Literature search services are currently unavailable. During our hosting provider's UPS upgrade we experienced a hardware failure and are currently working to resolve the issue.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Mice deficient in cellular retinoic acid binding protein II (CRABPII) or in both CRABPI and CRABPII are essentially normal.

We have disrupted the CRABPII gene using homologous recombination in embryonic stem cells, and shown that this disruption results in a null mutation. CRABPII null mutant mice are essentially indistinguishable from wild-type mice as judged by their normal development, fertility, life span and general behaviour, with the exception of a minor limb malformation. Moreover, CRABPI-/-/CRABPII-/- double mutant mice also appear to be essentially normal, and both CRABPII-/- single mutant and CRABPI-/-/CRABPII-/- double mutant embryos are not more sensitive than wild-type embryos to retinoic acid excess treatment in utero. Thus, CRABPI and CRABPII are dispensable both during mouse development and adult life. Our present results demonstrate that CRABPs are not critically involved in the retinoic acid signaling pathway, and that none of the functions previously proposed for CRABPs are important enough to account for their evolutionary conservation.

Pubmed ID: 7768191


  • Lampron C
  • Rochette-Egly C
  • Gorry P
  • DollĂ© P
  • Mark M
  • Lufkin T
  • LeMeur M
  • Chambon P


Development (Cambridge, England)

Publication Data

February 5, 1995

Associated Grants


Mesh Terms

  • Animals
  • Extremities
  • Limb Deformities, Congenital
  • Mice
  • Mice, Mutant Strains
  • Morphogenesis
  • Receptors, Retinoic Acid
  • Tretinoin