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TBX5 is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. Zusätzlich bieten wir Ihnen T-Box 5 Antikörper (74) und T-Box 5 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
we show TBX5 and TBX20 (zeige TBX20 ELISA Kits) can physically interact and map the interaction domains, and we show a cellular interaction for the two proteins in cardiac development
A novel heterozygous missense mutation in TBX5 gene identified in a case of ventricular septal defect. The mutation causes significant changes of the activity of TBX5 in vitro.
There is no difference in NKX2.5 (zeige NKX2-5 ELISA Kits) and TBX5 gene mutations between in vitro fertilization and naturally conceived children with congenital heart disease (CHD (zeige CHDH ELISA Kits)).
Rs7312625 of TBx5 gene was significantly associated with lone atrial fibrillation, and snp-snp interaction increased the risk of atrial fibrillation.
Hence, the variant distribution of NKX2-5 (zeige NKX2-5 ELISA Kits), GATA4 (zeige GATA4 ELISA Kits) and TBX5 are tightly associated with particular Congenital heart disease subtypes. Further structure-modelling analysis revealed that these mutated amino acid residuals maintain their DNA-binding ability and structural stability
Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4 (zeige GATA4 ELISA Kits), cand TBX5)genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.
Three genes-ATP6V1G1 (zeige ATP6V1G1 ELISA Kits) in 9q32, GMPS (zeige GMPS ELISA Kits) in 3q25.31, and TBX5 in 12q24.21-exhibited concomitant hypermethylation and decreased expression. The i(12p)-positive cells displayed global hypomethylation of gene-poor regions on 12p, a footprint previously associated with constitutional and acquired gains of whole chromosomes as well as with X-chromosome inactivation in females
report on the association between a TBX5 lossoffunction mutation and increased susceptibility to atrial fibrillation
Whole-genome microarray mRNA-expression profiles of myofibroblasts and skin fibroblasts revealed four additional genes that are significantly differentially expressed in these two cell types: NKX2-3 and LRRC17 (zeige LRRC17 ELISA Kits) in myofibroblasts and SHOX2 (zeige SHOX2 ELISA Kits) and TBX5 in skin fibroblasts
The Barrett-associated variants at GDF7 (zeige GDF7 ELISA Kits) and TBX5 also increase esophageal adenocarcinoma risk.
These include a patient with hypoplastic phalanges and absent hallux bilaterally with de novo deletion of 11.9 Mb on 7p21.1-22.1 spanning 63 genes including RAC1, another patient with severe Holt-Oram syndrome and a large de novo deletion 2.2 Mb on 12q24.13-24.21 spanning 20 genes including TBX3 (zeige TBX3 ELISA Kits) and TBX5, and a third patient with acheiropodia who had a nullizygous deletion of 102 kb on 7q36.3 spanning LMBR1 (zeige LMBR1 ELISA Kits)
Defined a transcriptional architecture for atrial rhythm control organized as an incoherent feed-forward loop, driven by TBX5 and modulated by PITX2 (zeige PITX2 ELISA Kits). TBX5/PITX2 (zeige PITX2 ELISA Kits) interplay provides tight control of atrial rhythm effector gene expression, and perturbation of the co-regulated network caused atrial fibrillation susceptibility.
The data also suggest that, in human, KLF13 (zeige KLF13 ELISA Kits) may be a genetic modifier of the Holt-Oram Syndrome gene TBX5.
Our data demonstrate an early, inherent asymmetry in the left and right limb-forming regions and that threshold levels of Tbx5 are required to overcome this asymmetry to ensure symmetric forelimb formation.
Data show that three transcriptional factors Gata4 (zeige GATA4 ELISA Kits), Mef2c (zeige MEF2C ELISA Kits), and Tbx5 (abbreviated as GMT (zeige GAMT ELISA Kits)) significantly improved murine embryonic stem cells (ESCs (zeige NR2E3 ELISA Kits)) differentiated into cardiomyocytes.
defines a TBX5-nucleosome remodeling and deacetylase interaction essential to cardiac development and the evolution of the mammalian heart
Study reports extensive and complex interdependent genomic occupancy of TBX5, NKX2-5 (zeige NKX2-5 ELISA Kits), and the zinc finger TF GATA4 (zeige GATA4 ELISA Kits) coordinately controlling cardiac gene expression, differentiation, and morphogenesis.
Tbx5 and Osr1 (zeige OSR1 ELISA Kits) interact to regulate posterior second heart field cell cycle progression for cardiac septation.
Haploinsufficiency of Tbx5 and trisomy affects alignment of the aorta and this effect may stem from deviations from normal left-right patterning in the heart; study unveiled a previously unknown interaction between the Tbx5 gene and trisomy, suggesting a connection between Tbx5 and trisomic genes important during heart development.
These findings elucidate mechanisms regulating the commitment of mesodermal cells in the early embryo and identify the Tbx5 cardiac transcriptome.
these data suggest that the molecular pathogenesis of ventricular septal defectss in Moz (zeige MYST3 ELISA Kits) germline mutant mice is due to loss of MOZ (zeige MYST3 ELISA Kits)-dependant activation of mesodermal Tbx1 (zeige TBX1 ELISA Kits) and Tbx5 expression.
a mesodermal Fgf24 convergence cue controlled by Tbx5a underlies this asymmetric convergent motility.
Results show that cul4a (zeige CUL4A ELISA Kits) but not cul4b (zeige CUL4B ELISA Kits) is required for the expression of tbx5a, an essential transcription factor in heart and limb development.
The tbx5 genes have essential roles in the establishment of cardiac laterality, dorsoventral retina axis organization and pectoral fin development.
tbx5 knockdown causes a pseudo GH deficiency in zebrafish during early embryonic stages, and supplementation of exogenous GH can partially restore dysmorphogenesis, apoptosis, cell growth inhibition, and abnormal cardiomyogenesis
tbx5 deficiency evoked apoptosis, distributed on multiple organs corresponding to dysmorphogenesis with the shortage of promising maturation, in tbx5 knockdown zebrafish embryos
data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5, tbx20 (zeige TBX20 ELISA Kits), and has2 (zeige HAS2 ELISA Kits) in the heart
Tbx5a confers anterior lateral plate mesodermal cells the competence to respond to Bmp signals and initiate proepicardial organ development.
Pdlim7 (zeige PDLIM7 ELISA Kits)/Tbx5 interactions affect the expression of Tbx5 target genes nppa (zeige NPPA ELISA Kits) and tbx2b at the atrio-ventricular boundary, and their domains of misexpression directly correlate with the identified valve defects.
The heartstrings mutation in zebrafish causes heart/fin Tbx5 deficiency syndrome.
overexpression of hrT (zeige TBX20 ELISA Kits) causes a significant downregulation of tbx5, indicating that one key role of hrT (zeige TBX20 ELISA Kits) is to regulate the levels of tbx5
This gene is a member of a phylogenetically conserved family of genes that share a common DNA-binding domain, the T-box. T-box genes encode transcription factors involved in the regulation of developmental processes. This gene is closely linked to related family member T-box 3 (ulnar mammary syndrome) on human chromosome 12. The encoded protein may play a role in heart development and specification of limb identity. Mutations in this gene have been associated with Holt-Oram syndrome, a developmental disorder affecting the heart and upper limbs. Several transcript variants encoding different isoforms have been described for this gene.
, T-box protein 5
, T-box transcription factor 5
, T-box transcription factor TBX5
, T-box transcription factor TBX5-like
, t-box transcription factor TBX5-like
, T-box gene 5
, T-box gene 5.1
, T-box transcription factor TBX5-A