Medical Journals

Hairless and Wnt Signaling: Allies in Epithelial Stem Cell Differentiation.

Authors:
  • Thompson Catherine C
  • Sisk Jeanne M
  • Beaudoin Gerard M J

From: Kennedy Krieger Research Institute, Baltimore, Maryland 21205, USA. thompsonc@kennedykrieger.org

Cell cycle (Georgetown, Tex.)

  • Publish Date: Sep 2006
  • ISSN: 1551-4005
  • Volume: 5
  • Issue: 17
  • Pages: 1913-7
  • Medium: Internet
  • Language: English
  • Citation (JAMA): Thompson Catherine C, Sisk Jeanne M, Beaudoin Gerard M J, et al. Hairless and Wnt Signaling: Allies in Epithelial Stem Cell Differentiation.. Cell Cycle Sep 2006;5:1913-7

Abstract

Nuclear receptors and Wnt signaling are both important regulators of developmental and physiological processes. Recent work linking these pathways in epithelial stem cell differentiation has come from studies analyzing the in vivo function of the nuclear receptor corepressor, Hairless (HR). The HR protein has long been suspected to regulate a stem cell-mediated process, hair cycling, as mutations in the Hr gene cause hair loss in both mice and men. The discovery that the HR protein is a nuclear receptor corepressor indicated that HR function in hair cycling is by regulating gene expression. A recent study revealed that HR represses expression of Wise, an inhibitor of Wnt signaling, leading to a model in which HR controls the timing of Wnt signaling required for hair cycling. Here we review these data, and provide new data showing that HR corepressor activity is essential for its in vivo function, and identify an additional putative Wnt inhibitor regulated by HR. This work complements previous studies demonstrating the role of Wnt signaling in epithelial stem cell differentiation.

Mesh Headings (Keywords): Animals, Cell Differentiation, Epithelial Cells, Gene Expression Regulation, Hair Follicle, Humans, Mice, Mutation, Regeneration, Repressor Proteins, Signal Transduction, Stem Cells, Transcription Factors, Wnt Proteins


Check for Full Text / PubMed Unique Identifier (PMID): 16929182


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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