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1 latory cascade ensuring adequate delivery of synaptic proteins.
2 of dendritic spine, neuronal structures and synaptic proteins.
3 ed by studies of patients lacking individual synaptic proteins.
4 des a powerful tool to study the function of synaptic proteins.
5 e lesion core and express reduced amounts of synaptic proteins.
6 changes coincide with altered expression of synaptic proteins.
7 mics analysis of kinesin complexes are known synaptic proteins.
8 cription factors, other splicing factors and synaptic proteins.
9 closely expression is associated with other synaptic proteins.
10 ts, resulting in increased levels of several synaptic proteins.
11 ta dimers or amyloid-beta trimers and tau or synaptic proteins.
12 showing a significant difference between the synaptic proteins.
13 Abeta oligomer level, and inhibited loss of synaptic proteins.
14 t (within 10 min) in the rate of addition of synaptic proteins.
15 omers, and marked down-regulation of several synaptic proteins.
16 cts were formed on cysteine residues of some synaptic proteins.
17 ophore assisted light inactivation (CALI) of synaptic proteins.
18 are commonly found in genes that encode for synaptic proteins.
19 cription factors, other splicing factors and synaptic proteins.
20 th concomitant increases in cAMP, pCREB, and synaptic proteins.
21 iate with antibodies against cell-surface or synaptic proteins.
22 bens neurons to glutamate, and through other synaptic proteins.
23 retrieve and to recycle vesicle membrane and synaptic proteins.
24 morphology, or the distribution of essential synaptic proteins.
25 f amyloid precursor protein, amyloid-beta or synaptic proteins.
26 tant for trafficking and function of several synaptic proteins.
27 d glutamatergic marker VGluT1, pre- and post-synaptic proteins.
28 glutamatergic synapses and interact with key synaptic proteins.
29 ion of the Golgi apparatus and missorting of synaptic proteins.
30 synaptic adhesion and recruitment of diverse synaptic proteins.
31 ole in the localization and function of many synaptic proteins.
32 c postsynaptic proteins and of glutamatergic synaptic proteins.
33 o chronic pain by regulating the turnover of synaptic proteins.
34 nscriptional and translational regulators to synaptic proteins.
35 s, involving recycling and/or degradation of synaptic proteins.
36 eins expressed in hair cells, including many synaptic proteins.
37 the expression levels of a subgroup of other synaptic proteins.
38 What came first: neurons or synaptic proteins?
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
46 monstrate SubSynMAP, a fast, multiplexed sub-synaptic protein analysis method using wide-field data f
47 owever, the influence of ovarian hormones on synaptic protein and opioid peptide levels in the aging
49 decreased fusion, abnormal mitochondrial and synaptic proteins and defective mitochondrial function i
51 un to quantify morphine-regulated changes in synaptic proteins and facilitate the generation of netwo
53 spectrometry, we quantified more than 7,000 synaptic proteins and identified 89 significantly reduce
54 lation of tau and promoted the expression of synaptic proteins and insulin signaling in the brain.
55 st that TOP1 controls the levels of multiple synaptic proteins and is required for normal excitatory
56 constitution of vesicle fusion from purified synaptic proteins and lipids has played a major role in
57 ir cell-like cells had hair bundle proteins, synaptic proteins and membrane proteins characteristic o
58 airs neuronal differentiation, expression of synaptic proteins and neuronal morphology, whereas reduc
59 loss of basal CA1 synaptic strength and key synaptic proteins and reduced the susceptibility to indu
60 vior in female rats, the decline observed in synaptic proteins and spine density in IS and in diestru
64 sets of genes including both those encoding synaptic proteins and those expressed during early devel
65 regulates the clustering and recruitment of synaptic proteins and vesicles to the synapse, adjusting
66 synaptic dysfunction, preventing the loss of synaptic proteins and/or have a positive effect on the i
68 of CaMKII are mediated by interactions with synaptic proteins, and activity-triggered translocation
70 ears earlier than the outer plexiform layer, synaptic proteins, and ribbons are first reliably recogn
71 antibodies against neuronal cell surface or synaptic proteins, and the differential diagnosis with i
72 xpression results in increased levels of the synaptic protein Arc and a concomitant impaired synaptic
74 nhibitory src homology 3 domain, and several synaptic proteins are known to bind to this SH3 domain a
77 early postnatal regulation of mRNAs encoding synaptic proteins are not altered in Fmr1 knockout mice.
80 nd signaling also becomes activated when pre-synaptic proteins are over-expressed, suggesting the exi
81 endent proteins is highly induced while some synaptic proteins are repressed in neurons missing the T
84 s a result of decreased levels of functional synaptic proteins as found in autopsied brains of patien
85 et that mediates intermolecular binding with synaptic proteins as resolved in complexes with TARPgamm
87 ctural plasticity of GCNs, and expression of synaptic proteins associated with learning and memory in
90 or-like protein 1 (APLP1) is a transmembrane synaptic protein belonging to the amyloid precursor prot
93 SD)-linked mutations disrupt the function of synaptic proteins, but no single gene accounts for >1% o
96 onstruction microscopy, the distributions of synaptic proteins can be measured with nanometer precisi
97 Previously, we showed that some GABAergic synaptic proteins change across the lifespan, but most s
98 an unbiased proteomic screen and identified synaptic protein changes in alphabetagamma-synuclein kno
99 These patterns of widespread, but diverse synaptic protein changes in response to global perturbat
100 detail the disease caused by absence of the synaptic protein CNKSR2 in 8 patients ranging from 6 to
102 es revealed individual synaptic proteins and synaptic protein complex densities at prefusion contact
103 proteomics data sets, systematic analysis of synaptic protein complexes showed that, compared with co
105 taking advantage of preparations lacking the synaptic protein complexin, which have elevated spontane
107 k3 gene in adult mice led to improvements in synaptic protein composition, spine density and neural f
109 ions of rapid estrogen-mediated signaling on synaptic proteins, connectivity, and synaptic function i
112 erences in developmental trajectory of these synaptic proteins could contribute to long-term differen
113 the CaMK family with unknown function, as a synaptic protein crucial for dendritic spine maintenance
114 several signaling molecules, receptors, and synaptic proteins currently implicated in ARM operate in
115 proteolytic processing did not accompany the synaptic protein declines, ADAMTS1 may play a nonproteol
116 Furthermore, this treatment prevented pre-synaptic protein deficit, decreased glycogen synthase ki
117 ly in deprived synapses, suggesting targeted synaptic protein degradation under sensory deprivation.
118 ein synapsin I, while antibodies to 16 other synaptic proteins discriminate among 4 subtypes of gluta
119 es reveals distinct, quantitative changes in synaptic proteins distributed across over 6,000 pairwise
120 vealed disease-specific modifications of sub-synaptic protein distributions across synapse classes an
121 by distinctly different firing features and synaptic protein distributions of neurons that innervate
122 an important mechanism for the generation of synaptic protein diversity, but few factors governing th
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 learning of a complex environment activates synaptic proteins essential for the stabilization of lon
127 expression in schizophrenia has an impact on synaptic protein expression and cognition and that these
128 t of mTORC1 whose translation and consequent synaptic protein expression are increased in the nucleus
134 pain-dependent degradation of the inhibitory synaptic protein gephyrin subsequently exacerbated SSC-m
136 halitis with autoantibodies directed against synaptic proteins has become an important component of t
139 bodies to ion channels, receptors, and other synaptic proteins have been recognised over the past 10
141 oline receptors are some of the most studied synaptic proteins; however, many questions remain that c
144 rt that the CIDE-N protein Drep-2 is a novel synaptic protein important for learning and behavioral a
145 boutons in NMJs lacking synapsin [Syn(-)], a synaptic protein important for vesicle clustering, neuro
147 e deficits, CST sprouting, and expression of synaptic proteins in an experimental model of closed hea
148 alpha-synuclein and the expression of other synaptic proteins in cholinergic axons in the guinea pig
149 rt the localization and amount of endogenous synaptic proteins in living neurons and thus may be used
151 r in concert with its regulation of numerous synaptic proteins in NAc as well as with SIRT1-mediated
153 tion concomitantly suppresses the buildup of synaptic proteins in neuronal cell bodies, hence may pla
158 aging on expression of prefrontal GABAergic synaptic proteins in relation to working memory decline,
160 set of dendritic spines and colocalized with synaptic proteins in specific nanodomains, as determined
163 letion results in altered levels of multiple synaptic proteins in the hippocampus, using both male an
165 lation, MAP2 overexpression and reduction of synaptic proteins in the spinal cord of diabetic rats, s
166 d to examine the localization of ciliary and synaptic proteins in Tmem67(bpck) mice and controls.
170 aptic release sites, and a redistribution of synaptic proteins including the vesicle-associated prote
172 striking reduction in the levels of several synaptic proteins, including CaMKII alpha/beta, AMPA, an
174 crease in the cluster size and number of key synaptic proteins, including N-methyl-d-aspartate recept
175 UPS) is known to regulate expression of many synaptic proteins, including presynaptic elements, to op
176 r localization and mediated large changes in synaptic proteins, including proteins implicated in fami
177 orted that estrogens increase levels of post-synaptic proteins, including PSD-95, and opioid peptides
180 ular determinants that are distinct from the synaptic protein interaction site (synprint) found in sy
181 1 in NAc D1+ neurons and increases levels of synaptic proteins involved in glutamatergic signaling.
182 post-transcriptional regulation of critical synaptic proteins involved in maintaining mature neurona
183 oing research efforts are largely focused on synaptic proteins involved in membrane fusion-and-fissio
184 ll as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release i
185 of these substrates, such as N-cadherin, are synaptic proteins involved in synapse remodeling and mai
186 that a striking induction of VGLUT2 mRNA and synaptic protein is triggered by a prolonged increase in
187 n that phosphorylation of serine residues on synaptic proteins is a major regulator of synaptic stren
188 asticity, suggesting that O-GlcNAcylation of synaptic proteins is likely as important as phosphorylat
190 ic GTPase-Activating Protein (SynGAP), a key synaptic protein, is determined by the combination of it
191 of this regulatory mechanism is Complexin, a synaptic protein known to regulate synaptic vesicle exoc
194 months of age, wildtype mice showed altered synaptic protein levels and relatively superior cognitiv
196 More prominently, there were declines in synaptic protein levels in the ADAMTS1 null female, but
197 the existence of a feedback circuit to match synaptic protein levels to the transport capacity of the
199 u dysregulation, which causes a reduction in synaptic protein levels, may be responsible for the cogn
200 -responsive changes in dendritic complexity, synaptic protein levels, spine density and morphology, a
202 molecules and their interactions with other synaptic proteins likely affect not only on synapse form
203 that nonpathogenic HTT can indeed influence synaptic protein localization and uncover a novel role o
204 rologic outcomes, such as protection against synaptic protein loss and synaptic plasticity impairment
206 emonstrate that epigenetic regulation of key synaptic proteins may be an underlying, yet reversible,
209 that ASD-associated mutations in a subset of synaptic proteins may target core cellular pathways that
210 nt depended on a direct interaction with the synaptic protein Munc13, because expression of the II-II
213 L BDNF to regulate excitatory and inhibitory synaptic proteins neuroligin 1 and neuroligin 2, which p
214 r expression of other glutamate receptors or synaptic proteins, number of synapses, dendritic spines,
216 ts were integrated into a software platform, Synaptic Protein/Pathways Resource (SyPPRes), enabling t
217 suggesting that MeCP2 likely regulates these synaptic proteins post-transcriptionally, directly or in
218 y, we demonstrate that SR interacts with the synaptic proteins, postsynaptic density protein 95 (PSD-
219 sis and the calpain-dependent degradation of synaptic proteins, potentially ameliorating the observed
220 tination-directed proteasomal degradation of synaptic proteins, presumably mediated by lysine 48 (K48
222 ogic alpha-syn led to selective decreases in synaptic proteins, progressive impairments in neuronal e
223 e association also impaired synthesis of the synaptic protein PSD-95, suggesting that this phenomenon
224 ent TimeSTAMP tag reveals that copies of the synaptic protein PSD95 are synthesized in response to lo
227 ply a convergent molecular pathway involving synaptic protein recycling that may also be involved in
231 ersible, and activity-dependent insertion of synaptic proteins required during the induction and expr
236 nvolved in translational regulation of major synaptic proteins; scaffolding proteins in excitatory sy
238 % of quantified proteins, including abundant synaptic proteins such as PSD-95 and gephyrin, exhibited
240 Neurotransmitter release is orchestrated by synaptic proteins, such as SNAREs, synaptotagmin, and co
241 ignificant decrease in expression of several synaptic proteins, suggesting a functional deficit of re
242 g/kg, and 5 mg/kg) on behavior and levels of synaptic proteins synapsin-1, postsynaptic density prote
244 oligodendrocytes, enhanced expression of the synaptic proteins synaptophysin and PSD95 in the hippoca
245 synaptic plasticity and a reduced density of synaptic proteins (synaptosomal-associated protein 25, s
246 spines, while disrupting the distribution of synaptic proteins (synaptotagmin 2 and gephyrin) associa
247 emonstrate defects in the trafficking of the synaptic proteins Syntaxin1a and PSD-95 and the TrkB and
248 retardation protein (FMRP), which regulates synaptic protein synthesis and is a key player to limit
249 GluR1/5 have yielded deeper insight into how synaptic protein synthesis and plasticity are regulated
250 target a key mediator of activity-dependent synaptic protein synthesis downstream of mechanistic tar
252 ine-induced increases in mTOR activation and synaptic protein synthesis were mimicked and occluded in
253 report that expression of a key regulator of synaptic protein synthesis, the metabotropic glutamate r
257 synaptic density protein 95 (PSD95), a major synaptic protein that clusters glutamate receptors and i
258 These results suggest that CARM1 is a post-synaptic protein that plays roles in dendritic maturatio
260 ent by controlling the degradation of Arc, a synaptic protein that promotes the internalization of th
262 primary cortical neurons, topotecan depleted synaptic proteins that are encoded by extremely long gen
263 s expansion of the number of cell surface or synaptic proteins that are targets of autoimmunity.
266 linked to synapse loss and/or alterations of synaptic proteins that impair function in regions such a
267 report an in vitro system with reconstituted synaptic proteins that meets the long-sought goal to pro
268 y pathway, endocytosis, and the stability of synaptic proteins, the nature of how this mutation affec
269 neurons by targeting two well-characterized synaptic proteins, the obligatory GluN1 subunit of the N
273 clerosis and the altered expression of three synaptic proteins to cognitive status and global cogniti
274 rms complexes with the clustering of various synaptic proteins to construct postsynaptic signaling ne
275 we use acute in vivo genetic manipulation of synaptic proteins to investigate the molecular basis for
277 ted with intellectual disability (ID) encode synaptic proteins, transcriptional defects leading to ID
280 e Rap1b small GTPase and an associated local synaptic protein translation network in this process.
281 translation of Dgkkappa, indirectly controls synaptic proteins translation and membrane properties by
285 of a specific serine residue (Ser322) on the synaptic protein UNC-18 as an end point for the Galphas-
287 icroglial activation, and loss of excitatory synaptic proteins under conditions in which no viable ba
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 positioning of non-neuronal cells expressing synaptic proteins, while allowing neurites to grow freel
298 pproaches were used to identify and validate synaptic proteins with novel links to heavy drinking in
300 characterized target transcripts of FMRP are synaptic proteins, yet targeting these proteins has not
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