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1 NRG1 could stimulate the stability of PSD-95 in the mann
2 NRG1 enhanced excitatory drive onto fast spiking interne
3 NRG1 enhanced the strength of excitatory synapses onto F
4 NRG1 has multiple isoforms that are generated by usage o
5 NRG1 is the ligand for ERBB3 and 4, members of the epide
6 NRG1 treatment prevents the loss of deprived eye visual
7 NRG1 type I-IV and NRG1-IVNV isoforms were evaluated wit
8 NRG1 was localized to the wound epithelium prior to blas
9 NRG1-ErbB4 signaling controls inhibitory circuit develop
10 NRG1-IVNV was expressed from 16 weeks gestation until ag
17 scued by the administration of neuregulin 1 (NRG1) and nerve growth factor (NGF) recombinant proteins
19 tudies revealed that the ErbB3-neuregulin 1 (NRG1) axis is a dominant pathway responsible for hematog
21 he only autonomous receptor of neuregulin 1 (NRG1) in the basolateral amygdala (BLA), was expressed i
26 protective missense variant in neuregulin 1 (NRG1) linked to schizophrenia by meta-analysis (ie, rs10
27 val, we obtained evidence that neuregulin 1 (NRG1) produced by TICs promotes their proliferation and
29 lines of evidence suggest that neuregulin 1 (NRG1) signaling may influence cognitive function and neu
32 that the signalling pathway of neuregulin 1 (NRG1), a protein involved in the regulation of skeletal
36 studies implicate variants of Neuregulin-1 (NRG1) and its neuronal receptor ErbB4 in schizophrenia a
40 of Schwann cells and neuronal Neuregulin-1 (NRG1) has emerged as the pivotal signal that controls Sc
41 sed by disruption of BMP10 and Neuregulin-1 (NRG1) signaling pathways, two central mediators of myoca
43 ance ectodomain sensitivity of neuregulin-1 (NRG1; epidermal-growth-factor) or CD44 (receptor-tyrosin
44 e critical period downregulates neuregulin-1(NRG1)/ErbB4 signaling in PV neurons, causing retraction
45 gulators, LIMK and SSH1, as end targets of a NRG1 signaling pathway and demonstrates that cofilin1 is
49 ly, we show that interneuronal DISC1 affects NRG1-ErbB4-mediated phenotypes in the fast spiking inter
50 tion and proliferation in HER2-amplified and NRG1-expressing cancer cells, and it displayed single-ag
51 In summary, Mycn acts downstream of BMP and NRG1 cardiogenic signaling pathways to promote normal my
53 levels of ErbB3 in ovarian cancer cells and NRG1 in the omentum allowed for tumor cell localization
54 a functional relationship between DISC1 and NRG1-ErbB4 signalling in mature cortical interneurons.
55 hanism by which cross-talk between DISC1 and NRG1-ErbB4 signalling may contribute to these deficits.
57 ession of GSTT2, CTSA, PPARG, CDA, ENPP1 and NRG1-Iis changing over time and correlates with disease
58 ter injury, probably by regulating ErbB2 and NRG1 levels, identifying a novel player in regulating re
60 rbB4 is highly abundant in interneurons, and NRG1-mediated erbB4 activation has been shown to modulat
63 autocrine signaling loop between Notch1 and NRG1 that controls melanoma growth and provide experimen
64 also demonstrate that the effects of RET and NRG1 are universal across European and Asian ancestries.
66 usceptibility variants at the RET, SEMA3 and NRG1 loci have been detected through genome-wide associa
68 suggest that BRCA1-IRIS and/or BDNF/TrkB and NRG1/ErbB2 could serve as rational therapeutic targets f
74 transgenic mice that expressed excess axonal NRG1-III exhibited continued remodeling, in contrast to
78 entified biological and disease link between NRG1-ErbB4, p110delta, and AKT; and suggest that p110del
82 ight of the association of the genes of both NRG1 and ErbB4 with schizophrenia and dysfunction of GAB
84 dies have strongly implicated membrane-bound NRG1 forms (type III) in the myelination at late stages,
85 ternative splicing, and association of brain NRG1 type IV isoform expression with the schizophrenia-r
86 growth factor neuregulin-1 (Nrg1, encoded by NRG1) is a key signalling factor controlling myelination
87 e found that the glutamatergic impairment by NRG1 overexpression required LIM domain kinase 1 (LIMK1)
88 , and LTP inhibition or reversal mediated by NRG1/ErbB signaling, which requires ErbB4 receptors in P
89 regulates Rac1 activation by BDNF but not by NRG1-Type III in Schwann cells, although both ligands ac
91 analysis confirms the recently reported CD74-NRG1 fusion and suggests that NRG1, NF1 and Hippo pathwa
93 deficits in ctoNrg1 mice require continuous NRG1 abnormality in adulthood, suggesting that relevant
103 ether, our results show that nerve-dependent NRG1/ErbB2 signaling promotes blastemal proliferation in
104 protective effects of fibroblast/CAF-derived NRG1 on cell growth properties of RAF inhibitor-treated
105 y, after the switch to a well-balanced diet, NRG1 cleavage ratio and ErbB4 amount were increased.
107 ronal deficits and involvement of the DISC1, NRG1 and ErbB4 genes in schizophrenia, respectively.
115 ore, overexpression of transcription factors NRG1 and UME6, to maintain yeast and hyphal morphologies
117 lthy individuals carrying risk genotypes for NRG1 and ERBB4, or these 2 together with AKT1, were disp
121 targeting ERBB3 and cMET, the receptors for NRG1 and HGF, respectively, overcome resistance to trame
123 ulate interneuron function, but the role for NRG1-erbB4 signaling in regulating interneuron dendritic
124 gy, and pharmacology, we identify a role for NRG1-IV in learning, memory, and cognition and determine
125 These data demonstrate a novel role for NRG1-IV in learning, memory, and neural circuit formatio
127 on a molecular level, and eight genes (e.g., NRG1 and ERBB4) displayed evidence for pleiotropy, revea
128 nctional analysis revealed that three genes, NRG1, MST1 and NAT9, were strongly correlated with the p
131 terneurons, and offer novel insight into how NRG1/ErbB4 signaling can impact hippocampal activity.
132 h occurs in schizophrenia, understanding how NRG1-erbB4 signaling modulates interneuron dendritic mor
133 T, DRD2, DTNBP1, GAD1, GRIA1, GRIN2B, HTR2A, NRG1, RELN, SNAP-25, TNIK), brain development, myelinati
134 enic mouse model engineered to express human NRG1-IV, an isoform of the NRG1 (Neuregulin 1) gene that
135 yos demonstrated that misexpression of human NRG1 type III results in ectopic Schwann cell migration,
136 mouse model (NRG1-IV/NSE-tTA) in which human NRG1-IV is selectively overexpressed in a neuronal speci
139 uble ectodomains of both type I and type III NRG1 significantly increased expression of Abeta-degradi
140 we have identified mutations within type III NRG1 that disrupt intramembranous proteolytic processing
141 possibility, full-length type I or type III NRG1 was overexpressed via lentiviral vectors in the hip
144 TP is an insuppressible form due to impaired NRG1/ErbB signaling, possibly through the loss of PV int
150 vant phenotypes similar to those observed in NRG1 or ErbB4 null mutant mice, including hyperactivity,
151 isease, however, consistent with its role in NRG1 processing we find that BACE1 inhibition significan
154 ough ligand-blocking HER3 antibodies inhibit NRG1-driven tumor growth, they are ineffective against H
157 ut the neurobiology of a novel NRG1 isoform, NRG1-IV, which is increased in the brains of individuals
160 and fail to increase DA in response to local NRG1 infusion into the dorsal hippocampus, medial prefro
162 iption of NRG1-IVNV, compared with the major NRG1 isoforms, across human prenatal and postnatal prefr
163 Here, we developed a transgenic mouse model (NRG1-IV/NSE-tTA) in which human NRG1-IV is selectively o
164 ," composed of the ErbB4 ligand, neuregulin (NRG1), fused to the avian viral receptor TVB (TVB-NRG1),
165 g from overexpression of HER2 or neuregulin (NRG1) in cancer leads to HER3-mediated oncogenic activat
168 the levels of membrane-tethered neuregulin1 (NRG1-III), a potent activator of SCs normally presented
169 liced proteins belonging to the neuregulin1 (NRG1) gene family of growth and differentiation factors
170 e is known about the neurobiology of a novel NRG1 isoform, NRG1-IV, which is increased in the brains
172 f Glycogen synthase kinase 3, or addition of NRG1 significantly enhanced the efficiency of transdiffe
175 le-phenotype analyses we find association of NRG1 with left ventricular hypertrophy phenotypes, fibri
180 bumin-positive cells mediates the effects of NRG1 on inhibitory circuit formation in the cortex.
182 These results indicate that expression of NRG1 isoforms is regulated by distinct mechanisms, which
185 he role of soluble, heparin-binding forms of NRG1 (type I/II) in regulating early Schwann cell develo
186 veral studies have addressed the function of NRG1 in brain, very little is known about the cleavage a
188 ich may contribute to versatile functions of NRG1 and pathologic mechanisms of brain disorders such a
189 ohistochemistry and in situ hybridization of NRG1 and its active receptor ErbB2 revealed that they ar
193 are associated in melanoma and inhibition of NRG1 signaling leads to melanoma cell growth inhibition
194 ted limbs, and pharmacological inhibition of NRG1 signaling reduced cell proliferation, blocked blast
195 indings highlight the targeted inhibition of NRG1-HER3 pathways as a potential target for the treatme
196 g high levels of phospho-ErbB3, knockdown of NRG1 reduced cell viability and was associated with decr
197 hat ctoNrg1 mice, which mimic high levels of NRG1 observed in forebrain regions of schizophrenic pati
201 study provides the first quantitative map of NRG1 isoform expression during human neocortical develop
202 lecular, cellular, and circuit mechanisms of NRG1/ErbB4 in regulating the initiation of critical peri
204 rophysiological and behavioral phenotypes of NRG1 mutant mice have been investigated extensively, pra
205 re we investigated proteolytic processing of NRG1 type III and demonstrate that the ectodomain can be
207 dependent transcriptional down-regulation of NRG1 and Sok1-mediated degradation of Nrg1 protein.
209 dings suggested a novel synaptogenic role of NRG1 in excitatory synapse development, possibly via sta
210 iched in GABAergic interneurons, the role of NRG1 in excitatory synapse formation in these neurons re
213 he type 2-oriented membrane-retained stub of NRG1 type III is further processed by signal peptide pep
215 ed the temporal dynamics of transcription of NRG1-IVNV, compared with the major NRG1 isoforms, across
218 e that the stimulatory effects of calcyon on NRG1 cleavage and shedding depend on clathrin-mediated e
222 (which encode proteins in the WNT pathway), NRG1 (which encodes an ERBB ligand), and IL16 (which enc
224 tor required for cellular migration, and pro-NRG1 (ADAM17 substrate), which releases the epidermal gr
228 Chronic exercise training also promoted NRG1 cleavage, resulting in increased ErbB4 phosphorylat
229 On the other end, addition of recombinant NRG1 can partially restore melanoma cell growth that is
233 is not only controlled by membrane-retained NRG1 type III, but also in a paracrine manner via proteo
235 se depends on the phosphorylation of several NRG1-ICD serines, in part mediated by protein kinase Cde
236 Here, we show that axon-derived soluble NRG1 translocates from axonal to Schwann cell surfaces i
237 ized, axoglial feedback loop through soluble NRG1 and BDNF critical for early Schwann cell survival a
241 e I/II NRG1 signaling either with a targeted NRG1 antagonist or by shRNA blocks their differentiation
242 ination, our findings identify axon-tethered NRG1 as a molecular determinant for SC-driven neuromuscu
244 and behavioral analyses, we demonstrate that NRG1-IV/NSE-tTA mice exhibit abnormal behaviors relevant
246 a tissue microarray analysis, we found that NRG1 expression and associated HER2 activation occurred
249 Together, these observations indicated that NRG1-ErbB4 signaling is critical to maintaining GABAergi
251 ) in GABAergic interneurons, indicating that NRG1 stimulates the formation of new synapses and streng
262 reported CD74-NRG1 fusion and suggests that NRG1, NF1 and Hippo pathway fusions may play important r
266 aining and a well-balanced diet activate the NRG1 signalling in skeletal muscle of obese rats, possib
267 training and well-balanced diet activate the NRG1-ErbB4 pathway, possibly via the metalloprotease ADA
268 besity, but did not significantly affect the NRG1/ErbB signalling pathway in rat skeletal muscle.
269 developmental risk for schizophrenia at the NRG1 locus, involving a novel class of NRG1 proteins.
270 orrected P values >.05), and affected by the NRG1 genotype (higher striatal responses in controls wit
271 ost robust associations were observed in the NRG1 gene (rs6996585, P=1.08 x 10(-10)) and this SNP was
272 to express human NRG1-IV, an isoform of the NRG1 (Neuregulin 1) gene that is increased in the brains
273 d by increases in cortical expression of the NRG1 receptor, ErbB4 and the downstream signaling target
274 ced obesity could lead to alterations of the NRG1 signalling pathway and that chronic exercise could
275 d diet is associated with alterations of the NRG1 signalling pathway and whether exercise and diet mi
277 sion of BRG1 influences the stability of the NRG1 transcript, thus controlling filamentation through
279 e conversely pharmacological blockade of the NRG1-ErbB pathway prevents myelination, providing direct
280 tify a genetic pathway that converges on the NRG1-responsive transcription factor ETV1 as a critical
281 studies support the rationale to target the NRG1-ErbB3-ErbB2 axis as a novel treatment strategy in a
283 adhesion kinase, and paxillin in response to NRG1, but fail to increase in size possibly due to stabi
284 genesis in rat Schwann cells, in response to NRG1, TGFbeta, and laminins, three major signals implica
287 ve inhibitory neurons infected using the TVB-NRG1 bridge protein receives inputs indiscriminately fro
288 , fused to the avian viral receptor TVB (TVB-NRG1), along with EnvB pseudotyped lentivirus (LV) and r
290 in glioblastoma, MSN-ROS1, TRIM4-BRAF, VAMP2-NRG1, TPM3-NTRK1 and RUFY2-RET in lung cancer, FGFR2-CRE
293 guingly, these deficits were diminished when NRG1 expression returned to normal in adult mice, sugges
295 The association of rs6994992 genotype with NRG1-IVNV expression and the subcellular distribution an
297 fact, synaptic SCs of these adult mice with NRG1-III overexpression exhibited behaviors evident in w
298 the adult rodent brain does not overlap with NRG1 and is more extensive than originally reported, inc
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