-
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.
-
Enrichment of induced cardiomyocytes derived from mouse fibroblasts can be achieved by reprogramming with cardiac transcription factors, Gata4, MEF2c, Tbx5, and Hand2.
-
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.
-
The data also suggest that, in human, KLF13 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, Mef2c, and Tbx5 (abbreviated as GMT) significantly improved murine embryonic stem cells (ESCs) 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, and the zinc finger TF GATA4 coordinately controlling cardiac gene expression, differentiation, and morphogenesis.
-
Tbx5 and Osr1 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 and Tbx5 expression.
-
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.
-
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
-
Disruption of myocardial Gata4 and Tbx5 results in defects in cardiomyocyte proliferation and atrioventricular septation.
-
TBX5 isoforms derived from novel exons have distinct expression domains and function. Alternative splicing regulates TBX5 function in heart and limb.
-
Tbx5 is a common node in the genetic pathways regulating forelimb and sternum development, enabling specific adaptations of thesefeatures without affecting other skeletal elements.
-
Data show that Hdac3 physically interacts with Tbx5 and modulates its acetylation to repress Tbx5-dependent activation of cardiomyocyte lineage-specific genes.
-
SRC-2 is critical to transcriptional control modulated by MEF2, GATA-4, and Tbx5, thereby enhancing gene expression associated with cardiac growth.
-
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.
