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TGFB-induced factor homeobox 1

TGIF, TG-interacting factor
The protein encoded by this gene is a member of the three-amino acid loop extension (TALE) superclass of atypical homeodomains. TALE homeobox proteins are highly conserved transcription regulators. This particular homeodomain binds to a previously characterized retinoid X receptor responsive element from the cellular retinol-binding protein II promoter. In addition to its role in inhibiting 9-cis-retinoic acid-dependent RXR alpha transcription activation of the retinoic acid responsive element, the protein is an active transcriptional co-repressor of SMAD2 and may participate in the transmission of nuclear signals during development and in the adult. Mutations in this gene are associated with holoprosencephaly type 4, which is a structural anomaly of the brain. Alternative splicing has been observed at this locus and eight variants, encoding four distinct isoforms, are described. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TGF-beta, CAN, ACID, Shh, Smad2
Papers on TGIF
TGIF function in oncogenic Wnt signaling.
Atfi et al., Cambridge, United States. In Biochim Biophys Acta, 29 Nov 2015
UNASSIGNED: Transforming growth-interacting factor (TGIF) has been implicated in the pathogenesis of many types of human cancer, but the underlying mechanisms remained mostly enigmatic.
The effect of PrP(Sc) accumulation on inflammatory gene expression within sheep peripheral lymphoid tissue.
Hopkins et al., Edinburgh, United Kingdom. In Vet Microbiol, 17 Nov 2015
RT-qPCR analysis of seven genes showed statistically significant correlation with the array data, although the results for IL1RN and TGIF were different between the two technologies.
Homeodomain proteins: an update.
Affolter et al., Basel, Switzerland. In Chromosoma, 13 Nov 2015
In animals, there are 16 major classes, ANTP, PRD, PRD-LIKE, POU, HNF, CUT (with four subclasses: ONECUT, CUX, SATB, and CMP), LIM, ZF, CERS, PROS, SIX/SO, plus the TALE superclass with the classes IRO, MKX, TGIF, PBC, and MEIS.
The human brain and face: mechanisms of cranial, neurological and facial development revealed through malformations of holoprosencephaly, cyclopia and aberrations in chromosome 18.
Herman et al., Washington, D.C., United States. In J Anat, Sep 2015
where the HPE gene, TGIF, resides, to the p terminus.
TGIF governs a feed-forward network that empowers Wnt signaling to drive mammary tumorigenesis.
Atfi et al., Boston, United States. In Cancer Cell, May 2015
Moreover, genetic experiments revealed that Tgif1 ablation impeded mammary tumor development in MMTV-Wnt1 mice, further underscoring a requirement of TGIF for oncogenic Wnt signaling.
Role of TG-interacting factor (Tgif) in lipid metabolism.
Parini et al., Huddinge, Sweden. In Biochim Biophys Acta, Jan 2015
Mutations in TGIF1 have been linked to holoprosencephaly, which is a human genetic disease that affects craniofacial development.
Molecular Biology of Pediatric Hydrocephalus and Hydrocephalus-related Diseases.
Kanemura et al., Takatsuki, Japan. In Neurol Med Chir (tokyo), Dec 2014
Sixteen causative genes for HPE have been identified, of which mutations are most often found in SHH, ZIC2, SIX3, and TGIF.
MicroRNA-34a inhibits tumor invasion and metastasis in gastric cancer by targeting Tgif2.
Lin et al., Chengdu, China. In Int J Clin Exp Pathol, Dec 2014
In gastric cancer cells transfected with miR-34a mimic/Tgif siRNA, Tgif2 expression was remarkably down-regulated.
Role of 5'TG3'-interacting factors (TGIFs) in Vorinostat (HDAC inhibitor)-mediated Corneal Fibrosis Inhibition.
Mohan et al., Morocco. In Mol Vis, Dec 2014
RNA isolation, cDNA preparation, and PCR were performed to detect the presence of TGIF1 and TGIF2 transcripts.
Overexpression of TG-interacting factor is associated with worse prognosis in upper urinary tract urothelial carcinoma.
Huang et al., Tainan City, Taiwan. In Am J Pathol, 2012
TGIF contributes to the progression of urothelial carcinoma via the phosphatidylinositol 3-kinase-AKT pathway.
Premature senescence and increased TGFβ signaling in the absence of Tgif1.
Wotton et al., Charlottesville, United States. In Plos One, 2011
Data suggest that in the absence of Tgif1, a persistent increase in TGFbeta responsive transcription and a reduced ability to deal with hyperoxic stress result in premature senescence in primary MEFs.
The TGF-β/Smad repressor TG-interacting factor 1 (TGIF1) plays a role in radiation-induced intestinal injury independently of a Smad signaling pathway.
Milliat et al., Fontenay-aux-Roses, France. In Plos One, 2011
TGF-beta/Smad co-repressor TGIF1 plays a role in radiation-induced normal tissue damage by a Smad-independent mechanism.
New findings for phenotype-genotype correlations in a large European series of holoprosencephaly cases.
Odent et al., Rennes, France. In J Med Genet, 2011
There was a positive correlation between the severity of the brain malformation and facial features for SHH, SIX3, and TGIF, but no such correlation was found for ZIC2 mutations.
Etiopathogenetic advances and management of holoprosencephaly: from bench to bedside.
Bona et al., Novara, Italy. In Panminerva Med, 2010
Genetic causes are responsible for about 20% of cases: they are chromosomal abnormalities and gene mutations: up to date, nine genes (SHH, ZIC2, SIX3, TGIF, PATCHED1, TDGF1/CRIPTO, FAST1, GLI2 and DHCR) are definitely associated with HPE, but many others candidate gene are under investigation.
PCTA: a new player in TGF-beta signaling.
Liu, United States. In Sci Signal, 2007
cPML is sequestered in the nucleus by the homeodomain protein TGIF (TG-interacting factor), a negative regulator of TGF-beta signaling.
Functional analysis of mutations in TGIF associated with holoprosencephaly.
Muenke et al., Bethesda, United States. In Mol Genet Metab, 2007
Of the eleven sequence variations in TGIF, all but four can be demonstrated to be functionally abnormal, associated with holoprosencephaly.
David et al., Rennes, France. In Orphanet J Rare Dis, 2006
To date, seven genes have been positively implicated in HPE: Sonic hedgehog (SHH), ZIC2, SIX3, TGIF, PTCH, GLI2 and TDGF1.
Mutations in TGIF cause holoprosencephaly and link NODAL signalling to human neural axis determination.
Elledge et al., Philadelphia, United States. In Nat Genet, 2000
Here we describe the involvement of the TG-interacting factor (TGIF), a homeodomain protein, in human HPE.
A Smad transcriptional corepressor.
Massagué et al., New York City, United States. In Cell, 1999
We identified the homeodomain protein TGIF as a Smad2-binding protein and a repressor of transcription.
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