization and function of many synaptic proteins.
9 c postsynaptic proteins and of glutamatergic synaptic proteins.
10 o chronic pain by regulating the turnover of synaptic proteins.
11 nscriptional and translational regulators to synaptic proteins.
12 ential subcellular sorting of family-related synaptic proteins.
13 eins expressed in hair cells, including many synaptic proteins.
14 the expression levels of a subgroup of other synaptic proteins.
15 latory cascade ensuring adequate delivery of synaptic proteins.
16 s downregulation of neurotrophic factors and synaptic proteins.
17  of dendritic spine, neuronal structures and synaptic proteins.
18 ed by studies of patients lacking individual synaptic proteins.
19 des a powerful tool to study the function of synaptic proteins.
20 e lesion core and express reduced amounts of synaptic proteins.
21  changes coincide with altered expression of synaptic proteins.
22 mics analysis of kinesin complexes are known synaptic proteins.
23 cription factors, other splicing factors and synaptic proteins.
24  closely expression is associated with other synaptic proteins.
25 ts, resulting in increased levels of several synaptic proteins.
26 ta dimers or amyloid-beta trimers and tau or synaptic proteins.
27  Abeta oligomer level, and inhibited loss of synaptic proteins.
28 t (within 10 min) in the rate of addition of synaptic proteins.
29 omers, and marked down-regulation of several synaptic proteins.
30 ophore assisted light inactivation (CALI) of synaptic proteins.
31 ith which to manipulate and understand these synaptic proteins.
32 c homology three and proline-rich domains of synaptic proteins.
33 al homeostasis through the redistribution of synaptic proteins.
34 s, involving recycling and/or degradation of synaptic proteins.
35 showing a significant difference between the synaptic proteins.
36 cts were formed on cysteine residues of some synaptic proteins.
37                  What came first: neurons or synaptic proteins?
38                   Here, we report Inhibitory Synaptic protein 1 (InSyn1) is a critical component of t
39 ted to two distinct classes of transmembrane synaptic proteins: (1) ion channel auxiliary factors suc
40 ochondrial dynamics, biogenesis proteins and synaptic proteins, (3) soluble Abeta levels and immunore
41 rder (ASD) and highlight the contribution of synaptic protein acetylation to synaptic processing.
42 ere linked with changes in the expression of synaptic proteins across various regions of the brain.
43 Immunoblotting findings of mitochondrial and synaptic proteins agreed with mRNA findings.
44 Immunoblotting findings of mitochondrial and synaptic proteins agreed with the mRNA findings.
45    Our findings formalize a link between the synaptic protein AIDA-1 and a rare, previously undefined
46                                              Synaptic protein alpha-synuclein (alpha-SYN) modulates n
47                                        These synaptic protein alterations are associated with a defic
48  of neuropeptides, transcription factors and synaptic proteins, among other gene categories.
49 monstrate SubSynMAP, a fast, multiplexed sub-synaptic protein analysis method using wide-field data f
50 ia, the nature, consistency and magnitude of synaptic protein and mRNA changes has not been systemati
51      Furthermore, stress-induced deficits in synaptic proteins and decreases in dendritic density and
52 un to quantify morphine-regulated changes in synaptic proteins and facilitate the generation of netwo
53                      Research has identified synaptic proteins and function as primary contributors t
54  spectrometry, we quantified more than 7,000 synaptic proteins and identified 89 significantly reduce
55 lation of tau and promoted the expression of synaptic proteins and insulin signaling in the brain.
56 st that TOP1 controls the levels of multiple synaptic proteins and is required for normal excitatory
57 constitution of vesicle fusion from purified synaptic proteins and lipids has played a major role in
58 ir cell-like cells had hair bundle proteins, synaptic proteins and membrane proteins characteristic o
59 airs neuronal differentiation, expression of synaptic proteins and neuronal morphology, whereas reduc
60 e (IEG) expression and changes in excitatory synaptic proteins and physiology in the basolateral amyg
61  loss of basal CA1 synaptic strength and key synaptic proteins and reduced the susceptibility to indu
62  PNs, but with differential transcription of synaptic proteins and signaling molecules.
63 vior in female rats, the decline observed in synaptic proteins and spine density in IS and in diestru
64                             The diversity of synaptic proteins and synapse types demands synapse anal
65 of the 5-HT(1A) receptor increased levels of synaptic proteins and synaptic function in the mPFC.
66               The images revealed individual synaptic proteins and synaptic protein complex densities
67 observed distinct morphologies of individual synaptic proteins and their complexes.
68  sets of genes including both those encoding synaptic proteins and those expressed during early devel
69 or reactive oxygen species-responsive genes, synaptic proteins and transcription regulators such as c
70  regulates the clustering and recruitment of synaptic proteins and vesicles to the synapse, adjusting
71 synaptic dysfunction, preventing the loss of synaptic proteins and/or have a positive effect on the i
72 s, autophagic/lysosomal dysfunction, loss of synaptic protein, and reduced life-span.
73  of CaMKII are mediated by interactions with synaptic proteins, and activity-triggered translocation
74 (seen by EM in the CA1 region), reduction of synaptic proteins, and localization to the nucleus.
75 hic factor signaling, increased synthesis of synaptic proteins, and most notably increased GluR1 and
76 ears earlier than the outer plexiform layer, synaptic proteins, and ribbons are first reliably recogn
77  antibodies against neuronal cell surface or synaptic proteins, and the differential diagnosis with i
78 xpression results in increased levels of the synaptic protein Arc and a concomitant impaired synaptic
79 he structure and function of these important synaptic proteins are accelerating understanding of thei
80    Antibodies against neuronal receptors and synaptic proteins are associated with a group of ill-def
81 nhibitory src homology 3 domain, and several synaptic proteins are known to bind to this SH3 domain a
82 -expressed genes enriched for those encoding synaptic proteins are liable to change with age.
83 isordered, possibly because interacting post-synaptic proteins are not present.
84 regulating the surveillance and clearance of synaptic proteins are not well understood.
85                     Furthermore, because key synaptic proteins are O-GlcNAcylated, this modification
86 nd signaling also becomes activated when pre-synaptic proteins are over-expressed, suggesting the exi
87 endent proteins is highly induced while some synaptic proteins are repressed in neurons missing the T
88 endent proteins is highly induced while some synaptic proteins are repressed.
89  The real-time surveillance and clearance of synaptic proteins are thought to be vital to the health,
90  evidence points toward aberrant activity of synaptic proteins as a critical contributing factor.
91 s a result of decreased levels of functional synaptic proteins as found in autopsied brains of patien
92 et that mediates intermolecular binding with synaptic proteins as resolved in complexes with TARPgamm
93                    We used iExM to visualize synaptic proteins, as well as the detailed architecture
94 ctural plasticity of GCNs, and expression of synaptic proteins associated with learning and memory in
95                               These included synaptic proteins at dendritic spines, myelination along
96 omposition and nanoscale organization of key synaptic proteins at these inputs remains largely elusiv
97  clathrin-specific co-chaperone, such as the synaptic protein auxilin.
98 or-like protein 1 (APLP1) is a transmembrane synaptic protein belonging to the amyloid precursor prot
99 brane molecules (Neurotactin/Neuroglian) and synaptic proteins (Bruchpilot/N-Cadherin).
100             CDKL5 was shown to interact with synaptic proteins, but an in vivo analysis of the role o
101 SD)-linked mutations disrupt the function of synaptic proteins, but no single gene accounts for >1% o
102                                 The abundant synaptic protein CaMKII is necessary for long-term poten
103                  Mutations in genes encoding synaptic proteins cause many neurodevelopmental disorder
104    Previously, we showed that some GABAergic synaptic proteins change across the lifespan, but most s
105  an unbiased proteomic screen and identified synaptic protein changes in alphabetagamma-synuclein kno
106    These patterns of widespread, but diverse synaptic protein changes in response to global perturbat
107  detail the disease caused by absence of the synaptic protein CNKSR2 in 8 patients ranging from 6 to
108                                              Synaptic protein co-expression was significantly decreas
109 es revealed individual synaptic proteins and synaptic protein complex densities at prefusion contact
110 he effect of detergent on activity-dependent synaptic protein complexes has not been rigorously exami
111 rograms that shape molecular repertoires and synaptic protein complexes.
112 taking advantage of preparations lacking the synaptic protein complexin, which have elevated spontane
113 k3 gene in adult mice led to improvements in synaptic protein composition, spine density and neural f
114 erences in developmental trajectory of these synaptic proteins could contribute to long-term differen
115  the CaMK family with unknown function, as a synaptic protein crucial for dendritic spine maintenance
116  Akt/mTOR signaling, and increases levels of synaptic proteins crucial for synaptic plasticity in the
117  several signaling molecules, receptors, and synaptic proteins currently implicated in ARM operate in
118    Furthermore, this treatment prevented pre-synaptic protein deficit, decreased glycogen synthase ki
119 ly in deprived synapses, suggesting targeted synaptic protein degradation under sensory deprivation.
120 hen bound to a two-PPXY motif peptide of the synaptic protein Dendrin.
121 es reveals distinct, quantitative changes in synaptic proteins distributed across over 6,000 pairwise
122 vealed disease-specific modifications of sub-synaptic protein distributions across synapse classes an
123  findings indicate that SUMO1-conjugation of synaptic proteins does not occur or is extremely rare an
124  distinct mutations within BRAG1, an Arf-GEF synaptic protein, each led to X-chromosome-linked intell
125 or synaptic function to recycle membrane and synaptic proteins enabling the continued release of syna
126  involve transcriptional changes in the core synaptic protein encoding genes bruchpilot, liprin and s
127                                     Arc is a synaptic protein essential for memory consolidation.
128  learning of a complex environment activates synaptic proteins essential for the stabilization of lon
129 , whereas inhibition mimics, the increase in synaptic proteins evoked by the knockdown of NP1.
130 his, we analyzed the motion of 45 GFP-tagged synaptic proteins expressed in cultured hippocampal neur
131 t of mTORC1 whose translation and consequent synaptic protein expression are increased in the nucleus
132 h exhibit strong caspase3 signal and reduced synaptic protein expression by 3 weeks of age.
133 olonged withdrawal recapitulated most of the synaptic protein expression profiles observed at early w
134 induced increases in tyrosine hydroxylase or synaptic protein expression.
135 nsmembrane protein 3 (LRRTM3) is member of a synaptic protein family.
136        Stoichiometric labeling of endogenous synaptic proteins for high-contrast live-cell imaging in
137 the utility of the ExCel toolbox for mapping synaptic proteins, for identifying previously unreported
138  long-distance delivery of newly synthesized synaptic proteins from the soma to distal synapses, rais
139 pain-dependent degradation of the inhibitory synaptic protein gephyrin subsequently exacerbated SSC-m
140  promote mTORC1-dependent translation of the synaptic proteins GluA1 and Homer.
141 halitis with autoantibodies directed against synaptic proteins has become an important component of t
142                    Dysregulated synthesis of synaptic proteins has been implicated in the pathophysio
143 hine effects nor changes in the abundance of synaptic proteins have been clearly delineated.
144                             We conclude that synaptic proteins have evolved to limit possible contact
145 apses causes a loss instead of the gain of a synaptic protein (i.e., GABAARs).
146 rt that the CIDE-N protein Drep-2 is a novel synaptic protein important for learning and behavioral a
147 boutons in NMJs lacking synapsin [Syn(-)], a synaptic protein important for vesicle clustering, neuro
148 isease, less is known about the role of this synaptic protein in AD.
149 e deficits, CST sprouting, and expression of synaptic proteins in an experimental model of closed hea
150  alpha-synuclein and the expression of other synaptic proteins in cholinergic axons in the guinea pig
151 rt the localization and amount of endogenous synaptic proteins in living neurons and thus may be used
152 depression-like behavior, spine density, and synaptic proteins in male and female rats.
153 r in concert with its regulation of numerous synaptic proteins in NAc as well as with SIRT1-mediated
154                                          Six synaptic proteins in NDE extracts were quantified by ELI
155 tion concomitantly suppresses the buildup of synaptic proteins in neuronal cell bodies, hence may pla
156                                    Decreased synaptic proteins in neuronal exosomes of frontotemporal
157            Using this method, we analyzed 15 synaptic proteins in normal and Fragile X mental retarda
158 Notch signaling is involved in expression of synaptic proteins in postmitotic neurons.
159  evidence for autoantibodies to cell surface synaptic proteins in psychosis and schizophrenia.
160  aging on expression of prefrontal GABAergic synaptic proteins in relation to working memory decline,
161 set of dendritic spines and colocalized with synaptic proteins in specific nanodomains, as determined
162 raining, combined treatment had no effect on synaptic proteins in the aged hippocampus.
163 s in multiple transcripts encoding important synaptic proteins in the brain's reward circuitry.
164 letion results in altered levels of multiple synaptic proteins in the hippocampus, using both male an
165 ver, the signals that regulate expression of synaptic proteins in the mature brain are incompletely u
166 approach to study the dynamics of endogenous synaptic proteins in vivo.
167 3/Deltaex13 mice compared to control are key synaptic proteins including CaMK2a.
168           54% of palmitoylation sites map to synaptic proteins including many GPCRs, receptors/ion ch
169 aptic release sites, and a redistribution of synaptic proteins including the vesicle-associated prote
170 ulates the localization and function of many synaptic proteins, including AMPARs and PSD-95.
171 interacts with a variety of PDZ domains from synaptic proteins, including MAGI-3.
172 crease in the cluster size and number of key synaptic proteins, including N-methyl-d-aspartate recept
173 tein phosphatase that regulates a variety of synaptic proteins, including NMDA receptors (NAMDRs).
174 UPS) is known to regulate expression of many synaptic proteins, including presynaptic elements, to op
175 r localization and mediated large changes in synaptic proteins, including proteins implicated in fami
176 ustering of aggregates with mitochondria and synaptic proteins, indicating that the amyloid-like adhe
177 ease risk factors and their placement within synaptic protein interaction networks.
178 not impair GluN2B binding, another important synaptic protein interaction of CaMKII.
179 1 in NAc D1+ neurons and increases levels of synaptic proteins involved in glutamatergic signaling.
180 ll as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release i
181 n that phosphorylation of serine residues on synaptic proteins is a major regulator of synaptic stren
182 asticity, suggesting that O-GlcNAcylation of synaptic proteins is likely as important as phosphorylat
183                            Synthesis of many synaptic proteins is under local control and much of thi
184 ic GTPase-Activating Protein (SynGAP), a key synaptic protein, is determined by the combination of it
185 of this regulatory mechanism is Complexin, a synaptic protein known to regulate synaptic vesicle exoc
186                                      Whereas synaptic protein labeling in the young hippocampus was s
187 neuroanatomically-based molecular changes in synaptic protein levels and astroglial cell marker in a
188                               The effects on synaptic protein levels and inhibitory neurotransmission
189  months of age, wildtype mice showed altered synaptic protein levels and relatively superior cognitiv
190            However, whether topotecan alters synaptic protein levels and synapse function is currentl
191 the existence of a feedback circuit to match synaptic protein levels to the transport capacity of the
192 ory, hippocampal long-term potentiation, and synaptic protein levels were assessed.
193 u dysregulation, which causes a reduction in synaptic protein levels, may be responsible for the cogn
194 -responsive changes in dendritic complexity, synaptic protein levels, spine density and morphology, a
195  molecules and their interactions with other synaptic proteins likely affect not only on synapse form
196  that nonpathogenic HTT can indeed influence synaptic protein localization and uncover a novel role o
197 used to guide the segmentation of individual synaptic protein locations and spatial extents, revealin
198 ected against TBI-induced motor deficits and synaptic protein loss.
199 emonstrate that epigenetic regulation of key synaptic proteins may be an underlying, yet reversible,
200                                          NDE synaptic proteins may be useful preclinical indices and
201 nt depended on a direct interaction with the synaptic protein Munc13, because expression of the II-II
202  (PSDs) and causes excessive cleavage of the synaptic protein N-cadherin (N-CAD).
203                                          The synaptic protein Neuroligin 1 (NLGN1), a cell adhesion m
204  We here tested the hypotheses that the post-synaptic protein Neuroligin-1 (NLGN1) is affected early
205                                          The synaptic protein neuroligin-3 (NLGN3) was identified as
206 L BDNF to regulate excitatory and inhibitory synaptic proteins neuroligin 1 and neuroligin 2, which p
207 t of three detergents commonly used to study synaptic proteins on activity-dependent protein interact
208 tmortem studies in schizophrenia quantifying synaptic protein or mRNA levels in brain tissue.
209 ave revealed that synaptic components (e.g., synaptic proteins, organelles, neurotransmitters and the
210 NA imaging probes to resolve nanometer-scale synaptic protein organization across nine distinct prote
211 ts were integrated into a software platform, Synaptic Protein/Pathways Resource (SyPPRes), enabling t
212 on leads to elevated levels of ubiquitinated synaptic proteins per se.
213 suggesting that MeCP2 likely regulates these synaptic proteins post-transcriptionally, directly or in
214 y, we demonstrate that SR interacts with the synaptic proteins, postsynaptic density protein 95 (PSD-
215 sis and the calpain-dependent degradation of synaptic proteins, potentially ameliorating the observed
216 tination-directed proteasomal degradation of synaptic proteins, presumably mediated by lysine 48 (K48
217 nd synaptic transmission implying changes in synaptic protein profile.
218 ion in cortical excitatory neurons disrupted synaptic protein profiles, altered neuronal morphology,
219 e association also impaired synthesis of the synaptic protein PSD-95, suggesting that this phenomenon
220 reveals coordinated upregulation of the post-synaptic proteins PSD-95, SHANK3 and Homer-1b/c, as well
221 ent TimeSTAMP tag reveals that copies of the synaptic protein PSD95 are synthesized in response to lo
222                                          The synaptic proteins PSD95 and NR2B were reduced in dendrit
223  administration also increased levels of the synaptic proteins, PSD95, GluA1, and Synapsin 1 and enha
224            We visualized functionally active synaptic proteins reconstituted into proteoliposomes and
225 ply a convergent molecular pathway involving synaptic protein recycling that may also be involved in
226        Postsynaptic density 95 (PSD-95) is a synaptic protein regulating glutamate receptor anchoring
227  CPT1C-overexpressing neurons, whereas other synaptic proteins remain unaltered.
228        Importantly, the mRNA levels of these synaptic proteins remains unchanged, suggesting that MeC
229 ersible, and activity-dependent insertion of synaptic proteins required during the induction and expr
230 SPIRE system regulates axonal trafficking of synaptic proteins required for proper connectivity and s
231                               The downstream synaptic protein response to HDACi administration is sim
232                  Next, we tested whether the synaptic protein response to HDACi treatment is similarl
233 situ structural characterization of numerous synaptic proteins simultaneously through multiplexed ima
234 r studies revealed a significant decrease of synaptic protein, specifically in the spinal dorsal horn
235               Because of its many effects on synaptic proteins, STEP has been implicated in regulatin
236 % of quantified proteins, including abundant synaptic proteins such as PSD-95 and gephyrin, exhibited
237                                        Other synaptic proteins, such as extracellular signal-regulate
238  Neurotransmitter release is orchestrated by synaptic proteins, such as SNAREs, synaptotagmin, and co
239 ignificant decrease in expression of several synaptic proteins, suggesting a functional deficit of re
240            Our findings implicate a role for synaptic proteins synapsin-1, postsynaptic density prote
241 g/kg, and 5 mg/kg) on behavior and levels of synaptic proteins synapsin-1, postsynaptic density prote
242 ects and restores normal distribution of the synaptic protein synaptophysin, confirming that Tat alte
243 oligodendrocytes, enhanced expression of the synaptic proteins synaptophysin and PSD95 in the hippoca
244 synaptic plasticity and a reduced density of synaptic proteins (synaptosomal-associated protein 25, s
245 spines, while disrupting the distribution of synaptic proteins (synaptotagmin 2 and gephyrin) associa
246 emonstrate defects in the trafficking of the synaptic proteins Syntaxin1a and PSD-95 and the TrkB and
247 drug development (e.g., agents that increase synaptic protein synthesis and plasticity).
248  target a key mediator of activity-dependent synaptic protein synthesis downstream of mechanistic tar
249                        Altered regulation of synaptic protein synthesis has been hypothesized to cont
250 ine-induced increases in mTOR activation and synaptic protein synthesis were mimicked and occluded in
251 report that expression of a key regulator of synaptic protein synthesis, the metabotropic glutamate r
252 (mTORC1), a signaling pathway that regulates synaptic protein synthesis.
253 yperactivity, seizures, and elevated de novo synaptic protein synthesis.
254 nd cleavage, exchange and religation using a synaptic protein tetramer.
255 synaptic density protein 95 (PSD95), a major synaptic protein that clusters glutamate receptors and i
256   These results suggest that CARM1 is a post-synaptic protein that plays roles in dendritic maturatio
257         Densin-180 (densin) is an excitatory synaptic protein that promotes Ca(2+)-dependent facilita
258 esynaptic Ca(2+) channels, K(+) channels, or synaptic proteins that affect transmitter release.
259 primary cortical neurons, topotecan depleted synaptic proteins that are encoded by extremely long gen
260 s expansion of the number of cell surface or synaptic proteins that are targets of autoimmunity.
261                      We found adaptations in synaptic proteins that control glutamatergic signaling i
262                 Complexins (Cplxs) are small synaptic proteins that cooperate with SNARE-complexes in
263 linked to synapse loss and/or alterations of synaptic proteins that impair function in regions such a
264 as genetic regulators of neurodevelopment or synaptic proteins that regulate neural activity.
265 y pathway, endocytosis, and the stability of synaptic proteins, the nature of how this mutation affec
266  neurons by targeting two well-characterized synaptic proteins, the obligatory GluN1 subunit of the N
267 ustering of mutant Htt with mitochondria and synaptic proteins, thereby restoring neuronal function.
268 ynaptic candidates and assign numerous known synaptic proteins to a specific cleft type.
269 clerosis and the altered expression of three synaptic proteins to cognitive status and global cogniti
270           This kinase interacts with various synaptic proteins to regulate expression and function of
271 gulated transport system to deliver selected synaptic proteins to synapses.
272 ted with intellectual disability (ID) encode synaptic proteins, transcriptional defects leading to ID
273                             How FMRP impacts synaptic protein translation and which mRNAs are most im
274 e Rap1b small GTPase and an associated local synaptic protein translation network in this process.
275  translation initiation factors that dampens synaptic protein translation.
276 translation of Dgkkappa, indirectly controls synaptic proteins translation and membrane properties by
277 d pathways, most prominently those involving synaptic proteins, translational regulation, and chromat
278             However, the mechanisms by which synaptic proteins turn over remain elusive.
279 ing that their action depends on concomitant synaptic protein turnover.
280 hought: NMDA receptors, L-VDCCs, CaMKII, and synaptic protein turnover.
281 of a specific serine residue (Ser322) on the synaptic protein UNC-18 as an end point for the Galphas-
282                            Additionally, the synaptic protein UNC-31 [calcium-activated protein for s
283 icroglial activation, and loss of excitatory synaptic proteins under conditions in which no viable ba
284  linked directly to phosphorylated tau (e.g. synaptic protein VAMP2, vacuolar-ATPase subunit ATP6V0D1
285 novel transport system that delivers certain synaptic proteins via the actin cytoskeleton within the
286         Additionally, abnormal expression of synaptic proteins was observed in amygdala and prefronta
287  majority of transcripts encoding excitatory synaptic proteins were lower in OFC but not significantl
288                        GABAergic markers and synaptic proteins were mainly abnormal in schizophrenia
289              One hundred fifty-five selected synaptic proteins were quantified by targeted mass spect
290             More than half of the quantified synaptic proteins were regulated, including pre- as well
291 PrP(C), residues 95-110), a highly expressed synaptic protein which mediates the neuronal binding and
292 er or similar autoimmune disorders affecting synaptic proteins, which are therefore treatable with im
293 le of LRP1 in the regulation and turnover of synaptic proteins, which may contribute to the reduced d
294   The loss of Brd4 function affects critical synaptic proteins, which results in memory deficits in m
295          Importantly, this screen identified synaptic proteins whose levels were affected by sensory
296                        Thus, PNKD is a novel synaptic protein with a regulatory role in neurotransmit
297 pproaches were used to identify and validate synaptic proteins with novel links to heavy drinking in
298            We modified genomic loci encoding synaptic proteins within bacterial artificial chromosome
299  and localization of PSD95, a dendritic post-synaptic protein, within oligodendrocytes.
300 characterized target transcripts of FMRP are synaptic proteins, yet targeting these proteins has not

 
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