anti-T-Box 5 (TBX5) Antibodies

Xenopus laevis T-Box 5 (TBX5) interaction partners

1. we show TBX5 and TBX20 can physically interact and map the interaction domains, and we show a cellular interaction for the two proteins in cardiac development

Human T-Box 5 (TBX5) interaction partners

1. TBX5 (rs6489957) is associated with congenital heart disease in Egyptian children.

2. miR-10a-5p in a relation with TBX5 regulates joint inflammation in arthritis.

3. The single nucleotide polymorphisms (SNPs) of NKX2.5, GATA4, and TBX5 are highly associated with congenital heart diseases in the Chinese population, but not significant in the SNPs of FOG2.

4. Study showed that thalidomide inhibited the TBX5/HAND2 physical interaction, and the in silico docking revealed that the same amino acids involved in the interaction of TBX5 with DNA are also involved in its binding to HAND2. Results establish a HAND2/TBX5 pathway implicated in heart development and diseases.

5. down-regulation of miR-10a-5p promotes proliferation and restricts apoptosis via targeting TBX5 in inflamed synoviocytes.

6. Diagnosis of Holt-Oram syndrome is possible as early as in prenatal period and it can be verified by genetic tests.

7. TBX5 overexpression markedly suppressed in vitro NSCLC cell proliferation, colony formation, and invasion and induced apoptosis.

8. TBX5 variants show possible pathogenic Fibrosis of the Cardiac Conduction system.

9. TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells

10. 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.

11. There is no difference in NKX2.5 and TBX5 gene mutations between in vitro fertilization and naturally conceived children with congenital heart disease (CHD).

12. Rs7312625 of TBx5 gene was significantly associated with lone atrial fibrillation, and snp-snp interaction increased the risk of atrial fibrillation.

13. Hence, the variant distribution of NKX2-5, GATA4 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

14. Findings suggest that a single introduction of the three cardiomyogenic transcription factor (GATA4, cand TBX5)genes using polyethyleneimine (PEI)-based transfection is sufficient for transdifferentiation of adipose-derived stem cells (hADSCs) towards the cardiomyogenic lineage.

15. Three genes-ATP6V1G1 in 9q32, GMPS 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

16. report on the association between a TBX5 lossoffunction mutation and increased susceptibility to atrial fibrillation

17. 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 in myofibroblasts and SHOX2 and TBX5 in skin fibroblasts

18. The Barrett-associated variants at GDF7 and TBX5 also increase esophageal adenocarcinoma risk.

19. 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 and TBX5, and a third patient with acheiropodia who had a nullizygous deletion of 102 kb on 7q36.3 spanning LMBR1

20. provide both genetic and functional evidence to support the contribution of TBX5 gene in the pathogenesis of Atrial fibrillation

Mouse (Murine) T-Box 5 (TBX5) interaction partners

1. Normal downregulation of the definitive arterial pole progenitor cell program in the posterior of the Second Heart Field (SHF) is dependent on both Tbx1 and Tbx5. Furthermore, retinoic acid (RA) signaling is required for Tbx5 activation in Tbx1-positive cells and blocking RA signaling at the time of Tbx5 activation results in atrioventricular septal defects at fetal stages.

2. Enrichment of induced cardiomyocytes derived from mouse fibroblasts can be achieved by reprogramming with cardiac transcription factors, Gata4, MEF2c, Tbx5, and Hand2.

3. Defined a transcriptional architecture for atrial rhythm control organized as an incoherent feed-forward loop, driven by TBX5 and modulated by PITX2. TBX5/PITX2 interplay provides tight control of atrial rhythm effector gene expression, and perturbation of the co-regulated network caused atrial fibrillation susceptibility.

4. The data also suggest that, in human, KLF13 may be a genetic modifier of the Holt-Oram Syndrome gene TBX5.

5. 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.

6. Data show that three transcriptional factors Gata4, Mef2c, and Tbx5 (abbreviated as GMT) significantly improved murine embryonic stem cells (ESCs) differentiated into cardiomyocytes.

7. defines a TBX5-nucleosome remodeling and deacetylase interaction essential to cardiac development and the evolution of the mammalian heart

8. Study reports extensive and complex interdependent genomic occupancy of TBX5, NKX2-5, and the zinc finger TF GATA4 coordinately controlling cardiac gene expression, differentiation, and morphogenesis.

9. Tbx5 and Osr1 interact to regulate posterior second heart field cell cycle progression for cardiac septation.

10. 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.

11. These findings elucidate mechanisms regulating the commitment of mesodermal cells in the early embryo and identify the Tbx5 cardiac transcriptome.

12. 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 and Tbx5 expression.

13. our findings reveal a novel mechanism for regulation of SCFFbox25-dependent Nkx2-5 and Tbx5 ubiquitination in cardiac development and provide a new insight into the regulatory mechanism of Nkx2-5 and Tbx5 transcriptional activity.

14. Our findings implicate Foxf genes in atrioventricular septation, describe the molecular underpinnings of the genetic interaction between Hedgehog signaling and Tbx5, and establish a molecular model for the selection of the SHF gene regulatory network

15. Disruption of myocardial Gata4 and Tbx5 results in defects in cardiomyocyte proliferation and atrioventricular septation.

16. TBX5 isoforms derived from novel exons have distinct expression domains and function. Alternative splicing regulates TBX5 function in heart and limb.

17. Tbx5 is a common node in the genetic pathways regulating forelimb and sternum development, enabling specific adaptations of thesefeatures without affecting other skeletal elements.

18. Data show that Hdac3 physically interacts with Tbx5 and modulates its acetylation to repress Tbx5-dependent activation of cardiomyocyte lineage-specific genes.

19. SRC-2 is critical to transcriptional control modulated by MEF2, GATA-4, and Tbx5, thereby enhancing gene expression associated with cardiac growth.

20. Data indicate that Nkx2-5, Tbx5, Gata4, or Myocd alone did not induce the de novo expression of cardiac marker proteins in 10T1/2 non-myoblastic cells.

Zebrafish T-Box 5 (TBX5) interaction partners

1. These studies highlight the importance of KAT2A and KAT2B modulation of TBX5 and their impact on heart and limb development.

2. IGF-I has an anti-apoptotic protective effect in zebrafish embryos with tbx5 deficiency.

3. loss of tbx5a function significantly impairs the ability of zebrafish hearts to regenerate after ventricular resection, indicating that Tbx5a plays an essential role in the transcriptional program of heart regeneration.

4. Tbx5a-expressing lineage demonstrates cardiomyocyte plasticity during zebrafish heart regeneration.

5. Regulatory evolution of Tbx5 and the origin of paired appendages, such as fins, is presented.

6. a mesodermal Fgf24 convergence cue controlled by Tbx5a underlies this asymmetric convergent motility.

7. Results show that cul4a but not cul4b is required for the expression of tbx5a, an essential transcription factor in heart and limb development.

8. The tbx5 genes have essential roles in the establishment of cardiac laterality, dorsoventral retina axis organization and pectoral fin development.

9. Despite similar spatio-temporal expression patterns, tbx5a and tbx5b have independent functions in heart and fin development.

10. 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

11. tbx5 deficiency evoked apoptosis, distributed on multiple organs corresponding to dysmorphogenesis with the shortage of promising maturation, in tbx5 knockdown zebrafish embryos

12. data demonstrate that elevated glucose alone induces cardiac defects in zebrafish embryos by altering the expression pattern of tbx5, tbx20, and has2 in the heart

13. Tbx5a confers anterior lateral plate mesodermal cells the competence to respond to Bmp signals and initiate proepicardial organ development.

14. Pdlim7/Tbx5 interactions affect the expression of Tbx5 target genes nppa and tbx2b at the atrio-ventricular boundary, and their domains of misexpression directly correlate with the identified valve defects.

15. The heartstrings mutation in zebrafish causes heart/fin Tbx5 deficiency syndrome.

16. overexpression of hrT causes a significant downregulation of tbx5, indicating that one key role of hrT is to regulate the levels of tbx5

17. Tbx5, in addition to its role governing forelimb identity, is both necessary and sufficient for limb outgrowth; Tbx5 functions downstream of WNT signaling to regulate Fgf10, which, in turn, maintains Tbx5 expression during limb outgrowth.

18. Sall gene family redundancy and tbx5 offer explanations for the similarity of individuals with Okihiro syndrome and Holt-Oram syndrome limb defects

19. heart failure caused by the knockdown of tbx5 gene might result from the down-regulation of cardiac myogenesis genes

20. redundant activities of Nkx2.5 and Nkx2.7 are required for cardiac morphogenesis, but Nkx2.7 plays a more critical function, regulating the expressions of tbx5 and tbx20 through the maturation stage