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Study identified and characterized new TBX18 binding partners that may influence the transcriptional activity of TBX18 in vivo. Proteomic screen strongly supports an exclusive nuclear function of TBX18 as a repressor of chromatin accessibility.
Tbx18-positive cells represent a part of PE cells in the initial phase of differentiation and subsequently include SMCs as well as fibroblasts. These results indicate that Tbx18-positive cells serve as a PE progenitor to supply a variety of cells that contribute to the formation of coronary arteries.
Gene product expressions of SHH, TBX18 and TSHZ3 are statistically higher in patients with UPJ obstruction, when compared with control group. The explanation may be the reactivation of the processes, which had shown their effects in the embryological period, due to the chronic inflammation and long-term micro-trauma created by the disease
Data indicate that human T-box 18 (TBX18) gene induces rat adipose-derived stem cells (ADSCs) to differentiate into pacemaker-like cells in the cardiac microenvironment.
Mutations in TBX18 cause dominant urinary tract malformations via transcriptional dysregulation of ureter development.
The DNA sequence variants within the TBX18 gene promoter identified in ventricular septal defects (VSD) patients may be involved in the VSD etiology.
connexin43 transcriptional suppression by TBX18 undermines cardiomyocyte cell-cell electrical coupling
Tbx18 interacts with Gata4 and Nkx2-5 and competes Tbx5-mediated activation of the cardiac Natriuretic peptide precursor type a-promoter. Tbx18 down-regulates Tbx6-activated Delta-like 1 expression in the somitic mesoderm in vivo
Areas of strong tbx18 expression are found in the developing somitic and presomitic mesoderm, in the heart and in pectoral fin mesenchyme, as well as the ventral neuroectoderm and the developing palate
Tbx18, Ripply2, and Hes7 repress the activation of the Hes7 essential region by the aforementioned transcription factors.
TBX18 gene transduction may facilitate the differentiation of brown adipose-derived stem cell and white adipose-derived stem cellinto pacemakerlike myocardial cells, and brown adipose-derived stem cell may have a higher capacity than white adipose-derived stem cell for this differentiation.
The expression of Tbx3 and shox2, the other two important transcription factors in the development of pacemaker cells, was decreased by silencing Tbx18, which suggests that Tbx18 mediates the differentiation of BATSCs into a pacemaker phenotype via these two downstream transcription factors.
hypoxia intervention was sufficient to induce the differentiation of Tbx18-positive epicardial cells to coronary vascular smooth muscle cells.
Tbx18 does not function redundantly with Tbx2 or Tbx20 in epicardial development.
We conclude that exclusion of Tbx18 expression from the developing atria and (right) ventricle is important to achieve normal cardiac left-right patterning and myocardial differentiation, and that Tbx18 is not sufficient to induce full SAN differentiation of chamber cardiomyocytes in fetal mice.
Tbx18 is essential to the differentiation and maintenance of the prostate periurethral mesenchyme; it indirectly regulates epithelial differentiation through control of stromal-epithelial signaling.
The temporal suppression of Tbx18 gene expression by the hypermethylation of its promoter seems to trigger the differentiation of mesenchymal cells into hypertrophic chondrocytes in the early stages of endochondral ossification.
A distant downstream enhancer directs essential expression of Tbx18 in urogenital tissues.
Tbx18 has a role in normal development of vasculature network and glomerular mesangium in the mammalian kidney
Tbx18, a T-box family member highly expressed in the proepicardium, controls critical early steps in coronary development.
Tbx18 is required to prepattern mouse ureteric mesenchyme
Tbx18 and Wt1 directly bound to the Slug promoter region and regulated Slug expression
Tbx18 is dispensable for epicardial development but that a transcriptional activator form of Tbx18 is sufficient to induce premature smooth muscle differentiation of epicardial cells.
Tbx18 is dispensable for normal dermal papilla function.
Data show that Tbx18- and Wt1-deficient mice additionally exhibit partial pericardial absence.
phenotypes result from competition between the ectopically expressed Tbx6 and the endogenously expressed Tbx18 and Tbx15 at the binding sites of target genes
SIX1 acts synergistically with TBX18 in mediating ureteral smooth muscle formation.
identification of Tbx18 as a candidate gene for osteosarcoma
This genes codes for a member of an evolutionarily conserved family of transcription factors that plays a crucial role in embryonic development. The family is characterized by the presence of the DNA-binding T-box domain and is divided into five sub-families based on sequence conservation in this domain. The encoded protein belongs to the vertebrate specific Tbx1 sub-family. The protein acts as a transcriptional repressor by antagonizing transcriptional activators in the T-box family. The protein forms homo- or heterodimers with other transcription factors of the T-box family or other transcription factors.
, T-box transcription factor TBX18-like
, t-box transcription factor TBX18-like
, T-box transcription factor TBX18
, transcription factor Tbx18
, T-box protein 18