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. 2022 Jun 16;9:897108. doi: 10.3389/fmed.2022.897108

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Copyright © 2022 Bing, Li, Li, Zhang and Chang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Molecular mechanisms underlying cholestasis associated with ATP8B1 deficiency. ATP8B1 consists of 10 transmembrane segments, and ATP8B1 and CDC50A assemble to form a heterodimer complex that participates in PS flipping. BESP is a canalicular bile salt transporter. FXR is a nuclear receptor involved in regulating bile acid metabolism. When ATP8B1 is defective, the nuclear translocation of FXR is disrupted, and BSEP expression on the hepatic duct membrane is reduced due to its transcriptional inhibition. *Dotted line indicated a negative effect.