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Please use this identifier to cite or link to this item:
http://hdl.handle.net/2239/31119
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| Title: | p73-deficient mice have neurological, pheromonal and inflammatory defects but lack spontaneous tumours. |
| Authors: | Yang, A.
Walker, N.
Bronson, R.
Kaghad, M.
Oosterwegel, M.
Bonnin, J.
Vagner, C.
Bonnet, H.
Dikkes, P.
Sharpe, A. |
| Keywords: | tumor suppressor proteins
DNA-binding proteins
protein isoforms
nervous system diseases
pheromones
biochemical pathways
inflammation
carcinogenesis
mice |
| Issue Date: | 17-Oct-2007 |
| Description: | p73 (ref. 1) has high homology with the tumour suppressor p53 (refs 2-4), as well as with p63, a gene implicated in the maintenance of epithelial stem cells5-7. Despite the localization of the p73 gene to chromosome 1p36.3, a region of frequent aberration in a wide range of human cancers1, and the ability of p73 to transactivate p53 target genes1, it is unclear whether p73 functions as a tumour suppressor. Here we show that mice functionally deficient for all p73 isoforms exhibit profound defects, including hippocampal dysgenesis, hydrocephalus, chronic infections and inflammation, as well as abnormalities in pheromone sensory pathways. In contrast to p53-deficient mice, however, those lacking p73 show no increased susceptibility to spontaneous tumorigenesis. We report the mechanistic basis of the hippocampal dysgenesis and the loss of pheromone responses, and show that new, potentially dominant-negative, p73 variants are the predominant expression products of this gene in developing and adult tissues. Our data suggest that there is a marked divergence in the physiological functions of the p53 family members, and reveal unique roles for p73 in neurogenesis, sensory pathways and homeostatic control. |
| URI: | http://seekspace.resip.ac.cn/handle/2239/31119 |
| Other Identifiers: | http://seekspace.resip.ac.cn/handle/10113/97 |
| Appears in Collections: | 网络开放学术资源
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