[HTML][HTML] MDM2 expression during mouse embryogenesis and the requirement of p53
T Léveillard, P Gorry, K Niederreither… - Mechanisms of …, 1998 - Elsevier
Mechanisms of development, 1998•Elsevier
We compared mouse embryonic expression of the MDM2 proto-oncogene, p21WAF1/CIP1
and their transcriptional regulator, p53. MDM2 expression is ubiquitous from 7.5 to 11.5 days
post coitum (dpc) and more restricted from 12.5 dpc, with the highest levels in the testes and
neural tube. From 14.5 to 18.5 dpc, the nasal respiratory epithelium expresses high levels of
MDM2 RNA and protein and p21WAF1/CIP1 RNA, in both wild type and p53 null embryos.
MDM2 expression during development is tissue-specific and, like p21WAF1/CIP1, is …
and their transcriptional regulator, p53. MDM2 expression is ubiquitous from 7.5 to 11.5 days
post coitum (dpc) and more restricted from 12.5 dpc, with the highest levels in the testes and
neural tube. From 14.5 to 18.5 dpc, the nasal respiratory epithelium expresses high levels of
MDM2 RNA and protein and p21WAF1/CIP1 RNA, in both wild type and p53 null embryos.
MDM2 expression during development is tissue-specific and, like p21WAF1/CIP1, is …
We compared mouse embryonic expression of the MDM2 proto-oncogene, p21WAF1/CIP1 and their transcriptional regulator, p53. MDM2 expression is ubiquitous from 7.5 to 11.5 days post coitum (dpc) and more restricted from 12.5 dpc, with the highest levels in the testes and neural tube. From 14.5 to 18.5 dpc, the nasal respiratory epithelium expresses high levels of MDM2 RNA and protein and p21WAF1/CIP1 RNA, in both wild type and p53 null embryos. MDM2 expression during development is tissue-specific and, like p21WAF1/CIP1, is independent of p53. MDM2 may have a developmental role after 6.5 dpc, when MDM2 null mice die (Jones, S.N., Roe, A.E., Donehower, L.A., Bradley, A., 1995. Rescue of embryonic lethality in Mdm2-deficient mice by absence of p53. Nature 378, 206–208; Montes de Oca Luna, R., Wagner, D.S., Lozano, G., 1995. Rescue of early embryonic lethality in mdm2-deficient mice by deletion of p53. Nature 378, 203–206).
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