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Human Polyclonal TGIF1 Primary Antibody pour ELISA, WB - ABIN543813
Ferrand, Demange, Prunier, Seo, Atfi: A mechanism for mutational inactivation of the homeodomain protein TGIF in holoprosencephaly. dans FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2007
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Chronic otitis media is associated with the TGIF1 and FBXO11 loci that are involved in TGF-beta signaling, suggesting this pathway may be important in the transition from acute to chronic middle ear inflammation, and a potential molecular target.
TGIF1 homeodomain interacts with Smad2/Smad4 MH1 domains and represses TGF-beta signaling.
Results suggest that silencing TGIF inhibited migration, invasion and metastasis of the human breast cancer cell line of MDAMB231 in vitro and in vivo.
Data suggest that expression of TGIF is up-regulated by carcinogen BaP [benzo(a)pyrene]; this process is involved in BaP-induced cell proliferation, cell migration, tumor invasiveness, and tumor metastasis of lung adenocarcinoma cells.
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 mediates at least part of this effect.
Knockdown of TGIF1 resulted in decreased protein expression of HOXD10 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 plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src/EGFR/AKT/FOXO3A pathway and redox signaling.
Corneal fibroblasts demonstrate the expression of TGIF1 and TGIF2 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 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/AKT is the upstream signaling that regulates TGIF-induced Nox4 activation and subsequent superoxide production.
TGIF1 has a role as a negative regulator of MLL-rearranged acute myeloid leukemia
TG-interacting factor transcriptionally induced by AKT/FOXO3A is a negative regulator that antagonizes arsenic trioxide-induced cancer cell apoptosis.
TG-interacting factor 1 (Tgif1) is an important repressor of SOAT2 gene expression.
TGIF1 is a relevant candidate gene with potential to contribute in the genesis of high myopia.
Alternative splicing of TGIF1 is deregulated in OSCC, with overexpression of some splicing variants, especially TGIF1v8, which is associated with advanced stages of OSCC.
Data demonstrate that homeobox gene TGIF-1 is a potential up-stream regulator of trophoblast differentiation and the altered TGIF-1 expression may contribute to aberrant villous trophoblast differentiation in FGR.
Tgifs play an important role in regulating basic energy metabolism in normal cells, and that this function of Tgifs is amplified in some cancers.
Tgif1 is a novel regulator of bone remodeling and an essential component of the PTH anabolic action.
Zic2-binding to the cis-regulatory element near the Tgif1 promoter may be involved in the mechanism underlying forebrain development and incidences of holoprosencephaly.
Proteomic analyses show that HOXA1 physically interacts on chromatin with PBX, MEIS, and PREP family members, but not with TGIF, suggesting that TGIF may have an independent input into HOXA1-bound regions.complex cross-regulatory network of HOXA1 and TALE proteins. This study provides new insight into a regulatory network involving combinatorial interactions between HOXA1 and TALE proteins
loss of Tgif1 causes axial patterning defects that are enhanced by mutations in Tgif2
Tgif2 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 signalling in the development of chronic OM.
Tgif1 mutation in mouse contributes to Holoprosencephaly pathogenesis due to disruption of the Shh pathway
TGIF1 plays a role in TNF-alpha- and radiation-induced inflammation and it could be a target in limiting this event in the vascular compartment
TGF-beta/Smad co-repressor TGIF1 plays a role in radiation-induced normal tissue damage by a Smad-independent mechanism.
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.
mRNA for positive regulators of Fshb expression, such as Fos and Jun, were up-regulated at slower pulse frequencies than a number of potential negative regulators, such as the corepressors Skil, Crem, and Tgif1.
Tgif1 can regulate nuclear receptor complexes, in addition to those containing retinoic acid receptors, but also indicates that there is some specificity to which NR target genes are repressed by Tgif1.
Data show that loss-of-function mutations in both Tgif1 and Tgif2 result in a failure of gastrulation.
Targeted disruption of Tgif in mice did not induce discernible derangements in forebrain, which point to a possible functional redundancy of Tgif, potentially provided by the closely related Tgif2.
loss of TGIF function is compensated by other TGF-beta antagonists such as c-Ski and SnoN during vertebrate anterior neural development
TGIF acts as a transcriptional corepressor, which regulates developmental signaling by retinoic acid, and raises the possibility that TGIF may repress other RXR-dependent transcriptional responses.
Tgif1 expression and regulation of TGFbeta 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