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Article

Aberrant activation of p53 due to loss of MDM2 or MDMX causes early lens dysmorphogenesis.

Developmental biology - 1 Dec 2014

Zhang Yiwei, Zhang Xin, Lu Hua

Abstract excerpt

Although forming a heterodimer or heterooligomer is essential for MDM2 and MDMX to fully control p53 during early embryogenesis, deletion of either MDM2 or MDMX in specific tissues using the loxp-Cre system reveals phenotypic diversity during organ morphogenesis, which can be completely rescued by loss of p53, suggesting the spatiotemporal independence and specificity of the regulation of p53 by MDM2 and MDMX. In...

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Share to Apoptosis
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Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Lens, Crystalline

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Share to Proto-Oncogene Proteins c-mdm2

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Share to Tumor Suppressor Protein p53

Source

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Identifiers

PMID: 25263199
DOI: 10.1016/j.ydbio.2014.09.017
PMCID: PMC5393629

Genes

MDM2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Aberrant activation of p53 due to loss of MDM2 or MDMX causes early lens dysmorphogenesis.PMID 25263199Read ↗

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