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1 flux transporter for bile acids on the liver canalicular membrane.
2 ile flow and transporter localization to the canalicular membrane.
3 r membrane before treatment, appeared at the canalicular membrane.
4  retrieval of bile salt export pump from the canalicular membrane.
5  the endoplasmic reticulum instead of at the canalicular membrane.
6 secretion into bile by targeting Mrp2 to the canalicular membrane.
7 es, and maintained an abnormal intracellular canalicular membrane.
8 ated Ca(2+) signals in targeting Mrp2 to the canalicular membrane.
9 tes, although Bsep remained localized to the canalicular membrane.
10 r (FXR) or by impairing the structure of the canalicular membrane.
11 esistance-associated protein 2 to the apical canalicular membrane.
12 traffic directly from Golgi membranes to the canalicular membrane.
13 solateral membranes, but only fused with the canalicular membrane.
14 compared with the amount present in the bile canalicular membrane.
15 d and nonbile acid organic anions across the canalicular membrane.
16 nce analysis, was due to interactions at the canalicular membrane.
17  is constitutively expressed in normal liver canalicular membrane.
18 ective bile acid transport at the hepatocyte canalicular membrane.
19 e tubulovesicle compartment, into the apical canalicular membrane.
20 P < 0.01) and its tissue localization at the canalicular membrane.
21 er of organic anions expressed in hepatocyte canalicular membranes.
22 ll, predominantly localizing with F-actin to canalicular membranes.
23 ile acid transporters on both sinusoidal and canalicular membranes.
24 a protein, which is highly enriched in mouse canalicular membranes.
25 te and dinitrophenyl-glutathione directly in canalicular membranes.
26 of DHE but not its enrichment in the apical (canalicular) membrane.
27                      Transport of DHE to the canalicular membrane after photobleaching was very rapid
28 tate distribution after 20 h of SPGP between canalicular membrane and a combined endosomal fraction.
29 nt of ATP-dependent transporters to the bile canalicular membrane and are accompanied by increased ca
30 ransport of bile acids across the hepatocyte canalicular membrane and for generation of bile acid-dep
31  revealed that BSEP-YFP was localized at the canalicular membrane and in tubulo-vesicular structures
32 suggests cycling of ABC transporters between canalicular membrane and intrahepatic sites before degra
33 ATP)-dependent transport of E217G in the rat canalicular membrane and protect against E217G-mediated
34 ated the exocytic insertion of Mrp2 into the canalicular membrane and the recovery of bile flow and b
35 ietal cells exhibited limited development of canalicular membranes and a virtual absence of tubuloves
36 Electron microscopy revealed abnormal apical canalicular membranes and loss of tubulovesicles in muta
37 ocytes, (2) altered targeting of BSEP to the canalicular membrane, and (3) increased ileal BA absorpt
38 8 expression was localized to the hepatocyte canalicular membrane, and bile Mn levels were increased
39 nt of ATP-dependent transporters to the bile canalicular membrane, and PI 3-kinase products are impor
40                  Transporters at the hepatic canalicular membrane are essential for the formation of
41 ved, and BSEP, which was not detected at the canalicular membrane before treatment, appeared at the c
42 omol/L E(2)17G, respectively, whereas in rat canalicular membrane, both E(2)17G and the choleretic es
43  by favoring bile acid-induced injury in the canalicular membrane but does not directly affect FXR ex
44  amounts of SPGP, MDR1, and MDR2 in the bile canalicular membrane by 3-fold; these effects abated aft
45 ut during stimulation, it is shuttled to the canalicular membrane by a poorly understood mechanism th
46 rter pools, one of which is mobilized to the canalicular membrane by cAMP and the other, by taurochol
47  (CsA), which is transported across the bile canalicular membrane by P-glycoprotein, on the biliary e
48 ering that BSEP activity directly depends on canalicular membrane cholesterol content, decreased BSEP
49                                          Rat canalicular membranes contain microdomains enriched in c
50 ic bile acid CDCA resulted in focal areas of canalicular membrane disruption by electron microscopy a
51                    We previously showed that canalicular membrane-enriched vesicles isolated from EHB
52  phosphatidylcholines and cholesterol to the canalicular membrane for ongoing biliary lipid secretion
53                    With both basolateral and canalicular membrane fractions, sulindac inhibited choly
54 ne proteins to their site of function at the canalicular membrane front.
55 nslocator specifically expressed at the bile canalicular membrane in hepatocytes, highly homologous t
56 ein that transports phospholipids across the canalicular membrane in hepatocytes.
57 thelial cells in the kidney, intestine, bile-canalicular membrane in the liver, blood-brain barrier,
58 strated endocytic retrieval of Mrp2 from the canalicular membrane into pericanalicular and intracellu
59 ny cell systems, and Ca(2+) release near the canalicular membrane is mediated by the type II inositol
60               Its localization in the apical canalicular membrane is physiologically regulated by the
61 istance-associated protein 2 (Mrp2) from the canalicular membrane leading to cholestasis.
62 ence colocalization analysis using CD13 as a canalicular membrane marker.
63             Knockout mice unable to make the canalicular membrane mdr2 P-glycoprotein exhibit normal
64  of human embryonic kidney HEK293 and at the canalicular membrane of Can 10 and HepG2 cells.
65 es phosphatidylcholine (PC) secretion at the canalicular membrane of hepatocytes and its genetic defe
66    The secretion of phospholipids across the canalicular membrane of hepatocytes occurs via the multi
67 inding cassette transporter localized at the canalicular membrane of hepatocytes that plays an import
68 wo sites (apical membrane of enterocytes and canalicular membrane of hepatocytes) to mediate choleste
69  cassette (ABC) transporter expressed at the canalicular membrane of hepatocytes, where it mediates p
70 tte (ABC) transporters and is located in the canalicular membrane of hepatocytes.
71  pump, which is exclusively expressed at the canalicular membrane of hepatocytes.
72 t the apical membrane of enterocytes and the canalicular membrane of hepatocytes.
73  the major bile salt transport system at the canalicular membrane of hepatocytes.
74       In the liver, P-gp is localized on the canalicular membrane of hepatocytes.
75        Mrp2 remained localized at the apical/canalicular membrane of NHERF-1(-/-) mouse hepatocytes,
76 ntly discovered that NPC1L1 localizes to the canalicular membrane of primate hepatocytes and that NPC
77           Transport of bile acids across the canalicular membrane of the hepatocyte provides the prim
78 alt export pump (Bsep), a transporter on the canalicular membrane of the hepatocyte.
79                        Slc30a10 localized to canalicular membranes of hepatocytes, but mice with live
80 tical trans-locator for phospholipids across canalicular membranes of hepatocytes, evidenced by the f
81 ABC transporters are targeted to the apical (canalicular) membrane of hepatocytes where they execute
82 tte transporters are targeted to the apical (canalicular) membrane of hepatocytes, where they mediate
83 d along basolateral (sinusoidal) and apical (canalicular) membranes of hepatocytes, are integral dete
84 ed that single BSEP-YFP molecules resided in canalicular membranes only transiently before exchanging
85  the internal to external hemileaflet of the canalicular membrane permits exovesiculation of the exte
86 ctivity and abundance of transporters in the canalicular membrane regulate bile flow; however, little
87 cid transporters on both the basolateral and canalicular membranes, resulting in intrahepatic cholest
88 as associated with a marked reduction in the canalicular membrane structure as observed by differenti
89 atocytes, thereby increasing exposure of the canalicular membrane to bile salts linking to increased
90            As a consequence, exposure of the canalicular membrane to bile salts was increased, allowi
91 2 and 4, which localize to granules and open canalicular membranes, together with the general target
92  the polarized targeting and/or retaining of canalicular membrane transporters and is a critical dete
93 tion, kinase activity, and protein levels in canalicular membrane vesicle (CMV) and sinusoidal membra
94 e and dinitrophenyl-glutathione transport in canalicular membrane vesicles above maximal ATP-dependen
95   HAX-1 was bound to BSEP, MDR1, and MDR2 in canalicular membrane vesicles and co-localized with BSEP
96  macrophages doubled PI 3-kinase activity in canalicular membrane vesicles and enhanced taurocholate
97 ate and PI 3-kinase activity were reduced in canalicular membrane vesicles isolated from rat liver th
98 ncrease in the amount of ABC transporters in canalicular membrane vesicles was observed, whereas the
99 a rat liver subcellular fraction enriched in canalicular membrane vesicles, and MLC2 colocalized with
100 rat liver subcellular fractions enriched for canalicular membrane vesicles, microsomes, and clathrin-
101                                           In canalicular membrane vesicles, translocase activity had
102 hosphate-dependent taurocholate transport in canalicular membrane vesicles, was induced by 90% (P < 0
103                      Release of DHE from the canalicular membrane was also ATP-independent but slower
104 , recombinant ABCG5 localized to the apical (canalicular) membrane when coexpressed with ABCG8, but n
105 bstrates by inducing Mrp2 retrieval from the canalicular membrane, whereas cyclic adenosine monophosp
106 anism of specific lipid recruitment from the canalicular membrane, which is essential to mitigate the
107 molecules and the ectoplasmic leaflet of the canalicular membrane, which result in biliary secretion

 
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