Scientific article

Selective inhibition of nuclear steroid receptor function by a protein from a human tumorigenic poxvirus

Published inVirology, vol. 274, no. 1, p. 17-25
Publication date2000

The poxvirus molluscum contagiosum (MC) has a worldwide distribution and its prevalence is on the rise. Here we report that the MCV MC013L protein inhibits glucocorticoid and vitamin D, but not retinoid or estrogen, nuclear receptor transactivation. A direct interaction of MC013L with glucocorticoid and vitamin D receptor is supported by yeast two-hybrid, GST pull-down, and far Western blot analyses. Glucocorticoids act as potent inhibitors of keratinocyte proliferation, while vitamin D and retinoids promote and block terminal differentiation, respectively. Therefore, MC013L may promote efficient virus replication by blocking the differentiation of infected keratinocytes. MC013L may be the first member of a new class of poxvirus proteins that directly modulate nuclear receptor-mediated transcription.

  • Amino Acid Sequence
  • Animals
  • COS Cells
  • Calcitriol/metabolism
  • Cell Nucleus
  • Gene Expression
  • Genes, Reporter
  • Growth Substances/genetics
  • HSP40 Heat-Shock Proteins
  • Heat-Shock Proteins/genetics/metabolism/ physiology
  • Humans
  • Molecular Sequence Data
  • Molluscum contagiosum virus/genetics/metabolism/ physiology
  • Receptors, Calcitriol/antagonists & inhibitors/genetics
  • Receptors, Estrogen/antagonists & inhibitors/genetics
  • Receptors, Glucocorticoid/antagonists & inhibitors/genetics
  • Receptors, Retinoic Acid/metabolism
  • Receptors, Steroid/ antagonists & inhibitors/genetics
  • Sequence Homology, Amino Acid
  • Transcription, Genetic
  • Viral Proteins/genetics/metabolism/ physiology
  • Virus Replication/physiology
Citation (ISO format)
CHEN, N. et al. Selective inhibition of nuclear steroid receptor function by a protein from a human tumorigenic poxvirus. In: Virology, 2000, vol. 274, n° 1, p. 17–25. doi: 10.1006/viro.2000.0410
Updates (1)
ISSN of the journal0042-6822

Technical informations

Creation06/21/2010 10:23:31 AM
First validation06/21/2010 10:23:31 AM
Update time03/14/2023 3:43:03 PM
Status update03/14/2023 3:43:03 PM
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