Disease relevance of Tcf2

• The level of phospho-activating transcription factor-2 appeared to be higher in CAI pyramidal cells than in dentate granule cells after ischemia [1].

High impact information on Tcf2

• Our results demonstrate that 2-AAF and some of its analogs can elicit a specific mitogenic response and induce expression of the "establishment" transcription factors, HNF1 beta and HNF3 gamma, in ductal cells [2].
• Whole-mount immunostaining demonstrates that, in the developing larvae, XDCoH is localized in the nuclei of the hepatocytes, the gut cells and the pronephric cells, tissues of mesodermal and endodermal origin known to contain LFB1 and LFB3 [3].
• Our results show that LFB3 transcripts can be detected in mesoderm-derived cells as soon as they are induced to differentiate into a polarized epithelium, while LFB1 transcripts appear only at a later stage when the three different segments of the nephron become apparent [4].
• Neither LFB1 nor LFB3 are expressed in the glomeruli or in the transition epithelia of the ureters and of the urinary bladder, none of which are involved in active transport mechanisms [4].
• This expression pattern suggests that LFB3 and LFB1 play a role in two critical stages of the developmentally regulated conversion of the nephric mesenchyme into a polarized epithelium: the early inductory phase (LFB3) and the postinductory phase (LFB1+LFB3) [4].

Biological context of Tcf2

• Tumor necrosis factor-alpha and interferon-gamma suppress both gene expression and deoxyribonucleic acid-binding of TTF-2 in FRTL-5 cells [5].

Anatomical context of Tcf2

• Thyroid transcription factor-2 (TTF-2) is a DNA-binding protein that modulates the expression of TG and TPO genes [5].
• Enhanced nuclear respiratory transcription factor-2 binding activity in hippocampus was accompanied by a nearly three-fold boost in mitochondrial DNA content over 5 days [6].

Associations of Tcf2 with chemical compounds

• Overexpression of HNF-1beta enhances dexamethasone-stimulated promoter activity [7].
• Thus, the synergistic effects of HNF-1beta and the GR on dexamethasone-stimulated promoter activity require that they are bound to the HNF-1 site and the GRE, respectively, and may involve protein-protein interactions between the transcription factors, or between them and the basal transcription machinery or a steroid receptor coactivator [7].
• Compensatory responses were found in nuclear gene expression for manganese superoxide dismutase, mitochondrial transcription factor A, and nuclear respiratory transcription factor-2 [6].

Physical interactions of Tcf2

• Formation of the TTF-2/DNA complex was decreased by TNF-alpha and/or IFN-gamma [5].
• In gel shift assays, HNF-1alpha and HNF-1beta in H4-II-E extracts bind to the palindromic HNF-1 site [7].

Other interactions of Tcf2

• TNF-alpha (50 ng/ml) only slightly suppressed (61+/-2% compared with control), whereas IFN-gamma (100 U/ml) modestly decreased TTF-2 messenger RNA (mRNA) levels (34+/-4%) [5].
• TNF-alpha and IFN-gamma simultaneously caused a marked decrease in TTF-2 mRNA levels (13+/-2%) [5].
• This expression was coincident with an increased expression of hepatocyte nuclear factor (HNF)-4 and a higher HNF-1alpha/HNF-1beta ratio, when compared with those cells that were cultured on collagen or E-C-L extracellular matrix [8].

Analytical, diagnostic and therapeutic context of Tcf2

• We have analyzed the expression pattern of LFB1 and LFB3 in the developing rat kidney by in situ hybridization [4].
• Northern blot analysis revealed that there were slightly more transcripts of C/EBP, HNF1 beta (n.s.) and HNF4 (p < 0.05), but fewer of HNF3 gamma (n.s.), in perivenous than in periportal lysates [9].

References