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anti-Human TGIF1 Antikörper:
anti-Mouse (Murine) TGIF1 Antikörper:
anti-Rat (Rattus) TGIF1 Antikörper:
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High TGIF-1 expression is associated with fetal growth restriction.
Tgifs regulate ciliogenesis and suggests that Evi5l (zeige EVI5L Antikörper) mediates at least part of this effect.
Knockdown of TGIF1 resulted in decreased protein expression of HOXD10 (zeige HOXD10 Antikörper) 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 (zeige IL10 Antikörper) plays an important role in low-dose arsenic-induced malignant transformation of HaCaT cells, which is regulated by c-Src (zeige SRC Antikörper)/EGFR (zeige EGFR Antikörper)/AKT (zeige AKT1 Antikörper)/FOXO3A (zeige FOXO3 Antikörper) pathway and redox signaling.
Corneal fibroblasts demonstrate the expression of TGIF1 and TGIF2 (zeige TGIF2 Antikörper) 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 (zeige IL10 Antikörper) 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 (zeige SRC Antikörper)/AKT (zeige AKT1 Antikörper) is the upstream signaling that regulates TGIF (zeige IL10 Antikörper)-induced Nox4 (zeige NOX4 Antikörper) activation and subsequent superoxide production.
TGIF1 has a role as a negative regulator of MLL (zeige MLL Antikörper)-rearranged acute myeloid leukemia (zeige BCL11A Antikörper)
loss of Tgif1 causes axial patterning defects that are enhanced by mutations in Tgif2 (zeige TGIF2 Antikörper)
Tgif2 (zeige TGIF2 Antikörper) 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 (zeige TGFB1 Antikörper) signalling in the development of chronic OM.
Tgif1 mutation in mouse contributes to Holoprosencephaly pathogenesis due to disruption of the Shh (zeige SHH Antikörper) pathway
TGIF1 plays a role in TNF-alpha (zeige TNF Antikörper)- and radiation-induced inflammation and it could be a target in limiting this event in the vascular compartment
TGF-beta (zeige TGFB1 Antikörper)/Smad (zeige SMAD1 Antikörper) co-repressor TGIF1 plays a role in radiation-induced normal tissue damage by a Smad (zeige SMAD1 Antikörper)-independent mechanism.
Data suggest that in the absence of Tgif1, a persistent increase in TGFbeta (zeige TGFB1 Antikörper) responsive transcription and a reduced ability to deal with hyperoxic stress result in premature senescence in primary MEFs.
Tgif1 expression and regulation of TGFbeta (zeige TGFB1 Antikörper) 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