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1 ctivating metabotropic glutamate receptor 3 (mGluR3).
2 y mGluR2 (the proposed treatment target) and mGluR3.
3 dy as a novel antipsychotic therapy aimed at mGluR3.
4  activates a group II metabotropic receptor, mGluR3.
5 uman mGluR2 and is without activity at human mGluR3.
6  RGT cells transfected with human mGluR2 and mGluR3.
7  RGT cells transfected with human mGluR2 and mGluR3.
8 re unable to discriminate between mGluR2 and mGluR3.
9 aptic glutamate release by its action at the mGluR3 (a group II metabotropic glutamate receptor).
10 tion of GCPII inflammatory signaling reduces mGluR3 actions and markedly diminishes dlPFC network fir
11 rated the antipsychotic efficacy of a mGluR2/mGluR3 agonist.
12 ceptor in the antipsychotic action of mGluR2/mGluR3 agonists.
13  increasing the duration of NAAG activity on mGluR3 and by reducing degradation into NAA and glutamat
14                            Alignment between mGluR3 and mGluR2, a closely related group II receptor,
15 al control to two additional family members: mGluR3 and mGluR6.
16 s indicate distinct functions for mGluR2 and mGluR3 and suggest a dynamic regulation of mGluR3 by PP2
17 I metabotropic glutamate receptor subtype 3 (mGluR3) and suppresses glutamate release.
18 bolize cAMP or inhibit its production (PDE4, mGluR3), and by proteins that bind calcium in the cytoso
19      The normal expression levels of mGluR2, mGluR3, and GCP II were determined for 10 regions of the
20 NAAG) is the selective endogenous agonist of mGluR3, and increasing NAAG may improve cognition.
21 etabotropic glutamate receptor (mGluR)-2 and mGluR3, and neuronal nitric oxide synthase.
22  group II metabotropic receptors (mGluR2 and mGluR3) are among different mechanisms that modulate pre
23 tabotropic glutamate receptor 2 (mGluR2) and mGluR3, bind to membranes and that this interaction can
24 e type 1 metabotropic GluR (mGluR1), mGluR2, mGluR3, but not the mGluR5 subtype of G protein-linked m
25 d mGluR3 and suggest a dynamic regulation of mGluR3 by PP2C.
26 ering the metabotropic glutamate receptor 3 (mGluR3) by pharmacology or genetics is associated with d
27 These findings indicate that mGluR2 (but not mGluR3) can selectively modulate GABAergic inhibition in
28            The minimal interacting domain of mGluR3 comprised residues 836-855.
29                                          The mGluR3 cytoplasmic C-terminal tail contains one phosphor
30              However, phosphorylation of the mGluR3 cytoplasmic tail at Ser-845 inhibits the interact
31 not PP1, PP2A, or PP2B, dephosphorylates the mGluR3 cytoplasmic tail in vitro.
32             The dephosphorylated form of the mGluR3 cytoplasmic tail, but not the equivalent region o
33                               Unlike mGluR2, mGluR3 displays basal dynamics, which are Ca(2+)-depende
34          Increased GCP II expression and low mGluR3 expression in the dorsolateral prefrontal cortex
35 COMT) and in metabotropic glutamate receptor mgluR3 (GRM3), respectively, suggest that these genes in
36 , this cooperativity is asymmetric in mGluR2/mGluR3 heterodimers.
37              Here we show that activation of mGluR3 in breast cancer cells activates Rab27-dependent
38 he only known specific endogenous agonist of mGluR3 in the mammalian brain.
39  metabotropic glutamate receptors mGluR2 and mGluR3 in the pathophysiology of schizophrenia.
40 rmine cryo-electron microscopy structures of mGluR3 in the presence of either an agonist or antagonis
41 onversely, activation of the Group II mGluR, mGluR3, induces long-term potentiation of electrical syn
42 oforms; however, among the mGluR family only mGluR3 interacted with PP2C.
43 hat the 50-aa C-terminal cytoplasmic tail of mGluR3 interacts specifically with protein phosphatase 2
44                                              mGluR3 interacts with PP2Calpha, beta, gamma, and delta
45                    GRM3 (the gene coding for mGluR3) is also genome-wide associated with risk for sch
46 tment in rodents did not influence GCP II or mGluR3 levels.
47 parallel fiber synapses, while mGluR2 and/or mGluR3 may modulate mossy terminal function.
48 metabotropic glutamate receptors (mGluR2 and mGluR3) may control relapse of alcohol seeking, but prev
49 adrenergic alpha(2A) adrenergic receptor and mGluR3 (metabotropic glutamate receptor 3) signaling but
50 botropic glutamate receptor subunits mGluR1, mGluR3, mGluR4, mGluR5, and mGluR7.
51 Rs (mGluRs), signals for mGluR1, mGluR2, and mGluR3 mRNAs were low or undetectable, whereas mGluR4 an
52 s process must be tightly regulated, e.g. by mGluR3 or alpha2A-AR on spines, to prevent loss of firin
53 lepticus did not alter expression of mGluR1, mGluR3, or mGluR5 mRNAs.
54 ncrease in GCP II protein and a reduction in mGluR3 protein in the dorsolateral prefrontal cortex in
55            Further, these data implicate the mGluR3 receptor in the antipsychotic action of mGluR2/mG
56  to distinguish the expression of mGluR2 and mGluR3 receptor proteins in schizophrenia and to quantif
57 ormed from NAA, and may be an agonist of the mGluR3 receptor.
58 ed to determine how activation of mGluR2 and mGluR3 receptors (Group II) might modulate visual respon
59 f LY354740 on IPSCs were not mimicked by the mGluR3-selective agonist N-acetyl-aspartyl-glutamate (NA
60 e mGluR2 is resistant to internalization and mGluR3 shows transient beta-arr coupling, which enables
61            Finally, we provide evidence that mGluR3 transducer coupling is controlled by CTD-membrane
62 metabotropic glutamate receptors (mGluR2 and mGluR3) were suggested as targets for addiction treatmen
63 metabotropic glutamate receptors, mGluR5 and mGluR3, which promoted IP3R2-dependent calcium release f
64                                 In contrast, mGluR3, whose activation inhibits adenylate cyclase but