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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, Six3
Papers on TGIF
4-Hydroxynonenal impairs transforming growth factor-β1-induced elastin synthesis via epidermal growth factor receptor activation in human and murine fibroblasts.
Nègre-Salvayre et al., Toulouse, France. In Free Radic Biol Med, Jun 2014
Concomitantly, 4-HNE modified and stimulated the phosphorylation of the epidermal growth factor receptor (EGFR) and subsequently ERK1/2 activation, leading to the phosphorylation/stabilization of the Smad transcriptional corepressor TGIF, which antagonizes TGF-β1 signaling.
Cerebral blood flow and apoptosis-associated factor with electroacupuncture in a traumatic brain injury rat model.
Kuo et al., Tainan City, Taiwan. In Acupunct Med, Dec 2013
Regional blood flow, cell infarction volume, extent of neuronal apoptosis, expression of cell apoptosis-associated factor transforming growth-interacting factor (TGIF) were studied, and functional outcome was assessed by running speed test.
Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells.
Hamid et al., In Mol Cell Biol, Dec 2013
TG-interacting factor 1 (TGIF1) is a transcriptional repressor that can modulate retinoic acid and transforming growth factor β signaling pathways.
Homeobox gene transforming growth factor β-induced factor-1 (TGIF-1) is a regulator of villous trophoblast differentiation and its expression is increased in human idiopathic fetal growth restriction.
Murthi et al., Melbourne, Australia. In Mol Hum Reprod, Oct 2013
Targeted disruption of homeobox gene transforming growth β-induced factor (TGIF-1) results in placental dysfunction in the mouse.
Identification of PHRF1 as a tumor suppressor that promotes the TGF-β cytostatic program through selective release of TGIF-driven PML inactivation.
Atfi et al., Paris, France. In Cell Rep, Sep 2013
The homeodomain protein TGIF (TG-interacting factor) restricts TGF-β/Smad cytostatic signaling by interfering with the nucleocytoplasmic transit of the tumor suppressor cPML.
Methylation of a novel panel of tumor suppressor genes in urine moves forward noninvasive diagnosis and prognosis of bladder cancer: a 2-center prospective study.
Sánchez-Carbayo et al., Madrid, Spain. In J Urol, Aug 2013
RESULTS: PRDM2, HLTF, ID4, DLC1, BNIP3, H2AFX, CACNA1G, TGIF and CACNA1A were methylated in bladder cancer.
Conditional loss of heparin-binding EGF-like growth factor results in enhanced liver fibrosis after bile duct ligation in mice.
Takehara et al., Ōsaka, Japan. In Biochem Biophys Res Commun, Aug 2013
Interestingly, HB-EGF did not prevent the TGF-β-induced nuclear accumulation of Smad3, but did lead to stabilization of the Smad transcriptional co-repressor TG-interacting factor.
Pituitary stalk interruption syndrome and isolated pituitary hypoplasia may be caused by mutations in holoprosencephaly-related genes.
Dacou-Voutetakis et al., Athens, Greece. In J Clin Endocrinol Metab, Apr 2013
In 10-15% of HPE patients, mutations in specific genes have been identified (eg, SHH, TGIF, SIX3).
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.
Hepatocyte growth factor in kidney fibrosis: therapeutic potential and mechanisms of action.
Liu, Pittsburgh, United States. In Am J Physiol Renal Physiol, 2004
In glomerular mesangial cells, HGF stabilizes another Smad corepressor, TGIF, by preventing it from degradation.
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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