High impact information on Dph1

• Furthermore, Ovca1; p53 double heterozygotes developed tumors quicker than p53 heterozygotes and with an increased carcinoma incidence [1].
• Ovca1 heterozygotes spontaneously develop cancer [1].
• Ovca1 regulates cell proliferation, embryonic development, and tumorigenesis [1].
• These in vivo findings demonstrate that Ovca1 is a tumor suppressor that can modify p53-induced tumorigenesis and suggest that it acts as a positive regulator for cell cycle progression [1].
• In this mutant, the Ovca1 gene was disrupted by gene trap mutagenesis, and this disruption well correlated with the toxin-resistant phenotype [2].

Biological context of Dph1

• Ovca1 mutant mice die during embryonic development and at birth with developmental delay and defects in multiple organ systems [1].

Analytical, diagnostic and therapeutic context of Dph1

• Multiple tumor burden in Ovca1 heterozygotes that were also p53 deficient was significantly higher than in p53 homozygous mutants [1].

References