Mice deficient for Rb are nonviable and show defects in neurogenesis and haematopoiesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1992-09

AUTHORS

Eva Y.-H. P. Lee, Chi-Yao Chang, Nanpin Hu, Yi-Chun J. Wang, Chen-Ching Lai, Karl Herrup, Wen-Hwa Lee, Allan Bradley

ABSTRACT

The retinoblastoma gene, a prototypic tumour-suppressor gene, encodes a nuclear phosphoprotein (Rb). To understand better the role of Rb in development and in tumorigenesis, mice with an insertional mutation in exon 20 of the Rb-1 locus were generated. Homozygous mutants die before the 16th embryonic day with multiple defects. The haematopoietic system is abnormal; there is a significant increase in the number of immature nucleated erythrocytes. In the nervous system, ectopic mitoses and massive cell death are found, particularly in the hindbrain. All spinal ganglion cells die, but the neural retina is unaffected. Transfer of the human retinoblastoma (RB) mini-transgene into the mutant mice corrects the developmental defects. Thus, Rb is essential for normal mouse development. More... »

PAGES

288-294

Journal

TITLE

Nature

ISSUE

6393

VOLUME

359

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/359288a0

DOI

http://dx.doi.org/10.1038/359288a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037982331

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1406932


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