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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
Disruption of the PHRF1 Tumor Suppressor Network by PML-RARα Drives Acute Promyelocytic Leukemia Pathogenesis.
Atfi et al., Paris, France. In Cell Rep, 11 Mar 2015
UNASSIGNED: PHRF1 functions as an essential component of the TGF-β tumor suppressor pathway by triggering degradation of the homeodomain repressor factor TGIF.
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.
TG-interacting factor mediates arsenic-induced malignant transformation of keratinocytes via c-Src/EGFR/AKT/FOXO3A and redox signalings.
Huang et al., Tainan City, Taiwan. In Arch Toxicol, Jan 2015
Surprisingly, low-dose arsenic could also transcriptionally increase TG-interacting factor (TGIF) expression via c-Src/EGFR/AKT/FOXO3A signaling involving superoxide production from NADPH oxidase.
Negative interplay of retinoic acid and TGF-β signaling mediated by TG-interacting factor to modulate mouse embryonic palate mesenchymal-cell proliferation.
Yu et al., Zhengzhou, China. In Birth Defects Res B Dev Reprod Toxicol, Dec 2014
Transforming growth-interacting factor (TGIF) is a transcriptional repressor that suppresses both TGF-β- and retinoid-driven gene transcription.
Involvement of TG-interacting factor in microglial activation during experimental traumatic brain injury.
Huang et al., Tainan City, Taiwan. In J Neurochem, Dec 2014
Previous mouse studies using high-density oligonucleotide array analysis have confirmed the upregulation of transforming growth-interacting factor (TGIF) mRNA in TBI.
Epidermal growth factor inhibits transforming growth factor-β-induced fibrogenic differentiation marker expression through ERK activation.
Schnaper et al., Chicago, United States. In Cell Signal, Oct 2014
Finally EGF induced the phosphorylation and expression of TGIF, a known TGF-β/Smad repressor.
Novel de novo heterozygous FGFR1 mutation in two siblings with Hartsfield syndrome: a case of gonadal mosaicism.
Babovic-Vuksanovic et al., Rochester, United States. In Am J Med Genet A, Sep 2014
Previous studies included a normal karyotype, oligonucleotide array, and single gene testing for nonsyndromic holoprosencephaly (SHH, SIX3, ZIC2, TGIF).
Hepatocyte growth factor regulates the TGF-β1-induced proliferation, differentiation and secretory function of cardiac fibroblasts.
Jiang et al., Wuhan, China. In Int J Mol Med, Aug 2014
Mechanistically, we identified that the phosphorylation of c‑Met, Akt and total protein of TGIF was significantly inhibited by the knockdown of HGF, but was significantly enhanced by HGF overexpression.
Molecular analysis of holoprosencephaly in South America.
Orioli et al., Rio de Janeiro, Brazil. In Genet Mol Biol, Mar 2014
Mutational analyses in genes SHH, ZIC2, SIX3 and TGIF were performed in 119 patients, revealing eight mutations in SHH, two mutations in SIX3 and two mutations in ZIC2.
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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