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1 ga target, the organic cation transporter 2 (OCT2).
2 n efficacy maximally in cells overexpressing OCT2.
3 d not significantly change the properties of OCT2.
4 D) values for binding to the model of rabbit OCT2.
5 f threonine 223 in the DNA-binding domain of OCT2.
6 t OBF1 extensively colocalizes with OCT1 and OCT2.
7 he POU family transcription factors OCT1 and OCT2.
8 fic enhancer, where the risk allele disrupts OCT2/4 binding, allowing increased interaction with the
10 s dependent on organic cation transporter 2 (OCT2), a dopamine transporter, providing an explanation
11 attenuated by saracatinib via inhibition of OCT2, a potential consideration for the clinical develop
17 one genes HIST1H1 B-E (27%) and mutations in OCT2 (also known as POU2F2; 8%), IRF8 (6%), and ARID1A (
18 a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors and tha
22 nding motifs that became heavily loaded with OCT2 and its GC-specific coactivator OCAB in GC B cells
23 and metformin, which is a probe for OCT1 and OCT2 and MATE1 and MATE2K (multidrug and toxin extrusion
24 c decreases in the kidney mRNA expression of Oct2 and Mate1, whereas Oct1 mRNA expression was only de
25 olocalization of IkappaBzeta with the POU TF OCT2 and NF-kappaB:p50 at hundreds of DNA elements harbo
28 es of exogenous organic cation transporters (OCT2 and OCT3), organic anion transporter (OAT1), and mo
30 redominantly B-cell-restricted expression of OCT2 and the absence of a systemic phenotype in our knoc
33 significant upregulation of organic cation (OCT2) and organic anion (OAT1/3) transporters, which lea
35 nockdown experiments demonstrated that OCT1, OCT2, and OBF1 regulate each other and are essential for
37 in cells overexpressing mouse Oct2 or human OCT2, and this process was associated with increased DNA
39 nd in vivo data indicate that mouse Oct1 and Oct2 are essential for facilitating the exit step of fre
41 d in OCT1 orthologs as one amino acid and in OCT2 as a different one, influence homolog-specific sele
42 ues on the activity of the human ortholog of OCT2, as expressed in Chinese hamster ovary-K1 cells.
43 hypothetical three-dimensional structure of OCT2 based on a homology model that used the Escherichia
47 SEs with high abundance of pre-positioned OCT2 binding preferentially formed long-range chromatin
49 is competition assays indicated that catfish Oct2 binds the consensus octamer motif with an apparentl
50 POU homeodomain transcription factors Oct1, Oct2, Brn4, SCIP, Skn1a or Skn1i, results in a strong su
51 y of OCT3 is different from that of OCT1 and OCT2 but correlates significantly with that of the extra
53 es suggest that pharmacological targeting of OCT2 could be exploited to afford neuroprotection in can
55 Our data indicate that the PORE-type Oct1 or Oct2 dimer, rather than the monomer, is the primary targ
56 lustering of regulatory elements enriched in OCT2 DNA-binding motifs that became heavily loaded with
57 and reduced tetraethylammonium transport by OCT2 expressed in Chinese hamster ovary cells, effects t
61 model of the three-dimensional structure of OCT2, Glu(447) was found in a putative docking region wi
62 of multiple octamer motifs suggests that an Oct2 homologue may play an important role in driving exp
63 cells are formed normally after depletion of OCT2 in a conditional knockout mouse, but their prolifer
66 al role of the organic cation transporter 2 (OCT2) in satellite glial cells in oxaliplatin-induced ne
67 istinct molecular properties of MATE1 versus OCT2 inhibitors and was used to screen the DrugBank in s
70 These data demonstrate that cysteine 474 of OCT2 is exposed to the aqueous milieu of the cleft and c
72 found that the organic cation transporter 2 (OCT2) is expressed on dorsal root ganglia cells within t
73 comparisons with mammalian Oct2, the catfish Oct2 isoforms show high sequence conservation in their N
74 subtly alters the DNA-binding preference of OCT2, leading to the transactivation of noncanonical tar
80 ntroducing mutations designed to disrupt the OCT2-OCA-B interface, we reveal a requirement for this p
81 uirement for the B-cell transcription factor OCT2 (octamer-binding protein 2, encoded by Pou2f2) in g
82 ransferase complex, and transcription factor OCT2 (octamer-binding transcription factor 2) bound coop
83 membrane of enterocytes and hepatocytes and OCT2 on the basolateral membrane of proximal tubular cel
85 16- to 35-fold in cells overexpressing mouse Oct2 or human OCT2, and this process was associated with
88 ifs were examined to determine if they bound Oct2 POU domains in monomeric or dimeric (PORE and MORE)
91 ermore, genetic or pharmacologic knockout of Oct2 protected mice from hypersensitivity to cold or mec
94 ganic cation transporters OCT1 (SLC22A1) and OCT2 (SLC22A2) are critically involved in absorption and
95 anion transporters Slc22a1 (Oct1), Slc22a2 (Oct2), Slc22a6 (Oat1), Slc22a8 (Oat3), and Slc47a1 (Mate
96 notype in our knockout mice, suggest that an OCT2-targeted therapeutic strategy would be efficacious
99 e broad transcriptional program regulated by OCT2 that includes the expression of STAT3, IL-10, ELL2,
101 some other multidrug transporters, including OCT2, the results suggest that substrate identity exerts
104 ments in HEK293 cells overexpressing OCT1 or OCT2, to identify and characterize novel endogenous subs
105 iched in motifs belonging to PU.1, TCF3, and OCT2 transcription factors and involved elevated MYD88/T
107 eurotoxicity, and demonstrate that targeting OCT2 using genetic and pharmacological approaches amelio
110 ng the humoral immune response, we show that OCT2 was the dominant transcription factor linked to dif
111 ounds plays a role in their interaction with OCT2, we examined the influence of external pH values on
113 inhibitors of organic cation transporter 2 (OCT2), which contributes to the cellular accumulation of