戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              SCAMs represent a unique tumor-specific TREM2(+) populat
2 ow been analyzed by scanning mutagenesis and SCAM.
3  to the accessibility patterns determined by SCAM studies of TMH6 in the opioid and dopamine D2 recep
4 y other GPCR in which TM6 has been mapped by SCAM.
5 sidues to thiol blockers (a technique called SCAM), we have identified the pore-lining residues of a
6                     The tumor rapidly drives SCAM differentiation, with intratumoral injections suffi
7                                 Furthermore, SCAMs actively proliferate and self-propagate through mu
8 TREM2(+) skin cancer-associated macrophages (SCAMs) support the proliferation of a distinct tumor epi
9 l substituted cysteine accessibility method (SCAM) and a new fluorescence binding assay.
10 e substituted cysteine accessibility method (SCAM) in transmembrane domains 6 (TM6) and 7 (TM7) and e
11 e substituted cysteine accessibility method (SCAM) to investigate the membrane-spanning domain struct
12 e substituted-cysteine accessibility method (SCAM) to map the residues in the sixth membrane-spanning
13 e substituted cysteine accessibility method (SCAM) to map the residues of the transmembrane helices (
14 d substituted cysteine accessibility method (SCAM) to provide new evidence for a centrally located ga
15 e substituted-cysteine-accessibility method (SCAM) to the M2 segment and the M1-M2 loop of the acetyl
16 e substituted cysteine accessibility method (SCAM) was applied to the first membrane-spanning segment
17 e substituted-cysteine accessibility method (SCAM) was applied to transmembrane span seven of the hum
18 e substituted-cysteine-accessibility method (SCAM), we are mapping the residues that contribute to th
19 e substituted cysteine accessibility method (SCAM), we defined the VirB2 IM topology and then identif
20 e substituted cysteine accessibility method (SCAM), we evaluated the role of possible pore-lining res
21 e substituted cysteine accessibility method (SCAM), we previously mapped the residues in the third, f
22 e substituted cysteine accessibility method (SCAM).
23 e substituted cysteine accessibility method (SCAM).
24 e substituted cysteine accessibility method (SCAM).
25 e substituted cysteine accessibility method (SCAM).
26 ituted cysteine (Cys) accessibility methods (SCAM) with sodium (2-sulfonatoethyl)methanethiosulfonate
27 e CB2 binding pocket, further confirming our SCAM results.
28                                            S-SCAM (synaptic cell adhesion molecule) and PSD-93 (posts
29                                            S-SCAM is a unique synaptic scaffolding protein that local
30                                            S-SCAM knockdown in cultured hippocampal neurons caused a
31                                            S-SCAM overexpression in the forebrain induces SCZ-like ph
32                                            S-SCAM transgenic mice showed an increased number of later
33                                            S-SCAM/MAGI-2 gene duplication is associated with schizoph
34 x proteins from glomerular lysates, MAGI-2/S-SCAM (membrane-associated guanylate kinase inverted 2/sy
35 he earliest identifiable podocytes, MAGI-2/S-SCAM is first detected in junctional complexes in podocy
36          However, consequences of aberrant S-SCAM expression on GABAergic synapses is little studied.
37        These results suggest that abnormal S-SCAM protein levels disrupt excitation/inhibition balanc
38                                 PSD-93 and S-SCAM bind to APC and its binding partner beta-catenin, r
39 ved in spine/synapse maturation, Shank and S-SCAM.
40 g N-cadherin, alpha-N-catenin, p120ctn and S-SCAM/Magi2.
41 inase inverted-2), a protein also known as S-SCAM (synaptic scaffolding molecule).
42                      MAGI-2 [also known as S-SCAM (synaptic scaffolding molecule)] is a multi-PDZ dom
43  supporting that GABAergic synapse loss by S-SCAM overexpression is due to the activity-induced dispe
44                     Conversely, decreasing S-SCAM levels by RNA interference-mediated knockdown cause
45 ptic Axin2 levels were increased in female S-SCAM Tg mice.
46                                   Finally, S-SCAM overexpression hampered NMDA-induced internalizatio
47                                   Further, S-SCAM increased surface AMPAR levels in the absence of PS
48                                We identify S-SCAM as a novel component of neuronal nicotinic synapses
49                               Importantly, S-SCAM regulated synaptic AMPAR levels in a manner, depend
50 of GSK3beta during long-term depression in S-SCAM overexpressing neurons.
51  and increased synaptic GSK3beta levels in S-SCAM overexpressing neurons.
52                                 Increasing S-SCAM levels in rat hippocampal neurons led to specific i
53                             Interestingly, S-SCAM Tg mice show male-specific impairments in synaptic
54 ion with S-SCAM, were also reduced in male S-SCAM Tg mice.
55 lication of Synaptic Scaffolding Molecule (S-SCAM, also called MAGI-2), which encodes a postsynaptic
56 rt that the synaptic scaffolding molecule (S-SCAM; also called membrane-associated guanylate kinase i
57 which may explain the pathogenic nature of S-SCAM copy number variations.
58           These results reveal the role of S-SCAM in controlling Axin-dependent synaptic localization
59               Here we report the effect of S-SCAM knockdown and overexpression on GABAergic synapses.
60 g the duplication conditions, elevation of S-SCAM levels in excitatory neurons of the forebrain was s
61  to decreased postsynaptic accumulation of S-SCAM, but not PSD-93.
62 e of PSD-95, while PSD-95 was dependent on S-SCAM to increase surface AMPAR levels.
63 validate a causal relationship of the rare S-SCAM CNV and provide supporting evidence for the rare CN
64                              Surprisingly, S-SCAM overexpression also attenuated GABAergic synapses,
65       Together, these results suggest that S-SCAM is an essential AMPAR scaffolding molecule for the
66                        Here we report that S-SCAM Tg mice have male-specific deficits in synaptic GSK
67                               We show that S-SCAM, PSD-93, neuroligin and neurexin are enriched at al
68  calcineurin inhibitor FK506 abolished the S-SCAM overexpression-induced loss of GABA(A) receptors, s
69 ated that Axin-binding is required for the S-SCAM overexpression-induced synaptic GSK3beta reduction.
70                           Furthermore, the S-SCAM transgenic mice provide a valuable new animal model
71                               Notably, the S-SCAM transgenic mice showed a unique sex difference in s
72  duplication and deletion mutations of the S-SCAM/MAGI-2 gene are associated with schizophrenia and i
73               Overexpression studies using S-SCAM mutants with various domain deletions indicated tha
74 e induction of long term-depression, while S-SCAM knockdown did not.
75 mGluR1 internalization by interacting with S-SCAM, a protein that has been implicated in vesicular tr
76 o which GSK3beta binds in competition with S-SCAM, were also reduced in male S-SCAM Tg mice.
77                                        Seven SCAM-sensitive residues (S3107.33, F3147.37, and I3167.3
78                                          The SCAM approach involved a systematic probe of receptor st
79                                          The SCAM data were consistent with a C-terminus at 4.58, but
80 the Xenopus oocyte expression system and the SCAM (substituted cysteine accessibility method), we fou
81                                Combining the SCAM data with rhodopsin-based molecular models of the r
82                           We previously used SCAM to identify water-accessible residues that line the
83 study, using a method coined as the "in vivo SCAM", identified several residues in the channel pore t
84 in vivo functional characterization, in vivo SCAM, electrophysiological studies, and disulfide-trappi