TLX

A master regulator for neural stem cell maintenance and neurogenesis

Mohammed M. Islam, Chun Li Zhang

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

The orphan nuclear receptor TLX, also known as NR2E1, is an essential regulator of neural stem cell (NSC) self-renewal, maintenance, and neurogenesis. In vertebrates, TLX is specifically localized to the neurogenic regions of the forebrain and retina throughout development and adulthood. TLX regulates the expression of genes involved in multiple pathways, such as the cell cycle, DNA replication, and cell adhesion. These roles are primarily performed through the transcriptional repression or activation of downstream target genes. Emerging evidence suggests that the misregulation of TLX might play a role in the onset and progression of human neurological disorders making this factor an ideal therapeutic target. Here, we review the current understanding of TLX function, expression, regulation, and activity significant to NSC maintenance, adult neurogenesis, and brain plasticity. This article is part of a Special Issue entitled: Nuclear receptors in animal development.

Original languageEnglish (US)
Pages (from-to)210-216
Number of pages7
JournalBiochimica et Biophysica Acta - Gene Regulatory Mechanisms
Volume1849
Issue number2
DOIs
StatePublished - Feb 1 2015

Fingerprint

Neural Stem Cells
Neurogenesis
Stem cells
Genes
Maintenance
Orphan Nuclear Receptors
Cell adhesion
Cytoplasmic and Nuclear Receptors
Prosencephalon
Nervous System Diseases
DNA Replication
Cell Adhesion
Plasticity
Vertebrates
Retina
Brain
Cell Cycle
Animals
Chemical activation
Cells

Keywords

  • Neural stem cell
  • Neurogenesis
  • NR2E1
  • Nuclear receptor
  • TLX

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Genetics
  • Molecular Biology
  • Structural Biology

Cite this

TLX : A master regulator for neural stem cell maintenance and neurogenesis. / Islam, Mohammed M.; Zhang, Chun Li.

In: Biochimica et Biophysica Acta - Gene Regulatory Mechanisms, Vol. 1849, No. 2, 01.02.2015, p. 210-216.

Research output: Contribution to journalArticle

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