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1 evidence of a role for allelic variation in SLCO1B1.
2 n the organic anion transporter polypeptide, SLCO1B1.
3 pe alleles (n = 10), SLCO1B1*1b/*1b (n = 8), SLCO1B1*15/*15 (n = 7), SLCO1B1*5/*15 (n = 1), SLCO1B1*1
4 CO1B1*15/*15 (n = 7), SLCO1B1*5/*15 (n = 1), SLCO1B1*1a/*5 (n = 6), and SLCO1B3*4/*4 (n = 4) by using
5 explained by UGT1A1*93, ABCC1 IVS11 -48C>T, SLCO1B1*1b, ANC baseline levels, sex, and race (P < .000
6 s of SLCO1B1/1B3 wild-type alleles (n = 10), SLCO1B1*1b/*1b (n = 8), SLCO1B1*15/*15 (n = 7), SLCO1B1*
7 cid were evaluated in 36 healthy carriers of SLCO1B1/1B3 wild-type alleles (n = 10), SLCO1B1*1b/*1b (
8 pair statin metabolism; the reduced function SLCO1B1*5 allele impairs statin clearance and is associa
11 he curve (AUC) is explained by ABCC2 -24C>T, SLCO1B1*5, HNF1A 79A>C, age, and CPT-11 dose (P < .0001)
12 O1B1*1b/*1b (n = 8), SLCO1B1*15/*15 (n = 7), SLCO1B1*5/*15 (n = 1), SLCO1B1*1a/*5 (n = 6), and SLCO1B
15 equenced CYP2D6, CYP2C8, CYP2C9, CYP3A4, and SLCO1B1 and tested 7 reduced function alleles for associ
16 n a multivariate analysis including TPMT and SLCO1B1 as covariates, consistent with its influence on
17 on study of children with ALL, we identified SLCO1B1 as harboring multiple common polymorphisms assoc
18 yet heretofore low-priority candidate gene, SLCO1B1, as important determinants of methotrexate's pha
19 orvastatin concentration was associated with SLCO1B1 c.388A>G (P<0.01) and c.521T>C (P<0.05) and 4bet
20 x, ethnicity, dose, and time from last dose, SLCO1B1 c.521T>C (P<0.001) and ABCG2 c.421C>A (P<0.01) w
21 tested the hypothesis that rare variants in SLCO1B1 could affect methotrexate clearance and compared
24 lded a single nucleotide polymorphism in the SLCO1B1 gene for the organic anion-transporting polypept
26 We verified lower function in vitro of four SLCO1B1 haplotypes that were associated with reduced met
27 ease processes, and the roles for UGT1A1 and SLCO1B1 in drug metabolism, these genetic findings have
33 e 12p12.2 region was a non-synonymous SNP in SLCO1B1 (rs4149056, P = 6.7 x 10(-13)), which gives rise
34 re damaging NS variants constituted 17.8% of SLCO1B1's effects (1.9% of total variation) and had larg
35 earance: SLC10A1, SLC22A1, SLC22A7, SLC47A1, SLCO1B1, SLCO1B3, SLCO2B1, ABCB1, ABCB11, ABCC2, ABCC3,
39 enotypes for the top UGT1A1 variant, the top SLCO1B1 variant remained highly significant (P = 7.3 x 1
40 or other genetic and non-genetic covariates, SLCO1B1 variants accounted for 10.7% of the population v
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