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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. Additionally we are shipping T-Box 5 Antibodies (74) and many more products for this protein.
Showing 5 out of 6 products:
we show TBX5 and TBX20 (show TBX20 Proteins) can physically interact and map the interaction domains, and we show a cellular interaction for the two proteins in cardiac development
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 (show NKX2-3 Proteins) and LRRC17 (show LRRC17 Proteins) in myofibroblasts and SHOX2 (show SHOX2 Proteins) and TBX5 in skin fibroblasts
The Barrett-associated variants at GDF7 (show GDF7 Proteins) 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 (show TBX3 Proteins) and TBX5, and a third patient with acheiropodia who had a nullizygous deletion of 102 kb on 7q36.3 spanning LMBR1 (show LMBR1 Proteins)
provide both genetic and functional evidence to support the contribution of TBX5 gene in the pathogenesis of Atrial fibrillation
In summary, our study implicated a gene network involving Tbx5, Osr1 (show OXSR1 Proteins) and Pcsk6 interaction in second heart field for atrial septation, providing a molecular framework for understanding the role of Tbx5 in congenital heart disease ontogeny.
The findings expand the mutational spectrum of TBX5 linked to Atrial fibrillation (AF), and provide new evidence that dysfunctional TBX5 may contribute to lone AF.
TBX5 microdeletion with microinsertion was detected in patient with Holt-Oram syndrome.
The crystal structure of cardiac TBX5 protein includes the N-terminal and DNA binding domains, which mediate intermolecular interactions.
Exome analysis revealed the splice mutation (c.148-1G>C) in TBX5 gene showing that haploinsufficiency of TBX5 protein caused the symptoms of the patients with Holt-Oram syndrome.
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 (show GATA4 Proteins), Mef2c (show MEF2C Proteins), and Tbx5 (abbreviated as GMT (show GAMT Proteins)) significantly improved murine embryonic stem cells (ESCs (show NR2E3 Proteins)) 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 (show NKX2-5 Proteins), and the zinc finger TF GATA4 (show GATA4 Proteins) coordinately controlling cardiac gene expression, differentiation, and morphogenesis.
Tbx5 and Osr1 (show OSR1 Proteins) 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 germline mutant mice is due to loss of MOZ-dependant activation of mesodermal Tbx1 (show TBX1 Proteins) and Tbx5 expression.
our findings reveal a novel mechanism for regulation of SCFFbox25-dependent Nkx2-5 (show NKX2-5 Proteins) and Tbx5 ubiquitination in cardiac development and provide a new insight into the regulatory mechanism of Nkx2-5 (show NKX2-5 Proteins) and Tbx5 transcriptional activity.
Our findings implicate Foxf (show FOXF1 Proteins) genes in atrioventricular septation, describe the molecular underpinnings of the genetic interaction between Hedgehog (show SHH Proteins) signaling and Tbx5, and establish a molecular model for the selection of the SHF (show SHF Proteins) gene regulatory network
a mesodermal Fgf24 convergence cue controlled by Tbx5a underlies this asymmetric convergent motility.
Results show that cul4a (show CUL4A Proteins) but not cul4b (show CUL4B Proteins) 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 (show TBX20 Proteins), and has2 (show HAS2 Proteins) in the heart
Tbx5a confers anterior lateral plate mesodermal cells the competence to respond to Bmp signals and initiate proepicardial organ development.
Pdlim7 (show PDLIM7 Proteins)/Tbx5 interactions affect the expression of Tbx5 target genes nppa (show NPPA Proteins) 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 (show TBX20 Proteins) causes a significant downregulation of tbx5, indicating that one key role of hrT (show TBX20 Proteins) 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