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1 f the enzymes prolyl 4-hydroxylase (P4H) and microsomal triglyceride transfer protein.
2 o LDL, and was greater than its affinity for microsomal triglyceride transfer protein.
3 ells were incubated with an inhibitor of the microsomal triglyceride transfer protein.
4 ed cellular apoB stability via activation of microsomal triglyceride transfer protein.
5 decreased expression of Mttp and its product microsomal triglyceride transfer protein.
6 posttranscriptional effects on the LDLR and microsomal triglyceride transfer protein.
7 was normalized by inactivating the gene for microsomal triglyceride transfer protein.
8 er conditional knockout of the gene encoding microsomal triglyceride transfer protein.
9 including apolipoprotein B (apoB), apoE, and microsomal triglyceride transfer protein.
10 al apoB synthetic rate, and abundance of the microsomal triglyceride transfer protein 97-kDa subunit
11 Finally, mRNA levels of the large subunit of microsomal triglyceride transfer protein, a required com
12 /-) mice contain higher levels of intestinal microsomal triglyceride transfer protein, absorb more li
13 tion both in vivo and in vitro, inhibits the microsomal triglyceride transfer protein activity as wel
16 ylase alpha(2)beta(2)-tetramer (P4H) and the microsomal triglyceride transfer protein alphabeta-dimer
19 and/or vit genes, the orthologs of mammalian microsomal triglyceride transfer protein and apolipoprot
20 ry-low-density lipoprotein (VLDL) synthesis (microsomal triglyceride transfer protein and apolipoprot
21 id absorption in the small intestine, namely microsomal triglyceride transfer protein and apolipoprot
22 osis by enhancing proteasomal degradation of microsomal triglyceride transfer protein and can be part
23 ApoB-independent pathways do not require microsomal triglyceride transfer protein and involve eff
24 activity of beta-apocarotenoids and identify microsomal triglyceride transfer protein and its transcr
25 ts that block VLDL assembly: an inhibitor of microsomal triglyceride transfer protein and siRNA direc
26 a conditional allele for Mttp (the gene for microsomal triglyceride transfer protein) and the induci
27 in part by transcriptional effects on apoB, microsomal triglyceride transfer protein, and lipogenic
28 lipoprotein lipase and reduced expression of microsomal triglyceride transfer protein, apolipoprotein
31 ates transcription and activity of placental microsomal triglyceride transfer protein as well as expr
32 a stable lipoprotein structure by inhibiting microsomal triglyceride transfer protein attenuates the
33 duce cytosolic Hsp70 or with an inhibitor of microsomal triglyceride transfer protein; both treatment
34 monensin, cycloheximide, and an inhibitor of microsomal triglyceride transfer protein but remains unc
40 ol and mitigates atherosclerosis by reducing microsomal triglyceride transfer protein expression and
41 ons, plasma apoB-containing lipoproteins and microsomal triglyceride transfer protein expression exhi
42 hibits triglyceride secretion and intestinal microsomal triglyceride transfer protein expression in v
43 ts length, its requirement for lipidation or microsomal triglyceride transfer protein expression.
45 ed lipoprotein production by down-regulating microsomal triglyceride transfer protein expression.
47 reversed by conditional inactivation of the microsomal triglyceride transfer protein gene, were plac
48 ssion of genes encoding apolipoprotein B and microsomal triglyceride transfer protein, (ii) an increa
49 been made towards understanding the role of microsomal triglyceride transfer protein in lipoprotein
50 summarizes recent advances about the role of microsomal triglyceride transfer protein in plasma and t
51 Acyl-CoA:Cholesterol acyltransferase 1, and microsomal triglyceride transfer protein in the intestin
52 id levels of BMS-201038, an inhibitor of the microsomal triglyceride transfer protein, in six patient
55 duce apoB degradation, but the addition of a microsomal triglyceride transfer protein inhibitor led t
56 med to assess the efficacy and safety of the microsomal triglyceride transfer protein inhibitor lomit
58 Upon omitting fatty acids from, or adding a microsomal triglyceride transfer protein inhibitor to, c
60 us expression systems, as well as the use of microsomal triglyceride transfer protein inhibitors in h
61 second-generation antisense oligonucleotide, microsomal triglyceride transfer protein inhibitors that
62 ay is induced by oleic acid, is repressed by microsomal triglyceride transfer protein inhibitors, and
63 ydrogenase 1A1, and catalase, as well as the microsomal triglyceride transfer protein, involved in re
67 poprotein secretion (e.g., in heart-specific microsomal triglyceride transfer protein knockout mice)
70 at physiological levels increased intestinal microsomal triglyceride transfer protein levels and acti
76 ted by either 6 mM OA or 20% Intralipid, but microsomal triglyceride transfer protein mRNA was signif
77 ve expression of 7alpha-hydroxylase mRNA and microsomal triglyceride transfer protein mRNA, a gene pr
78 ing or genetic or pharmacologic reduction in microsomal triglyceride transfer protein (MTP) activity,
81 strated protein-protein interactions between microsomal triglyceride transfer protein (MTP) and apoli
83 hylomicron and HDL pathways are dependent on microsomal triglyceride transfer protein (MTP) and ATP-b
84 lesterol absorption pathways and the role of microsomal triglyceride transfer protein (MTP) and ATP-b
85 by inhibiting lipid transfer mediated by the microsomal triglyceride transfer protein (MTP) and is pr
87 f a complex between apolipoprotein (apo)B, a microsomal triglyceride transfer protein (MTP) and prote
95 oth the apolipoprotein B (apoB) gene and the microsomal triglyceride transfer protein (MTP) gene is r
100 of biarylamide-substituted diaminoindanes as microsomal triglyceride transfer protein (MTP) inhibitor
102 ation across the endoplasmic reticulum by an microsomal triglyceride transfer protein (MTP) inhibitor
105 h accumulate triglycerides when treated with microsomal triglyceride transfer protein (MTP) inhibitor
113 h lipid synthesis, proteasomal activity, and microsomal triglyceride transfer protein (MTP) lipid-tra
115 ty lipoprotein (VLDL) secretion and elevated microsomal triglyceride transfer protein (MTP) mRNA and
118 The first involves transfer of lipid by the microsomal triglyceride transfer protein (MTP) to apoB d
121 eins, increased cellular lipids, and reduced microsomal triglyceride transfer protein (MTP) without d
130 n of IL-10, CD1d, and its critical regulator microsomal triglyceride transfer protein (MTP), as well
131 lipoproteins, a process that is dependent on microsomal triglyceride transfer protein (MTP), can cont
133 teinemia, a disease caused by defects in the microsomal triglyceride transfer protein (MTP), do not p
137 d lipidated apoB forms despite their lack of microsomal triglyceride transfer protein (MTP), which me
139 s observed in Chinese hamster ovary cells, a microsomal triglyceride transfer protein (MTP)-negative
151 defect can be overcome by coexpression with microsomal triglyceride transfer protein (MTP); moreover
153 rough genetic or pharmacologic inhibition of microsomal triglyceride transfer protein (Mttp) causes h
157 l mediates the transcriptional regulation of microsomal triglyceride transfer protein via hepatic nuc
158 low density lipoprotein receptor) as well as microsomal triglyceride transfer protein were elevated a
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