c-Jun is essential for normal mouse development and hepatogenesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1993-09

AUTHORS

Frank Hilberg, Adriano Aguzzi, Norma Howells, Erwin F. Wagner

ABSTRACT

THE proto-oncogene c-jun is the cellular homologue of v-jun, the transforming oncogene of the avian sarcoma virus 17 (ref. 1). c-jun encodes one major component of the AP-1 transcription fac-tor complex and is expressed in many organs during mouse development and in the adult2–4. Because of its rapid induction in cells following growth stimulation and the presence of AP-1 binding sites in the promoter regions of many genes, the c-Jun protein is thought to have important functions in cell proliferation and differentiation2,5–10. But embryonic stem (ES) cells lacking c-Jun are viable and have a normal in vitro differentiation capacity, although c-Jun appears to be important for growth of teratocarcinomas in vivo11. To define the function of c-jun better, targeted ES cells were used to generate mice lacking c-Jun. Here we report that heterozygous mutant mice appear normal, but embryos lacking c-Jun die at mid- to late-gestation and exhibit impaired hepatogenesis, altered fetal liver erythropoiesis and generalized oedema. Interestingly, c-jun-/- ES cells can More... »

PAGES

179-181

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/365179a0

DOI

http://dx.doi.org/10.1038/365179a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009910352

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/8371760


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