|Calculated MW||43013 Da|
|Other Names||Homeobox protein TGIF1, 5'-TG-3'-interacting factor 1, TGIF1, TGIF|
|Target/Specificity||A synthetic peptide corresponding to residues on the C-terminus of human TGIF was used as an immunogen. This antibody detects both phosphorylated and unphosphorylated TGIF.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||TGIF Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Binds to a retinoid X receptor (RXR) responsive element from the cellular retinol-binding protein II promoter (CRBPII- RXRE). Inhibits the 9-cis-retinoic acid-dependent RXR alpha transcription activation of the retinoic acid responsive element. Active transcriptional corepressor of SMAD2. Links the nodal signaling pathway to the bifurcation of the forebrain and the establishment of ventral midline structures. May participate in the transmission of nuclear signals during development and in the adult, as illustrated by the down-modulation of the RXR alpha activities.|
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Novel homeobox gene, denoted TGIF (5TG3' interacting factor), belongs to an expanding TALE (three amino acid loop extension) superclass of atypical homeodomains. The TGIF homeodomain binds to a previously characterized retinoid X receptor (RXR) responsive element from the cellular retinol-binding protein II promoter (CRBPII-RXRE), which contains an unusual DNA target for a homeobox (1). 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 (2). It has been reported that TGIF plays an unexpected role in the inhibition of Smad2 phosphorylation, which occurs by a mechanism independent of its association with Smad2. This inhibitory function of TGIF is executed in concert with c-Jun, which facilitates the interaction of TGIF with cPML, resulting in the nuclear sequestration of cPML and the disruption of the cPML-SARA complex (3).
1. Bertolino E, et al. J Biol Chem 270(52):31178-88, 1995.
2. Shen J, et al. Mol Cell Biol 25(9):3639-47, 2005.
3. Seo SR, et al. Mol Cell, 23(4):547-59, 2006.
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