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Based on the analysis of the TGIF1-homeodomain (HD) NMR structure determined here, the roles of two holoprosencephaly-related residues P192 and R219 in sufficient folding of TGIF1-HD were revealed. Mutations of these two residues, P192A and R219C found in holoprosence patients previously, resulted in structural change and less folding of TGIF1-HD, and thereby severely impaired the DNA-binding affinity of TGIF1-HD.
High TGIF-1 expression is associated with fetal growth restriction.
Tgifs regulate ciliogenesis and suggests that Evi5l (show EVI5L Antibodies) mediates at least part of this effect.
Knockdown of TGIF1 resulted in decreased protein expression of HOXD10 (show HOXD10 Antibodies) and increased resistance to colistin cytotoxicity in renal cells.
Data show that the silencing of TG-interacting factor (TGIF) inhibited A549 lung cancer cell proliferation, growth of tumor xenograft in vivo, and arrested the cell cycle in the G1 phase.
we suggest that TGIF (show IL10 Antibodies) plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src (show SRC Antibodies)/EGFR (show EGFR Antibodies)/AKT (show AKT1 Antibodies)/FOXO3A (show FOXO3 Antibodies) pathway and redox signaling.
Corneal fibroblasts demonstrate the expression of TGIF1 and TGIF2 (show TGIF2 Antibodies) transcription factors. These transcriptional repressors are critical, at least partially, in mediating the antifibrotic effect of vorinostat in the cornea.
Our results suggested that elevated expression of TGIF (show IL10 Antibodies) was involved in lung carcinogenesis.
our study demonstrated the oncogenic role of TGIF1 in NSCLC, and TGIF1 might be a therapeutic target for non-small cell lung cancer .
c-Src (show SRC Antibodies)/AKT (show AKT1 Antibodies) is the upstream signaling that regulates TGIF (show IL10 Antibodies)-induced Nox4 (show NOX4 Antibodies) activation and subsequent superoxide production.
Proteomic analyses show that HOXA1 (show HOXA1 Antibodies) physically interacts on chromatin with PBX, MEIS, and PREP (show PREP Antibodies) family members, but not with TGIF, suggesting that TGIF may have an independent input into HOXA1 (show HOXA1 Antibodies)-bound regions.complex cross-regulatory network of HOXA1 (show HOXA1 Antibodies) and TALE proteins. This study provides new insight into a regulatory network involving combinatorial interactions between HOXA1 (show HOXA1 Antibodies) and TALE proteins
loss of Tgif1 causes axial patterning defects that are enhanced by mutations in Tgif2 (show TGIF2 Antibodies)
Tgif2 (show TGIF2 Antibodies) participates in photoreceptor cell differentiation in the early stages of retinal development and regulates proper subretinal localization of the cone photoreceptors.
Tgif1 counterbalances the activity of core pluripotency factors, Oct4, Sox2, and Nanog, in mouse embryonic stem cells.
Tgif1 suppresses stem cell self-renewal.
The identification and characterization of the Tgif mutant supports the role of TGFbeta (show TGFB1 Antibodies) signalling in the development of chronic OM.
Tgif1 mutation in mouse contributes to Holoprosencephaly pathogenesis due to disruption of the Shh (show SHH Antibodies) pathway
TGIF1 plays a role in TNF-alpha (show TNF Antibodies)- and radiation-induced inflammation and it could be a target in limiting this event in the vascular compartment
TGF-beta (show TGFB1 Antibodies)/Smad (show SMAD1 Antibodies) co-repressor TGIF1 plays a role in radiation-induced normal tissue damage by a Smad (show SMAD1 Antibodies)-independent mechanism.
Tgif1 expression and regulation of TGFbeta (show TGFB1 Antibodies) signaling are implicated in the function of several types of stem cells, but this is the first demonstration that this regulatory network is necessary for regeneration of neurons.
Tgif is necessary for normal initiation of genes that control RA synthesis and degradation, resulting in defects in RA-dependent central nervous system patterning in Tgif-depleted embryos.
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.
5'-TG-3'-interacting factor 1
, TALE homeobox TG-interacting factor
, homeobox protein TGIF1
, transforming growth factor-beta-induced factor
, TALE family homeobox
, TG interacting factor 1
, TG interacting factor
, TGFB-induced factor (TALE family homeobox)
, avian knotted-related protein
, homeobox protein AKR
, homeodomain protein AKR
, TG-interacting factor
, TGFB-induced factor homeobox 1
, TG-interacting homeobox protein
, TGFB induced factor homeobox 1 S homeolog