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1 ch we term mitochondrial inner NEET protein (MiNT).
2 s APP, presenilins, and Ca(2+) channels (all Mints).
3  interaction data from IntAct, DIP, BIND and MINT.
4 brane cargo protein that works together with MINTs.
5                                              Mint 1 also inhibited transactivation by the "precleaved
6                             CASK, Velis, and Mint 1 are evolutionarily conserved in Caenorhabditis el
7 d mapping studies revealed that Caskin 1 and Mint 1 bind to the same site on the N-terminal CaM kinas
8 sing knockout mice, we show that deletion of Mint 1 does not impair survival or alter the overall bra
9 ulse depression, suggesting that deletion of Mint 1 impairs the regulation of gamma-aminobutyric acid
10 that bind to synaptic proteins such as CASK (Mint 1 only) and Munc18-1 (Mints 1 and 2) and conserved
11 alternative tripartite complexes with either Mint 1 or Caskin 1 that may couple CASK to distinct down
12 neurons selectively express higher levels of Mint 1 than Mint 2.
13 les was used to assay methylation changes at MINT 1, 2, 3, 12, 17, 25, and 31 in sets of normal, aden
14       The CaM kinase domain of CASK binds to Mint 1, and the region between the CaM kinase and PDZ do
15 unoprecipitations showed that Caskin 1, like Mint 1, is stably bound to CASK in the brain.
16                              Unlike CASK and Mint 1, no Caskin homolog was detected in C. elegans.
17                                     Thus the Mint 1-CASK complex is not required for AMPA- and NMDA-r
18 t an essential developmental function of the Mint 1-CASK complex.
19 aptic plasticity in excitatory synapses from Mint 1-deficient mice and detected no alterations in the
20 t synaptic functions that become apparent in Mint 1-deficient mice in inhibitory interneurons because
21 rons that contain selectively high levels of Mint 1.
22              The approximately 20% surviving Mint 1/2 double knock-out mice exhibit a decrease in wei
23 ression in cultured neurons from conditional Mint 1/2/3 triple knock-in mice also revealed a decline
24                                 We find that Mints 1 and 2 are similarly expressed in most neurons ex
25                        Our data suggest that Mints 1 and 2 but not Mint 3 have a specific effect on A
26 h all Mints were biochemically similar, only Mints 1 and 2 but not Mint 3 strongly inhibited transact
27  among Mints are unexpected, suggesting that Mints 1 and 2 have a brain-specific function related to
28                       Our data indicate that Mints 1 and 2 perform redundant synaptic functions that
29 mmunocytochemistry revealed that in neurons, Mints 1 and 2 were colocalized with APP in the trans-Gol
30 ins such as CASK (Mint 1 only) and Munc18-1 (Mints 1 and 2) and conserved C-terminal PTB- and PDZ-dom
31              Mints/X11s are neuron-specific (Mints 1 and 2) and ubiquitous (Mint 3) adaptor proteins
32  lacking both neuron-specific Mint isoforms (Mints 1 and 2) die at birth, whereas mice lacking any ot
33  composed of three isoforms: neuron-specific Mints 1 and 2, and the ubiquitously expressed Mint 3.
34 nscriptional factor, transient expression of MINT(1-812) suppresses the FGF/forskolin-activated OC pr
35  CpG islands in hMLH1, methylated in tumors (MINT) 1, MINT 2, MINT 31, and CDKN2A (p16).
36               The scaffolding protein LIN-10/Mint-1 also regulates GLR-1 abundance in the nerve cord.
37                           The MALS/Veli-CASK-Mint-1 complex of PDZ proteins occurs on both sides of t
38                                     X11alpha/Mint-1 has multiple protein-protein interaction domains,
39 ectionally regulates the abundance of LIN-10/Mint-1 in the ventral cord.
40                  CDK-5 phosphorylates LIN-10/Mint-1 in vitro and bidirectionally regulates the abunda
41 but six markers (CACNA1G, IGF2, RUNX3, MGMT, MINT-1, and SOCS1) were differentially clustered with CI
42 4a), CHFR, CRABP1, HIC1, IGF2, IGFBP3, MGMT, MINT-1, MINT-31, MLH1, NEUROG1, p14 (CDKN2A/arf), RUNX3,
43                               Methylation at MINT 2, 3, and 31 increased 11-fold (P = .005), 15-fold
44 nds in hMLH1, methylated in tumors (MINT) 1, MINT 2, MINT 31, and CDKN2A (p16).
45 ctively express higher levels of Mint 1 than Mint 2.
46  Our data suggest that Mints 1 and 2 but not Mint 3 have a specific effect on APP function that canno
47 emically similar, only Mints 1 and 2 but not Mint 3 strongly inhibited transactivation by APP-Gal4/VP
48 ron-specific (Mints 1 and 2) and ubiquitous (Mint 3) adaptor proteins composed of isoform-specific N-
49 ints 1 and 2, and the ubiquitously expressed Mint 3.
50 o APP that is not executed by the ubiquitous Mint 3.
51      A yeast two-hybrid screening identified Mint-3 as the EWV-binding protein.
52       siRNA-mediated knockdown of endogenous Mint-3 decreased MT5-MMP activity.
53                                 Furthermore, Mint-3 significantly increased the level of MT5-MMP on t
54                                              Mint-3 stimulates MT5-MMP activity when expressed at low
55 for internalized MT5-MMP by interacting with Mint-3, a protein with two type III PDZ domains.
56 MLH1, methylated in tumors (MINT) 1, MINT 2, MINT 31, and CDKN2A (p16).
57 R, CRABP1, HIC1, IGF2, IGFBP3, MGMT, MINT-1, MINT-31, MLH1, NEUROG1, p14 (CDKN2A/arf), RUNX3, SOCS1,
58                                              Mint adaptor proteins bind to the amyloid precursor prot
59                                              Mint adaptor proteins bind to the membrane-bound amyloid
60   In confocal immunofluorescence microscopy, MINT adopts a reticular nuclear matrix distribution that
61                                              Mints (also called X11-like proteins) are adaptor protei
62 n detect certain lipophilic irritants (e.g., mints, ammonia), the epithelium also houses a population
63 mical analyses, this novel protein was named MINT, an acronym for Msx2-interacting nuclear target pro
64  determined that conditional inactivation of Mint, an inhibitor of Notch-RBP-J interaction, resulted
65 O, and protein-protein interaction data from MINT and BIND.
66 hane lactones may contribute individually to mint and coconut odors, sensory studies suggested for th
67 th CSL, and we also delineate the domains of MINT and CSL that are necessary and sufficient for compl
68  OMIM; protein-protein interaction data from MINT and DIP; functional domain information from Pfam; p
69                                Recently, the MINT and IntAct databases decided to merge their separat
70                                              MINT and OC mRNAs are reciprocally regulated during diff
71 have studied functional interactions between MINT and Runx2, a master regulator of osteoblast differe
72  such as IntAct, BioGRID, ChEMBL, iRefIndex, MINT and STRING.
73                                      Various Mint and/or CASK-containing complexes can be assembled o
74 ted from other databases (IntAct, DIP, BIND, MINT) and are linked to 24,060 experimental evidences (P
75 the Msx2 interacting nuclear target protein (MINT) and Runx2/Cbfa1.
76                              Both IntAct and MINT are active contributors to the IMEx consortium.
77                              We propose that MINTs are a family of Arf-dependent, vesicle-coat protei
78                                              Mints are adaptor proteins that directly interact with t
79               Our studies thus indicate that Mints are important regulators of presynaptic neurotrans
80 the endocytic motif of APP, we proposed that Mints are involved in APP intracellular trafficking, whi
81              These findings demonstrate that Mints are necessary for activity-induced APP and PS1 tra
82 similarity, the functional differences among Mints are unexpected, suggesting that Mints 1 and 2 have
83                 Munc18 interacting proteins (MINTs) are a family of three proteins implicated in the
84 e survival advantage over less mature, newly minted ASCs, by enhancing pro-survival cytokine signalin
85 teoblasts (with endogenous Runx2 and FGFR2), MINT augments transcription driven by the OCFRE that is
86                                 We show that MINTs bind Arfs directly, co-localize with Arf and the A
87                          We demonstrate that MINTs bind Arfs through a region of the PTB domain and t
88 tion of membrane-bound APP via endosomes and Mints bind directly to the endocytic motif of APP, we pr
89                   We now show that all three Mints bind to the cytoplasmic tail of amyloid-beta precu
90 data indicate that the novel nuclear protein MINT binds the homeoprotein Msx2 and coregulates OC duri
91                                    Since X11/Mint binds to APP, and abnormal trafficking of APP contr
92                                     Msx2 and MINT both target an information-dense, osteoblast-specif
93                       Compared to spearmint, mint bush showed comparable antioxidant capacity, strong
94 e show in cultured cells that this region of MINT can inhibit Notch signaling in transcriptional repo
95 aptic proteins showed that acute deletion of Mints caused a selective increase in Munc18-1 and Fe65 p
96 testis library were sequenced to construct a MINT cDNA contig of 11 kb.
97 tative thermodynamic binding analysis of CSL-MINT complexes.
98             All data manually curated by the MINT curators have been moved into the IntAct database a
99 h, and enhanced paired-pulse facilitation in Mint-deficient mice, suggesting a decreased presynaptic
100 ute to the presynaptic phenotype observed in Mint-deficient mice.
101               These results suggest that X11/Mint-dependent endocytosis in dendrites may serve to pro
102 to interesting odorant zones, reminiscent of mint, detected in the studied wine.
103 2 abrogates Runx2-MINT OCFRE activation, and MINT-directed RNA interference reduces endogenous OC exp
104 cellular and molecular mechanisms underlying Mints effect on amyloid production are unclear.
105 reas Fe65 (which binds to APP as strongly as Mints) enhanced transactivation.
106                                        Thus, MINT enhances Runx2 activation of multiprotein complexes
107            Aqueous methanolic extract of the mint exhibited comparable antioxidant capacity to the co
108                            Acute ablation of Mint expression in cultured neurons from conditional Min
109 ps such as the sunflower, potato, coffee and mint families, totalling over 80,000 species(3).
110 (Mentha x piperita) and its relatives in the mint family (Lamiaceae) are accumulated in specialized a
111 er's sage, is an ethnomedicinal plant of the mint family (Lamiaceae).
112 lvinorin A, is a hallucinogenic plant in the mint family that has been used in traditional spiritual
113 stems of sage and other Lamiaceae (Labiatae; mint family) or Scrophulariaceae (figwort family) specie
114         In the MabThera International Trial (MInT) for young good-prognosis patients and the Rituxima
115 l titration calorimetry, we demonstrate that MINT forms a high affinity complex with CSL, and we also
116       Protein sequence analysis reveals that MINT has three N-terminal RNA recognition motifs (RRMs)
117                          However, cultivated mints have complex polyploid genomes and are sterile.
118                            Australian native mints have traditionally been used by the aboriginal peo
119 d event-free survival (EFS; hazard ratio for MInT [HRMInT] = 0.4, P > 001; hazard ratio for RICOVER-6
120 taneous release, confirming that deletion of Mints impair presynaptic function.
121 Mint knock-out neurons, revealing a role for Mints in APP trafficking.
122      Acute conditional deletion of all three Mints in cultured neurons suppresses the accumulation of
123 redox enzymes of monoterpene biosynthesis in mint indicates that these genes arose from different anc
124 Verticillium wilt are top priorities for the mint industry.
125  the PTB domain and the PDZ2 domain, and Arf-MINT interaction is necessary for the increased cellular
126 % identity) to the monoterpene reductases of mint involved in (-)-menthol biosynthesis.
127 port a model whereby one of the functions of Mints is to localize the vesicle fusion protein Munc18 t
128 ely 80% of mice lacking both neuron-specific Mint isoforms (Mints 1 and 2) die at birth, whereas mice
129 hereas mice lacking any other combination of Mint isoforms survive normally.
130  show that APP endocytosis was attenuated in Mint knock-out neurons, revealing a role for Mints in AP
131  analyzed neuronal cultures from control and Mint knockout neurons that were treated with either glut
132 ficking and Abeta generation were blocked in Mint knockout neurons.
133  rescue APP internalization and insertion in Mint knockout neurons.
134 e), dogwoods (Cornaceae), lilies (Liliales), mints (Lamiaceae p.p.), orchids (Orchidaceae), roses (Ro
135 iological studies indicate that knockdown of MiNT leads to increased accumulation of mitochondrial la
136 f curry leaf (EHEC) and the water extract of mint leaf (WEM) showed higher DPPH and ABTS(+) activity.
137 y of different solvent extracts of curry and mint leaf and their effect on colour and oxidative stabi
138   Menthol is a cooling compound derived from mint leaves and is extensively used as a flavoring chemi
139 y in peppermint oil, known for their potent, mint-like olfactory properties.
140 in and syndecan and the cytoplasmic proteins Mint/LIN-10 and Veli/LIN-7.
141 ge/zona occludens-1)-containing protein dX11/Mint/Lin-10, which also regulates synapse expansion down
142 thylation of 16 tumor suppressor genes and 3 MINT loci (acknowledged classifiers of CIMP) in 344 blad
143                         Increased MI of both MINT loci 1 and 31 was significantly associated with MSI
144 P < 0.0001) between methylation of the three MINT loci and methylation index, although the distributi
145               Methylation levels of specific MINT loci can be used as prognostic variables in patient
146 gned to determine whether the methylation of MINT loci during the progression of adenoma to CRC is re
147 ve assessment of methylated alleles at seven MINT loci in primary CRC with contiguous adenomatous and
148                               MI of specific MINT loci may be prognostic indicators of colorectal ade
149 mic hypermethylation of methylated-in-tumor (MINT) loci are both strong prognostic indicators in a su
150 sue at multiple genomic methylated-in-tumor (MINT) loci sequences.
151                                    Increased MINT locus methylation appears to precede MSI and may ha
152  to Alzheimer's disease, deregulation of X11/Mint may be important for Alzheimer's disease pathogenes
153                              In osteoblasts, MINT may serve as a nuclear matrix platform that organiz
154                                   Therefore, Mints may be the adaptor proteins that regulate the traf
155 quality attributes of refrigerated fresh-cut mints (Menthaxpiperita and M. spicata) was studied.
156  used for the p16 and hMLH1 genes, and three MINT (methylated in tumor) loci (MINT1, MINT2, and MINT3
157 supervised grouping analyses of quantitative MINT methylation data of TME trial patients demonstrated
158                                              MINT MI was found to be correlated with mismatch repair
159 nce the selection of one meaning (e.g., coin-mint-money) but failed to emerge when competition betwee
160 aning appropriate to the context (e.g., coin-mint-money) or under conditions of increased competition
161 d was unresolved by the context (e.g., candy-mint-money).
162 olution to a particular meaning (e.g., candy-mint-money).
163                              The corepressor MINT (Msx2-interacting nuclear target protein) has been
164 nding of vesicles to the active zone via the Mint.Munc18-1 complex in conjunction with syntaxin 1.
165 es, and strongly enhance defects seen in X11/Mint mutants.
166  a significant accentuation of freshness and mint notes.
167                         Msx2 abrogates Runx2-MINT OCFRE activation, and MINT-directed RNA interferenc
168 factor Gal4/VP16, we examined the effects of Mints on the proteolytic processing and putative transcr
169                                              MINT only partially co-localizes with Runx2; however, co
170 x odor but not other, nonthreatening, odors (mint or orange) rapidly decreased the number of prolifer
171            Instead, EGL-9 interacts with the Mint orthologue LIN-10, a mediator of GLR-1 membrane rec
172 9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate rec
173                   In addition, we found that Mint overexpression increased excitatory synaptic activi
174 ased cellular levels of beta-APP produced by MINT overexpression.
175 ometimes called "superpostdocs," offer newly minted PhDs instant independence and enable them to unde
176    We developed the Methylation INTegration (mint) pipeline to support the comprehensive analysis of
177 major active component of the hallucinogenic mint plant Salvia divinorum Epling and Jativa (Lamiaceae
178                Acting as a scaffold protein, MINT potentially exerts both positive and negative regul
179 inal) and approximately 250 kDa (C-terminal) MINT protein fragments accumulate in chromatin and nucle
180  Taken together, our study suggests that the MiNT protein functions in the same pathway as its homodi
181                                              Mint proteins are detectable only in brain and are compo
182                                    In brain, Mint proteins are part of a multimeric complex containin
183           Here we report that Drosophila X11/Mint proteins are required for targeting several protein
184 es have shown that loss of each of the three Mint proteins delays the age-dependent production of amy
185 e show that deletion of all three individual Mint proteins delays the age-dependent production of amy
186  with regions of similarity to mammalian X11/mint proteins, containing a phosphotyrosine-binding and
187 tus, Garland thorn, honeydew, heather, lime, mint, rapeseed, sage, strawberry tree, sulla flower, sav
188 however, the molecular mechanisms underlying Mint regulation in APP binding and processing remain unc
189 iated by an endocytic motif, and loss of X11/Mint results in a dramatic increase in cell-surface leve
190 ton, UK) IntAct, the Molecular Interactions (MINT, Rome, Italy) database, the Protein-Protein Interac
191                               The N-terminal MINT RRM domain represents an authentic dsDNA binding mo
192                     In gel shift assays, the MINT RRM domain selectively binds T- and G-rich DNA sequ
193 nction, but it shares homology with the spen/Mint/SHARP family of proteins defined by three amino-ter
194                 The genus Mentha encompasses mint species cultivated for their essential oils, which
195 development of genomic resources for fertile mint species.
196 for participants with chronic low back pain (Mint study) were conducted in 16 multidisciplinary pain
197                                In CV1 cells, MINT synergizes with Runx2 to enhance OCFRE activity in
198 ed in p-menthane monoterpene biosynthesis in mint: the large and small subunits of peppermint (Mentha
199  family, Spen, which includes the vertebrate MINT transcriptional regulator.
200 s from five primary databases: IntAct, HPRD, MINT, UniProt and the Gene Ontology.
201  structural studies reveal that synergy with MINT uniquely requires Runx2 activation domain 3.
202  the levels of the CASK-interacting proteins Mints, Veli/Mals, and neurexins are decreased, whereas t
203 ion threshold of this terpene reminiscent of mint was 0.9mug/L in model hydroalcoholic solution and 7
204             One of the zones, reminiscent of mint, was found in red wines with a prune flavor.
205  assayed for packaging and storing fresh-cut mints were adequate to achieve a relatively long shelf l
206                                 Although all Mints were biochemically similar, only Mints 1 and 2 but
207          The RNA recognition motif domain of MINT (which binds the OCFRE) is required.
208  release, suggesting that the interaction of Mints with Munc18-1 may contribute to the presynaptic ph
209 ase; however, the biological significance of Mint/X11 binding to APP and their possible role in Abeta
210              Previous studies suggested that Mint/X11 proteins influence APP cleavage and affect prod
211         These results suggest that the three Mint/X11 proteins regulate Abeta production by a novel m
212 ind to synaptic-signaling molecules, such as MINT/X11.
213                                              Mints/X11s are adaptor proteins composed of three isofor
214                                              Mints/X11s are neuron-specific (Mints 1 and 2) and ubiqu
215                                              Mints/X11s are neuronal adaptor proteins that bind to am
216 and conditional knock-out mice for all three Mints/X11s.

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