Full-Length cDNA Cloning and Genomic Organization of the Mouse Liver-Specific Organic Anion Transporter-1 (lst-1)

2000 ◽  
Vol 272 (2) ◽  
pp. 563-570 ◽  
Author(s):  
Kenichiro Ogura ◽  
Supratim Choudhuri ◽  
Curtis D. Klaassen
1996 ◽  
Vol 71 ◽  
pp. 291
Author(s):  
Takashi Sekine ◽  
Makoto Hosoyamada ◽  
Yoshikatsu Kanai ◽  
Hitoshi Endou

2010 ◽  
Vol 25 (4-5) ◽  
pp. 511-522 ◽  
Author(s):  
Hiroki Tsuchida ◽  
Naohiko Anzai ◽  
Ho Shin ◽  
Michael Wempe ◽  
Promsuk Jutabha ◽  
...  

2007 ◽  
Vol 28 (2) ◽  
pp. 291-301 ◽  
Author(s):  
Chun Chu ◽  
Jian Yi Li ◽  
Ruben J Boado ◽  
William M Pardridge

A novel organic anion transporter selectively expressed at the blood—brain barrier (BBB), originally designated BBB-specific anion transporter type 1 (BSAT1), and now classified as Slco1c1, has been cloned from a BBB genomics program as a partial cDNA; this study describes the cloning and expression of the full-length cDNA from a rat brain capillary cDNA library. Northern analysis revealed the selective expression of the transporter at the BBB, and the transporter was expressed after permanent transfection of human 293 cells with cDNA encoding either the full length or open reading frame mRNA. The full-length transporter cDNA was 2.6 kb, and the mRNA was highly expressed at the rat brain microvasculature, but not in kidney, liver, heart, or lung, or in glial cells or brain glial tumors. Blood—brain barrier-specific anion transporter type 1 expression in 293 cells was poor after the transfection of the full-length cDNA, whereas transporter expression in 293 cells was high after transfection of the open reading frame. The transporter showed asymmetric kinetic properties in comparison of the influx and efflux of model substrates, thyroxine (T4), triiodothyronine (T3), and estradiol-glucuronide (E2G). Thyroxine and T3 inhibited the influx of E2G, but E2G did not inhibit thyroxine influx, and T3 only weakly inhibited the influx of T4. Extracellular E2G stimulated the transefflux of intracellular T4. Blood—brain barrier-specific anion transporter type 1 is a novel organic anion transporter that is a sodium-independent exchanger that may participate in the active efflux of iodothyronines and steroid conjugates at the BBB.


1999 ◽  
Vol 341 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Ana M. WIELANDT ◽  
Valeska VOLLRATH ◽  
Marlene MANZANO ◽  
Soledad MIRANDA ◽  
Luigi ACCATINO ◽  
...  

The canalicular multispecific organic anion transporter, cMoat, is an ATP-binding-cassette protein expressed in the canalicular domain of hepatocytes. In addition to the transport of endo- and xenobiotics, cMoat has also been proposed to transport GSH into bile, the major driving force of bile-acid-independent bile flow. We have shown previously that the herbicide 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), a peroxisome-proliferator agent, significantly increases bile-acid-independent bile flow in mice. On this basis, the effect of the herbicide on cMoat gene expression was studied. A 3.6-fold increase in cMoat mRNA levels and a 2.5-fold increase in cMoat protein content were observed in the liver of mice fed on a diet supplemented with 0.125% 2,4,5-T. These effects were due to an increased rate of gene transcription (3.9-fold) and were not associated with peroxisome proliferation. Significant increases in bile flow (2.23±0.39 versus 1.13±0.15 μl/min per g of liver; P < 0.05) and biliary GSH output (7.40±3.30 versus 2.65±0.34 nmol/min per g of liver; P < 0.05) were observed in treated animals. The hepatocellular concentration of total glutathione also increased in hepatocytes of treated mice (10.95±0.84 versus 5.12±0.47 mM; P < 0.05), because of the induction (2.4-fold) of the heavy subunit of the γ-glutamylcysteine synthetase (GCS-HS) gene. This is the first model of co-induction of cMoat and GCS-HS genes in vivo in the mouse liver, associated with increased glutathione synthesis and biliary glutathione output. Our observations are consistent with the hypothesis that the cMoat transporter plays a crucial role in the secretion of biliary GSH.


2004 ◽  
Vol 42 (08) ◽  
Author(s):  
A Geier ◽  
CG Dietrich ◽  
C Gartung ◽  
F Lammert ◽  
HE Wasmuth ◽  
...  

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