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1 secretion into bile by targeting Mrp2 to the canalicular membrane.
2 es, and maintained an abnormal intracellular canalicular membrane.
3 ated Ca(2+) signals in targeting Mrp2 to the canalicular membrane.
4 tes, although Bsep remained localized to the canalicular membrane.
5 r (FXR) or by impairing the structure of the canalicular membrane.
6 esistance-associated protein 2 to the apical canalicular membrane.
7 traffic directly from Golgi membranes to the canalicular membrane.
8 solateral membranes, but only fused with the canalicular membrane.
9 compared with the amount present in the bile canalicular membrane.
10 r membrane before treatment, appeared at the canalicular membrane.
11 d and nonbile acid organic anions across the canalicular membrane.
12 retrieval of bile salt export pump from the canalicular membrane.
13 nce analysis, was due to interactions at the canalicular membrane.
14 is constitutively expressed in normal liver canalicular membrane.
15 ective bile acid transport at the hepatocyte canalicular membrane.
16 the endoplasmic reticulum instead of at the canalicular membrane.
17 e tubulovesicle compartment, into the apical canalicular membrane.
18 P < 0.01) and its tissue localization at the canalicular membrane.
19 ll, predominantly localizing with F-actin to canalicular membranes.
20 ile acid transporters on both sinusoidal and canalicular membranes.
21 a protein, which is highly enriched in mouse canalicular membranes.
22 te and dinitrophenyl-glutathione directly in canalicular membranes.
23 of DHE but not its enrichment in the apical (canalicular) membrane.
25 tate distribution after 20 h of SPGP between canalicular membrane and a combined endosomal fraction.
26 nt of ATP-dependent transporters to the bile canalicular membrane and are accompanied by increased ca
27 ransport of bile acids across the hepatocyte canalicular membrane and for generation of bile acid-dep
28 revealed that BSEP-YFP was localized at the canalicular membrane and in tubulo-vesicular structures
29 suggests cycling of ABC transporters between canalicular membrane and intrahepatic sites before degra
30 ATP)-dependent transport of E217G in the rat canalicular membrane and protect against E217G-mediated
31 ated the exocytic insertion of Mrp2 into the canalicular membrane and the recovery of bile flow and b
32 ietal cells exhibited limited development of canalicular membranes and a virtual absence of tubuloves
33 Electron microscopy revealed abnormal apical canalicular membranes and loss of tubulovesicles in muta
34 ocytes, (2) altered targeting of BSEP to the canalicular membrane, and (3) increased ileal BA absorpt
35 8 expression was localized to the hepatocyte canalicular membrane, and bile Mn levels were increased
36 nt of ATP-dependent transporters to the bile canalicular membrane, and PI 3-kinase products are impor
38 ved, and BSEP, which was not detected at the canalicular membrane before treatment, appeared at the c
39 omol/L E(2)17G, respectively, whereas in rat canalicular membrane, both E(2)17G and the choleretic es
40 by favoring bile acid-induced injury in the canalicular membrane but does not directly affect FXR ex
41 amounts of SPGP, MDR1, and MDR2 in the bile canalicular membrane by 3-fold; these effects abated aft
42 ut during stimulation, it is shuttled to the canalicular membrane by a poorly understood mechanism th
43 rter pools, one of which is mobilized to the canalicular membrane by cAMP and the other, by taurochol
44 (CsA), which is transported across the bile canalicular membrane by P-glycoprotein, on the biliary e
45 ering that BSEP activity directly depends on canalicular membrane cholesterol content, decreased BSEP
47 ic bile acid CDCA resulted in focal areas of canalicular membrane disruption by electron microscopy a
49 phosphatidylcholines and cholesterol to the canalicular membrane for ongoing biliary lipid secretion
52 nslocator specifically expressed at the bile canalicular membrane in hepatocytes, highly homologous t
54 strated endocytic retrieval of Mrp2 from the canalicular membrane into pericanalicular and intracellu
55 ny cell systems, and Ca(2+) release near the canalicular membrane is mediated by the type II inositol
59 es phosphatidylcholine (PC) secretion at the canalicular membrane of hepatocytes and its genetic defe
60 The secretion of phospholipids across the canalicular membrane of hepatocytes occurs via the multi
61 inding cassette transporter localized at the canalicular membrane of hepatocytes that plays an import
62 wo sites (apical membrane of enterocytes and canalicular membrane of hepatocytes) to mediate choleste
63 cassette (ABC) transporter expressed at the canalicular membrane of hepatocytes, where it mediates p
70 ntly discovered that NPC1L1 localizes to the canalicular membrane of primate hepatocytes and that NPC
73 tical trans-locator for phospholipids across canalicular membranes of hepatocytes, evidenced by the f
74 ABC transporters are targeted to the apical (canalicular) membrane of hepatocytes where they execute
75 tte transporters are targeted to the apical (canalicular) membrane of hepatocytes, where they mediate
76 d along basolateral (sinusoidal) and apical (canalicular) membranes of hepatocytes, are integral dete
77 ed that single BSEP-YFP molecules resided in canalicular membranes only transiently before exchanging
78 the internal to external hemileaflet of the canalicular membrane permits exovesiculation of the exte
79 ctivity and abundance of transporters in the canalicular membrane regulate bile flow; however, little
80 cid transporters on both the basolateral and canalicular membranes, resulting in intrahepatic cholest
81 as associated with a marked reduction in the canalicular membrane structure as observed by differenti
82 2 and 4, which localize to granules and open canalicular membranes, together with the general target
83 the polarized targeting and/or retaining of canalicular membrane transporters and is a critical dete
84 tion, kinase activity, and protein levels in canalicular membrane vesicle (CMV) and sinusoidal membra
85 e and dinitrophenyl-glutathione transport in canalicular membrane vesicles above maximal ATP-dependen
86 HAX-1 was bound to BSEP, MDR1, and MDR2 in canalicular membrane vesicles and co-localized with BSEP
87 macrophages doubled PI 3-kinase activity in canalicular membrane vesicles and enhanced taurocholate
88 ate and PI 3-kinase activity were reduced in canalicular membrane vesicles isolated from rat liver th
89 ncrease in the amount of ABC transporters in canalicular membrane vesicles was observed, whereas the
90 a rat liver subcellular fraction enriched in canalicular membrane vesicles, and MLC2 colocalized with
91 rat liver subcellular fractions enriched for canalicular membrane vesicles, microsomes, and clathrin-
93 hosphate-dependent taurocholate transport in canalicular membrane vesicles, was induced by 90% (P < 0
95 , recombinant ABCG5 localized to the apical (canalicular) membrane when coexpressed with ABCG8, but n
96 bstrates by inducing Mrp2 retrieval from the canalicular membrane, whereas cyclic adenosine monophosp
97 molecules and the ectoplasmic leaflet of the canalicular membrane, which result in biliary secretion
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