PMID: 10728790

Kullak-Ublick GA, Beuers U, Paumgartner G
Hepatobiliary transport.
J Hepatol. 2000;32(1 Suppl):3-18., [PubMed]
Sentences
No. Mutations Sentence Comment
223 ABCC7 p.Glu217Gly
X
ABCC7 p.Glu217Gly 10728790:223:199
status: NEW
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 How- 10 ever, the major pathogenetic factor in estradiol-induced cholestasis appears to be inhibition of Bsep transport function by the cholestatic estrogen metabolite estradiol- 17fl-D-glucuronide (E217G) (152). Login to comment 224 ABCC7 p.Glu217Gly
X
ABCC7 p.Glu217Gly 10728790:224:0
status: NEW
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ABCC7 p.Glu217Gly
X
ABCC7 p.Glu217Gly 10728790:224:174
status: NEW
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 E217G, which is an mrp2 substrate (153), probably trans-inhibits Bsep function from within the canalicular lumen, since mrp2-deficient rat strains that are unable to secrete E217G into the bile canaliculus do not develop cholestasis (154). Login to comment 225 ABCC7 p.Glu217Gly
X
ABCC7 p.Glu217Gly 10728790:225:333
status: NEW
view ABCC7 p.Glu217Gly details
 In accordance with these observations, it has been shown that Bsep function is inhibited neither in canalicular plasma membrane vesicles of mrp2-deficient GY/TR rat liver, nor in Bsep expressing membrane vesicles from baculovirus-infected Sf9 cells (68), indicating that intact mrp2 function is a prerequisite for the development of E217G induced cholestasis. Login to comment