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1                                              OCT1 and OCT2 are involved in renal secretion of cationi
2                                              OCT1 has a broad spectrum of structurally diverse substr
3                                              OCT1 inhibition decreased AP uptake of pentamidine by ap
4                                              OCT1 is the most highly expressed cation transporter in
5                                              OCT1 transports structurally highly diverse substrates.
6                                              OCT1/2 did not transport ethanolamine at physiologically
7  as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG prom
8 c variation in organic cation transporter 1 (OCT1) affects the response to the widely used biguanide
9  metformin via organic cation transporter 1 (OCT1) could increase metformin concentration in the inte
10                Organic cation transporter 1 (OCT1) is a membrane transporter that affects hepatic upt
11                Organic cation transporter 1 (OCT1) is located in the sinusoidal membrane of human hep
12                Organic cation transporter 1 (OCT1) plays a critical role in the hepatocellular uptake
13                Organic cation transporter 1 (OCT1) plays a role in the hepatic uptake of metformin, b
14        Hepatic organic cation transporter 1 (OCT1, SLC22A1) has a broad spectrum of structurally dive
15 1 encoding the organic cation transporter-1 (OCT1) may affect the response of hepatocellular carcinom
16                We analyzed the uptake of 144 OCT1 substrates for the phenylalanine 244 to alanine sub
17 f the Y361A, E386A, and R439A mutants for 15 OCT1 substrates.
18 is accompanied by the appearance of aberrant OCT1 variants that, together with decreased OCT1 express
19                      Both variants abolished OCT1-mediated uptake of tetraethylammonium, a typical OC
20 cytes, but the literature is ambiguous about OCT1 (mOct1) localization, with some evidence suggesting
21 heep and macaques, given relatively abundant OCT1 transporter expression and hepatic uptake following
22 unctional analyses suggest that W354 affects OCT1 transport by forming a hydrogen bond with N453 in t
23 of the CAAT box by an ATF binding site or an OCT1 binding site had no phenotypic effect in an otherwi
24 ment shifted substrate selectivity toward an OCT1-like phenotype.
25 , there was high overlap among MATE1/-2K and OCT1/-2 substrates.
26 -represented in these genes, as were AP1 and OCT1 sites.
27  binding factors, including FOXA1, CTCF, and OCT1.
28 61C, OCT1-P341L, OCT1-G220V, OCT1-G401S, and OCT1-G465R) altered evolutionarily conserved amino acid
29 scription, the homeodomain proteins MSX1 and OCT1.
30  Furthermore, we showed that OBF1, OCT2, and OCT1 bind widely to the promoters or enhancers of genes
31 th the observed differences between OCT3 and OCT1 and to the mechanisms of substrate recognition by O
32 ymorphone, and meptazinol were identified as OCT1 substrates.
33                                      Because OCT1 interacts with a variety of structurally diverse or
34     The ethanolamine influx K(t) mediated by OCT1/2 ranged from 7.6 +/- 3.7 mmol/L (mouse Oct2) to 13
35                    In contrast, transport by OCT1 was less stereoselective, although (R)-tamsulosin w
36 , although (R)-tamsulosin was transported by OCT1 with higher apparent affinity than the (S)-enantiom
37 l-l-carnitine (IBC), as a potential clinical OCT1 biomarker for DDI assessment.
38  29332 metabolites predicted 146 competitive OCT1 ligands, of which an endogenous neurotoxin, 1-benzy
39                           Thirty competitive OCT1 ligands, defined as ligands predicted in silico as
40 forms enhance MSX1 repression and counteract OCT1 activation of the GnRH gene.
41  OCT1 variants that, together with decreased OCT1 expression, may dramatically affect the ability of
42 rce optical coherence tomography device (DRI-OCT1 Atlantis; Topcon).
43             We show the transcription factor OCT1 binds TNF(-857T) but not TNF(-857C), and interacts
44 pon the octamer-binding transcription factor OCT1.
45 ates the expression of transcription factors OCT1 and OBF1, which are known to be critical for the ge
46 ator of the POU family transcription factors OCT1 and OCT2.
47 r assay, and the basal transcription factors OCT1 and SP1 were shown to bind the first and the second
48  trials to evaluate potential biomarkers for OCT1 and additional cation transporters (renal OCT2, MAT
49    Our data suggest that W354 is crucial for OCT1 function by mediating the switch from an inward-occ
50 confirms that the YER motif is essential for OCT1 transport and points to Y361 as a lever that intera
51 rnitine, and metformin, which is a probe for OCT1 and OCT2 and MATE1 and MATE2K (multidrug and toxin
52 001) as was carriage of two reduced-function OCT1 alleles compared with carriage of one or no deficie
53 01) in individuals with two reduced-function OCT1 alleles who were treated with OCT1 inhibitors.
54  the phenotype, carriage of reduced-function OCT1 variants, and concomitant prescribing of drugs know
55 ariants that reduced or eliminated function (OCT1-R61C, OCT1-P341L, OCT1-G220V, OCT1-G401S, and OCT1-
56           A variant with increased function (OCT1-S14F) changed an amino acid residue such that the h
57               In cells expressing functional OCT1 variants, OCT1 inhibition with quinine prevented so
58 function (OCT1-R61C, OCT1-P341L, OCT1-G220V, OCT1-G401S, and OCT1-G465R) altered evolutionarily conse
59 be safer for use in individuals with genetic OCT1 deficiency.
60 nity but at ninefold lower capacity by human OCT1.
61 r the closing of the binding pocket of human OCT1.
62 bstrate ASP(+) in cells overexpressing human OCT1.
63 acterization of all known and possible human OCT1 polymorphisms.
64         Recent studies have shown that human OCT1 is highly polymorphic.
65 ive characterization of phenylalanine 244 in OCT1 function.
66     It showed 86-fold higher accumulation in OCT1-overexpressing cells compared to control cells.
67 " i.e. the 24 residues that are conserved in OCT1 orthologs as one amino acid and in OCT2 as a differ
68 rmin in the kidney was severely decreased in OCT1/2(-/-) mice when evaluated with [(11)C]-Metformin a
69         Conversely, a reciprocal mutation in OCT1 (F161L) shifted the polyamine-sensitivity phenotype
70 cket of OCT3 to the corresponding residue in OCT1 (L166F, F450L, and E451Q) reduced the rate of MPP(+
71 ctional analyses to determine their roles in OCT1 transport, in general, and in substrate specificity
72 ansporters, we tested metformin treatment in OCT1/2(-/-) mice.
73 apeutic action and that genetic variation in OCT1 may contribute to variation in response to the drug
74 er prolonged androgen stimulation, including OCT1 and NKX3-1.
75 omitant use of medications, known to inhibit OCT1 activity, was associated with intolerance (odds rat
76 mitant prescribing of drugs known to inhibit OCT1 transport in 251 intolerant and 1,915 fully metform
77  vitro data and supported its use as a liver OCT1 biomarker.
78                 A short hairpin RNA-mediated OCT1 knockdown in Caco-2 cells decreased AP uptake of pe
79                        We discuss metformin, OCT1, pharmacogenetics, and how the integrative genomics
80 n transport kinetics between human and mouse OCT1 orthologs to identify amino acids that contribute t
81 we identified competitive and noncompetitive OCT1-interacting ligands in a library of 1780 prescripti
82 CR revealed expression of OCT3 mRNA, but not OCT1 or OCT2 mRNA, in the medial hypothalamus.
83 ain reaction detected OCT2 and OCT3, but not OCT1, mRNA expression in CP.
84                                     Notably, OCT1-420del (allele frequency of about 20% in white Amer
85       The organic cation transporters (OCTs) OCT1 on the basolateral membrane of enterocytes and hepa
86                                  Ablation of OCT1 and OCT2 significantly reduced the distribution of
87 ings suggest that structure-function data of OCT1 is not directly transferrable between substrates or
88 report single amino acids as determinants of OCT1 polyspecificity.
89                                Expression of OCT1 and OCT2 in Xenopus oocytes increased hemicholinium
90                                Expression of OCT1 variants in Xenopus laevis oocytes and determinatio
91 ppear to be independent of the expression of OCT1/2 and AMPK-beta1, the most abundant AMPK-beta isofo
92 sess clinical DDI risk for the inhibition of OCT1/2 and MATEs in clinical studies with new drug candi
93 r opioids to be substrates and inhibitors of OCT1.
94 S, competitive and noncompetitive ligands of OCT1 can be predicted.
95 equivocally show AP membrane localization of OCT1 (mOct1) in Caco-2 cells and human and mouse intesti
96 tudy aims at determining the localization of OCT1 (mOct1) in Caco-2 cells, and human and mouse entero
97 l three systems confirmed AP localization of OCT1 (mOct1).
98 liminary findings showing AP localization of OCT1 in Caco-2 cell monolayers, an established model of
99 sions were drawn assuming BL localization of OCT1 in enterocytes.
100 s work provides a complete functional map of OCT1 variants along with a framework for integrating fun
101 e C-terminal half of the rabbit orthologs of OCT1/2.
102 ithin the substrate translocation pathway of OCT1.
103         Seven nonsynonymous polymorphisms of OCT1 that exhibited reduced uptake of metformin were ide
104 s carrying reduced function polymorphisms of OCT1.
105 ds that contribute to the polyspecificity of OCT1.
106 ges at evolutionarily conserved positions of OCT1 are strong predictors of decreased function and sug
107 igher sensitivity pharmacological profile of OCT1.
108 nonymous variants across the 554 residues of OCT1, a key liver xenobiotic transporter.
109  contributes to the substrate specificity of OCT1.
110          Even without a crystal structure of OCT1, machine learning algorithms predict substrates acc
111  characterize novel endogenous substrates of OCT1/2.
112 ensitivity of OCT3 is different from that of OCT1 and OCT2 but correlates significantly with that of
113  also to a better molecular understanding of OCT1 in general.
114         I446 showed only marginal effects on OCT1 transport.
115  measurements in HEK293 cells overexpressing OCT1 or OCT2, to identify and characterize novel endogen
116  eliminated function (OCT1-R61C, OCT1-P341L, OCT1-G220V, OCT1-G401S, and OCT1-G465R) altered evolutio
117 yeast mitochondrial intermediate peptidase ( OCT1 gene, YMIP polypeptide), a metalloprotease required
118        In conclusion, although polyspecific, OCT1 possesses a strong selectivity for its ligands.
119 rmidine, spermine) and polyamine-like potent OCT1 blockers (1,10-diaminodecane, decamethonium, bistri
120 s have previously been screened as potential OCT1 substrates and verified by virtual docking.
121 ng with transport experiment data to predict OCT1 substrates based on classic molecular descriptors,
122 t reduced or eliminated function (OCT1-R61C, OCT1-P341L, OCT1-G220V, OCT1-G401S, and OCT1-G465R) alte
123               Recent data performed with rat OCT1 (rOCT1) suggest that currently performed in vitro t
124             Our results suggest that reduced OCT1 transport is an important determinant of metformin
125 eas only the W354Y mutant partially retained OCT1 activity.
126  transmembrane helix 10, thereby stabilizing OCT1 in its outward open conformation.
127            Methylnaltrexone is the strongest OCT1 substrate currently reported.
128 te peptidase (YMIP polypeptide; gene symbol, OCT1) promotes mitochondrial iron uptake by catalyzing t
129 ad significantly more overlap with OCT2 than OCT1.
130 graphy-dual mass spectrometry confirmed that OCT1 is able to transport sorafenib and that R61S fs*10
131  RNA knockdown experiments demonstrated that OCT1, OCT2, and OBF1 regulate each other and are essenti
132         Collectively, the data indicate that OCT1 is important for metformin therapeutic action and t
133              Further analysis indicated that OCT1 and OCT3 can recognize essentially the same substra
134 tes and elsewhere because it has stated that OCT1 is basolaterally localized in enterocytes.
135 e human protein matched the consensus of the OCT1 mammalian orthologs.
136   The N353L and R403I substitutions (OCT2 to OCT1) did not significantly change the properties of OCT
137       The major metformin uptake transporter OCT1 is expressed in the fetal liver, and fetal hepatic
138 c variants in the hepatic uptake transporter OCT1, observed in 9% of Europeans and white Americans, a
139  the human liver organic cation transporter, OCT1, in Xenopus oocytes.
140              The organic cation transporter, OCT1, is a major hepatic transporter that mediates the u
141                  Organic cation transporters OCT1 (SLC22A1) and OCT2 (SLC22A2) are critically involve
142 and synergy with organic cation transporters OCT1 and OCT2 remain incompletely understood.
143 eviously cloned organic cation transporters (OCT1, OCT2, NKT, NLT, RST, and OCTN1).
144 ated uptake of tetraethylammonium, a typical OCT1 substrate, and were not able to induce sorafenib se
145                                        Using OCT1 and CYP2D6 co-overexpressing cells, an additive eff
146                     Functional studies using OCT1-specific substrate pentamidine showed transporter-m
147 n cells expressing functional OCT1 variants, OCT1 inhibition with quinine prevented sorafenib-induced
148 hat the protective effects of metformin were OCT1/2 independent when tested in this model.
149                      We investigated whether OCT1 plays a role in the action of metformin and whether
150 ncing that OBF1 extensively colocalizes with OCT1 and OCT2.
151 on of metformin and whether individuals with OCT1 polymorphisms have reduced response to the drug.
152 ycodone and hydrocodone do not interact with OCT1 and may be safer for use in individuals with geneti
153 4 interacts in a highly specific manner with OCT1 substrates and inhibitors.
154 -function OCT1 alleles who were treated with OCT1 inhibitors.

 
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