Targeted disruption of Tgif, the mouse ortholog of a human holoprosencephaly gene, does not result in holoprosencephaly in mice.

ABSTRACT: 5'-TG-3'-interacting factor or transforming growth factor beta (TGF-beta)-induced factor (TGIF) belongs to a family of evolutionarily conserved proteins that are characterized by an atypical three-amino-acid loop extension homeodomain. In vitro studies have implicated TGIF as a transcriptional repressor and corepressor in retinoid and TGF-beta signaling pathways that regulate several important biological processes. Heterozygous nonsense and missense mutations of the human TGIF gene have been associated with holoprosencephaly, the most common congenital malformation of the forebrain. In mice, Tgif mRNA is expressed ubiquitously in the ventricular neuroepithelium at embryonic day 10.5 (E10.5) but displays a medial to lateral gradient in the developing cerebral cortex at E12.5. The expression

SUBMITTER: Shen J 

PROVIDER: S-EPMC1084278 | biostudies-literature | 2005 May

REPOSITORIES: biostudies-literature