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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 Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 74 products:
Human Monoclonal TBX5 Primary Antibody für RNAi, ELISA - ABIN563098
Ghosh, Song, Packham, Buxton, Robinson, Ronksley, Self, Bonser, Brook: Physical interaction between TBX5 and MEF2C is required for early heart development. in Molecular and cellular biology 2009
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Cow (Bovine) Polyclonal TBX5 Primary Antibody für IHC, WB - ABIN2777915
Zaragoza, Lewis, Sun, Wang, Li, Said-Salman, Feucht, Huang: Identification of the TBX5 transactivating domain and the nuclear localization signal. in Gene 2004
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Human Polyclonal TBX5 Primary Antibody für ICC, IF - ABIN4358060
Lian, Zhang, Azarin, Zhu, Hazeltine, Bao, Hsiao, Kamp, Palecek: Directed cardiomyocyte differentiation from human pluripotent stem cells by modulating Wnt/β-catenin signaling under fully defined conditions. in Nature protocols 2012
Show all 2 Pubmed References
Human Polyclonal TBX5 Primary Antibody für IHC (p), WB - ABIN658694
Baban, Pitto, Pulignani, Cresci, Mariani, Gambacciani, Digilio, Pongiglione, Albanese: Holt-Oram syndrome with intermediate atrioventricular canal defect, and aortic coarctation: functional characterization of a de novo TBX5 mutation. in American journal of medical genetics. Part A 2014
Human Monoclonal TBX5 Primary Antibody für ELISA, WB - ABIN969432
Collavoli, Hatcher, He, Okin, Deo, Basson: TBX5 nuclear localization is mediated by dual cooperative intramolecular signals. in Journal of molecular and cellular cardiology 2003
we show TBX5 and TBX20 (zeige TBX20 Antikörper) 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 Antikörper) and TBX5 gene mutations between in vitro fertilization and naturally conceived children with congenital heart disease (CHD (zeige CHDH Antikörper)).
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 Antikörper), GATA4 (zeige GATA4 Antikörper) 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 Antikörper), 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 Antikörper) in 9q32, GMPS (zeige GMPS Antikörper) 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 (zeige NKX2-3 Antikörper) and LRRC17 (zeige LRRC17 Antikörper) in myofibroblasts and SHOX2 (zeige SHOX2 Antikörper) and TBX5 in skin fibroblasts
The Barrett-associated variants at GDF7 (zeige GDF7 Antikörper) 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 Antikörper) and TBX5, and a third patient with acheiropodia who had a nullizygous deletion of 102 kb on 7q36.3 spanning LMBR1 (zeige LMBR1 Antikörper)
The data also suggest that, in human, KLF13 (zeige KLF13 Antikörper) 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 Antikörper), Mef2c (zeige MEF2C Antikörper), and Tbx5 (abbreviated as GMT (zeige GAMT Antikörper)) significantly improved murine embryonic stem cells (ESCs (zeige NR2E3 Antikörper)) 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 Antikörper), and the zinc finger TF GATA4 (zeige GATA4 Antikörper) coordinately controlling cardiac gene expression, differentiation, and morphogenesis.
Tbx5 and Osr1 (zeige OSR1 Antikörper) 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 Antikörper) germline mutant mice is due to loss of MOZ (zeige MYST3 Antikörper)-dependant activation of mesodermal Tbx1 (zeige TBX1 Antikörper) and Tbx5 expression.
our findings reveal a novel mechanism for regulation of SCFFbox25-dependent Nkx2-5 (zeige NKX2-5 Antikörper) and Tbx5 ubiquitination in cardiac development and provide a new insight into the regulatory mechanism of Nkx2-5 (zeige NKX2-5 Antikörper) and Tbx5 transcriptional activity.
a mesodermal Fgf24 convergence cue controlled by Tbx5a underlies this asymmetric convergent motility.
Results show that cul4a (zeige CUL4A Antikörper) but not cul4b (zeige CUL4B Antikörper) 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 Antikörper), and has2 (zeige HAS2 Antikörper) 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 Antikörper)/Tbx5 interactions affect the expression of Tbx5 target genes nppa (zeige NPPA Antikörper) 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 Antikörper) causes a significant downregulation of tbx5, indicating that one key role of hrT (zeige TBX20 Antikörper) 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