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RXR gamma null mice are apparently normal and compound RXR alpha +/-/RXR beta -/-/RXR gamma -/- mutant mice are viable.

The RXR gamma (RXR, retinoid X receptor) gene was disrupted in the mouse. Homozygous mutant mice developed normally and were indistinguishable from their RXR gamma +/- or wild-type littermates with respect to growth, fertility, viability, and apparent behavior in the animal facility. Moreover, RXR alpha -/-/RXR gamma -/- and RXR beta -/-/RXR gamma -/- mutant phenotypes were indistinguishable from those of RXR alpha -/- and RXR beta -/- mutants, respectively. Strikingly, RXR alpha +/-/RXR beta -/-/RXR gamma -/- triple mutants were viable. Thus, it appears that RXR gamma does not exert any essential function that cannot be performed by RXR alpha or RXR beta, and one copy of RXR alpha is sufficient to perform most of the functions of the RXRs.

Pubmed ID: 8799145

Authors

  • Krezel W
  • DupĂ© V
  • Mark M
  • Dierich A
  • Kastner P
  • Chambon P

Journal

Proceedings of the National Academy of Sciences of the United States of America

Publication Data

August 20, 1996

Associated Grants

None

Mesh Terms

  • Animals
  • Body Weight
  • Heterozygote
  • Homozygote
  • Mice
  • Mice, Knockout
  • Molecular Sequence Data
  • Muscle Development
  • Muscle, Skeletal
  • RNA, Messenger
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Tissue Distribution
  • Transcription Factors