ABCG2 - A transporter for all seasons

Research output: Contribution to journalArticle

223 Citations (Scopus)

Abstract

The human ABCG2 (ABCP/MXR/BCRP) protein is a recently recognized ABC half-transporter, which forms homodimers in the plasma membrane and actively extrudes a wide variety of chemically unrelated compounds from the cells. This protein protects our cells and tissues against various xenobiotics, with a crucial role in the intestine, liver, placenta, and the blood-brain barrier. Moreover, ABCG2 seems to have a key function in stem cell protection/regulation, and also in hypoxic defense mechanisms. Widely occurring single nucleotide polymorphisms in ABCG2 may affect absorption and distribution, altering the effectiveness and toxicity of drugs in large populations. At the clinics, overexpression of ABCG2 in tumor cells confers cancer multidrug resistance to a variety of newly developed anticancer agents. On the other hand, specific substrate mutants of ABCG2 are advocated for use as selectable markers in stem-cell based gene therapy.

Original languageEnglish
Pages (from-to)116-120
Number of pages5
JournalFEBS Letters
Volume567
Issue number1
DOIs
Publication statusPublished - Jun 1 2004

Fingerprint

Stem cells
Gene therapy
Xenobiotics
Stem Cells
Cell membranes
Polymorphism
Liver
Antineoplastic Agents
Toxicity
Tumors
Proteins
ATP-Binding Cassette Transporters
Cytoprotection
Nucleotides
Cells
Multiple Drug Resistance
Tissue
Drug-Related Side Effects and Adverse Reactions
Blood-Brain Barrier
Genetic Therapy

Keywords

  • ABC transporters, ATP-binding cassette transporters
  • ABCG2
  • ABCP, placenta-specific ABC transporter
  • Cancer drug resistance
  • Gene therapy
  • Hypoxic defense
  • Multidrug transporter
  • Polymorphic variant
  • Stem cell regulation
  • Xenobiotic transport

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

ABCG2 - A transporter for all seasons. / Sarkadi, B.; Özvegy-Laczka, C.; Német, K.; Váradi, A.

In: FEBS Letters, Vol. 567, No. 1, 01.06.2004, p. 116-120.

Research output: Contribution to journalArticle

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