TGIF1 Antibody (N-term) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | Q15583 |
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Clone Names | 100507169 |
Gene ID | 7050 |
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Other Names | Homeobox protein TGIF1, 5'-TG-3'-interacting factor 1, TGIF1, TGIF |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | TGIF1 |
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Synonyms | TGIF |
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. |
Cellular Location | Nucleus. |
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Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene is a member of thethree-amino acid loop extension (TALE) superclass of atypicalhomeodomains. TALE homeobox proteins are highly conservedtranscription regulators. This particular homeodomain binds to apreviously characterized retinoid X receptor responsive elementfrom the cellular retinol-binding protein II promoter. In additionto its role in inhibiting 9-cis-retinoic acid-dependent RXR alphatranscription activation of the retinoic acid responsive element,the protein is an active transcriptional co-repressor of SMAD2 andmay participate in the transmission of nuclear signals duringdevelopment and in the adult. Mutations in this gene are associatedwith holoprosencephaly type 4, which is a structural anomaly of thebrain. Alternative splicing has been observed at this locus andeight variants, encoding four distinct isoforms, are described.
References
Bengoechea-Alonso, M.T., et al. Oncogene 29(38):5322-5328(2010)Paulussen, A.D., et al. Eur. J. Hum. Genet. 18(9):999-1005(2010)Jugessur, A., et al. PLoS ONE 5 (7), E11493 (2010) :Demange, C., et al. Mol. Cell 36(6):1073-1085(2009)Hamid, R., et al. Mol Oncol 3 (5-6), 451-463 (2009) :
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