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Gene product expressions of SHH (zeige SHH Antikörper), TBX18 and TSHZ3 (zeige ZNF537 Antikörper) 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 (zeige GJA1 Antikörper) transcriptional suppression by TBX18 undermines cardiomyocyte cell-cell electrical coupling
Tbx18 interacts with Gata4 (zeige GATA4 Antikörper) and Nkx2-5 (zeige NKX2-5 Antikörper) and competes Tbx5 (zeige TBX5 Antikörper)-mediated activation of the cardiac Natriuretic peptide precursor type a-promoter. Tbx18 down-regulates Tbx6 (zeige TBX6 Antikörper)-activated Delta-like 1 (zeige DLL1 Antikörper) 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 does not function redundantly with Tbx2 (zeige TBX2 Antikörper) or Tbx20 (zeige TBX20 Antikörper) 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.
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