Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome.

@article{Caspary1999OppositelyIG,
  title={Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome.},
  author={Tamara Caspary and Michele A. Cleary and Elizabeth J Perlman and Ping-Wu Zhang and Stephen J Elledge and Shirley M. Tilghman},
  journal={Genes & development},
  year={1999},
  volume={13 23},
  pages={3115-24}
}
Beckwith-Wiedemann syndrome (BWS) is a clinically variable disorder characterized by somatic overgrowth, macroglossia, abdominal wall defects, visceromegaly, and an increased susceptibility to childhood tumors. The disease has been linked to a large cluster of imprinted genes at human chromosome 11p15.5. A subset of BWS patients has been identified with loss-of-function mutations in p57(KIP2), a maternally expressed gene encoding a G(1) cyclin-dependent kinase inhibitor. Some patients display… CONTINUE READING

Citations

Publications citing this paper.
Showing 1-10 of 56 extracted citations

Placental growth retardation due to loss of imprinting of Phlda2

Mechanisms of Development • 2004
View 4 Excerpts
Highly Influenced

Developmental Endocrinology

SE RIES
Contemporary Endocrinology • 2002
View 4 Excerpts
Highly Influenced

References

Publications referenced by this paper.
Showing 1-10 of 56 references

Similar Papers

Loading similar papers…