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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 (68) und und viele weitere Produktgruppen zu diesem Protein an.
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we show TBX5 and TBX20 (zeige TBX20 Proteine) can physically interact and map the interaction domains, and we show a cellular interaction for the two proteins in cardiac development
TBX5 overexpression markedly suppressed in vitro NSCLC cell proliferation, colony formation, and invasion and induced apoptosis.
TBX5 variants show possible pathogenic Fibrosis of the Cardiac Conduction system.
TBX5 deficiency-mediated downregulation of NFAT3 (zeige NFATC4 Proteine) is crucial for the high cytokine-producing activity of T cells
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 Proteine) and TBX5 gene mutations between in vitro fertilization and naturally conceived children with congenital heart disease (CHD (zeige CHDH Proteine)).
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 Proteine), GATA4 (zeige GATA4 Proteine) 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 Proteine), 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 Proteine) in 9q32, GMPS (zeige GMPS Proteine) 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
Enrichment of induced cardiomyocytes derived from mouse fibroblasts can be achieved by reprogramming with cardiac transcription factors, Gata4 (zeige GATA4 Proteine), MEF2c (zeige MEF2C Proteine), Tbx5, and Hand2 (zeige HAND2 Proteine).
Defined a transcriptional architecture for atrial rhythm control organized as an incoherent feed-forward loop, driven by TBX5 and modulated by PITX2 (zeige PITX2 Proteine). TBX5/PITX2 (zeige PITX2 Proteine) 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 Proteine) 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 Proteine), Mef2c (zeige MEF2C Proteine), and Tbx5 (abbreviated as GMT (zeige GAMT Proteine)) significantly improved murine embryonic stem cells (ESCs (zeige NR2E3 Proteine)) 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 Proteine), and the zinc finger TF GATA4 (zeige GATA4 Proteine) coordinately controlling cardiac gene expression, differentiation, and morphogenesis.
Tbx5 and Osr1 (zeige OSR1 Proteine) 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.
Regulatory evolution of Tbx5 and the origin of paired appendages, such as fins, is presented.
a mesodermal Fgf24 convergence cue controlled by Tbx5a underlies this asymmetric convergent motility.
Results show that cul4a (zeige CUL4A Proteine) but not cul4b (zeige CUL4B Proteine) 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 Proteine), and has2 (zeige HAS2 Proteine) 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 Proteine)/Tbx5 interactions affect the expression of Tbx5 target genes nppa (zeige NPPA Proteine) 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.
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