ABCC2/Abcc2: a multispecific transporter with dominant excretory functions

ABCC2/Abcc2 (MRP2/Mrp2) is expressed at major physiological barriers, such as the canalicular membrane of liver cells, kidney proximal tubule epithelial cells, enterocytes of the small and large intestine, and syncytiotrophoblast of the placenta. ABCC2/Abcc2 always localizes in the apical membranes....

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Published inDrug metabolism reviews Vol. 42; no. 3; pp. 402 - 436
Main Authors Jemnitz, Katalin, Heredi-Szabo, Krisztina, Janossy, Judit, Ioja, Eniko, Vereczkey, Laszlo, Krajcsi, Peter
Format Journal Article
LanguageEnglish
Published England Informa UK Ltd 01.08.2010
Taylor & Francis
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Abstract ABCC2/Abcc2 (MRP2/Mrp2) is expressed at major physiological barriers, such as the canalicular membrane of liver cells, kidney proximal tubule epithelial cells, enterocytes of the small and large intestine, and syncytiotrophoblast of the placenta. ABCC2/Abcc2 always localizes in the apical membranes. Although ABCC2/Abcc2 transports a variety of amphiphilic anions that belong to different classes of molecules, such as endogenous compounds (e.g., bilirubin-glucuronides), drugs, toxic chemicals, nutraceuticals, and their conjugates, it displays a preference for phase II conjugates. Phenotypically, the most obvious consequence of mutations in ABCC2 that lead to Dubin-Johnson syndrome is conjugate hyperbilirubinemia. ABCC2/Abcc2 harbors multiple binding sites and displays complex transport kinetics.
AbstractList ABCC2/Abcc2 (MRP2/Mrp2) is expressed at major physiological barriers, such as the canalicular membrane of liver cells, kidney proximal tubule epithelial cells, enterocytes of the small and large intestine, and syncytiotrophoblast of the placenta. ABCC2/Abcc2 always localizes in the apical membranes. Although ABCC2/Abcc2 transports a variety of amphiphilic anions that belong to different classes of molecules, such as endogenous compounds (e.g., bilirubin-glucuronides), drugs, toxic chemicals, nutraceuticals, and their conjugates, it displays a preference for phase II conjugates. Phenotypically, the most obvious consequence of mutations in ABCC2 that lead to Dubin-Johnson syndrome is conjugate hyperbilirubinemia. ABCC2/Abcc2 harbors multiple binding sites and displays complex transport kinetics.
Author Jemnitz, Katalin
Vereczkey, Laszlo
Heredi-Szabo, Krisztina
Ioja, Eniko
Krajcsi, Peter
Janossy, Judit
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  givenname: Krisztina
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  fullname: Heredi-Szabo, Krisztina
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  organization: 1Chemical Research Center, Institute of Biomolecular Chemistry, HAS, Budapest, Hungary
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  organization: 1Chemical Research Center, Institute of Biomolecular Chemistry, HAS, Budapest, Hungary
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  givenname: Peter
  surname: Krajcsi
  fullname: Krajcsi, Peter
  email: krajcsi@solvo.com, krajcsi@solvo.com
  organization: 1Chemical Research Center, Institute of Biomolecular Chemistry, HAS, Budapest, Hungary
BackLink https://www.ncbi.nlm.nih.gov/pubmed/20082599$$D View this record in MEDLINE/PubMed
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  publication-title: Oncol Rep
  contributor:
    fullname: Hagenauer B.
– ident: CIT0258
  doi: 10.1016/j.neuroscience.2008.06.015
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Snippet ABCC2/Abcc2 (MRP2/Mrp2) is expressed at major physiological barriers, such as the canalicular membrane of liver cells, kidney proximal tubule epithelial cells,...
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StartPage 402
SubjectTerms ABC transporter
ABCC2
ADME
Animals
Biological Transport, Active
Cloning, Molecular
conjugate hyperbilirubinemia
Drug Resistance, Multiple
Dubin-Johnson syndrome
Humans
Kinetics
Mice
Mice, Knockout
MRP2
Multidrug Resistance-Associated Proteins - biosynthesis
Multidrug Resistance-Associated Proteins - chemistry
Multidrug Resistance-Associated Proteins - genetics
Multidrug Resistance-Associated Proteins - metabolism
pharmacokinetics
Protein Conformation
toxicity
Xenobiotics - metabolism
Title ABCC2/Abcc2: a multispecific transporter with dominant excretory functions
URI https://www.tandfonline.com/doi/abs/10.3109/03602530903491741
https://www.ncbi.nlm.nih.gov/pubmed/20082599
Volume 42
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