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Delivering Alcohol Neurotoxicity into Nucleus, When Clusterin Meets Bcl XL: A Commentary

Research output: Contribution to journalArticlepeer-review

Abstract

The study by Kim and colleagues (in press) demonstrated that the expression of nuclear isoform of clusterin is induced by ethanol (EtOH) to participate in apoptotic cell death of neurons in developing rodent brain. EtOH-induced nuclear clusterin interacts with Bcl XL, thereby liberating proapoptotic Bax. This study indicates the proapoptotic role of nuclear clusterin in EtOH-exposed neurons, linking specific nuclear events to alcohol neurotoxicity. The study provides novel insights into the molecular mechanisms underlying fetal alcohol spectrum disorders.

Original languageEnglish
Pages (from-to)745-747
Number of pages3
JournalAlcoholism: Clinical and Experimental Research
Volume36
Issue number5
DOIs
StatePublished - May 2012

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Apoptosis
  • Bcl-2 Family Proteins
  • Clusterin
  • Fetal Alcohol Spectrum Disorders

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