Ask about this productRelated genes to: TBX5 antibody
- Gene:
- TBX5 NIH gene
- Name:
- T-box 5
- Previous symbol:
- HOS
- Synonyms:
- -
- Chromosome:
- 12q24.21
- Locus Type:
- gene with protein product
- Date approved:
- 1997-05-22
- Date modifiied:
- 2019-04-23
Related products to: TBX5 antibody
Related articles to: TBX5 antibody
- Cardiac ischemia induces substantial metabolomic reprogramming, which dysregulates cardiomyocytes (CMs) and non-myocyte stromal cell populations. The stromal cells derived from epicardial adipose tissue (EAT) and ventricle are critical for extracellular matrix (ECM) remodeling, paracrine signaling, and myocardial homeostasis. However, the metabolomic content and responses of EAT-derived stromal cells (EATDS) and ventricular stromal cells (VSCs) remain unknown. - Source: PubMed
Publication date: 2026/04/29
Sun DongweiPostajian AlexRostomian EdgminChen YuPark Junyoung OHatamian VediVartanian Kevin BabakhanThankam Finosh G - Heterozygous TBX4 variants are the second most common genetic cause of pediatric pulmonary hypertension (PH), yet mechanisms underlying TBX4-related lung disease remain poorly understood. This study developed a lung mesenchyme-specific Tbx4 loss-of-function (Tbx4cKO) mouse model that bypasses embryonic lethality to investigate this condition. Adult Tbx4cKO mice demonstrated significantly impaired pulmonary flow acceleration consistent with PH. Three-dimensional analysis of embryonic lungs revealed reduced lobe volumes and decreased distance between pleural edges and muscularized vessels. In adult Tbx4cKO lungs, we identified extensive vascular remodeling characterized by medial thickening and the extension of muscularized arteries into normally non-muscularized subpleural parenchymal zones. Contrary to previous reports suggesting vascular simplification, three-dimensional analysis demonstrated an elaborated pulmonary artery (PA) tree in addition to pathologic wall muscularization. Depletion of a single Tbx5 allele in addition to both Tbx4 alleles exacerbated histologic phenotypes with worsened right ventricular dilation. This model also demonstrated dysregulated airway smooth muscle patterning and prominent subpleural smooth muscle bands, similar to those in human TBX4 syndrome. We identify TBX4 as a critical regulator of smooth muscle differentiation and patterning across multiple lung compartments. Our model recapitulates key features of human TBX4 syndrome and identifies dysregulated smooth muscle differentiation as a potential future therapeutic target. - Source: PubMed
Publication date: 2026/04/23
Steffes Lea CChiles Kaylie AMasud Sehar RRahman AleenDawson MadelineGalambos CsabaKumar Maya EArora Ripla - Maternal sucralose exposure during pregnancy has been demonstrated to interfere embryonic development, yet limited studies have investigated its potential hazards on fetal cardiogenesis. In the present study, we employed a mice model to investigate the impact of sucralose exposure in early pregnancy on the risk of heart defects in offspring. Pregnant C57BL/6J mice received either control or sucralose water. The incidence of heart defects in the sucralose group was 13.86%, significantly higher than that in the control group. Transcriptional downregulation of cardiogenic genes involving , , , and were confirmed, potentially due to increased CREB phosphorylation. N-acetylcysteine (NAC) reduced CREB phosphorylation, partially reversed sucralose-induced suppression of cardiogenic genes, and reduced the incidence of heart defects from 16.67% to 4.81%. Our study demonstrates that sucralose exposure during early pregnancy increases the risk of heart defects via transcriptional suppression of cardiogenic genes, while NAC potentially functions as a protective factor. - Source: PubMed
Publication date: 2026/04/04
Zhang ZehuaYu ZiwenShi HaiqunDing TongShi YanZhao JianyuanCai KeWang Feng - The developing vertebrate forelimb expresses seven T-box transcription factors, with several in overlapping expression domains. All T-box transcription family members share similarity within their DNA binding domain, the T-domain. Outside of the T-domain, these factors share little similarity, allowing family members to have different transcriptional properties and binding partners. Several human T-box genes show haploinsufficiency in the limb, including Tbx5 and Tbx3 that, when mutated, cause Holt-Oram and ulnar-mammary syndrome, respectively. This dosage sensitivity combined with the shared T-domain leads to our hypothesis that when co-expressed a competition between T-box factors at target genes can occur. To test this, we ectopically expressed two exogenous T-box factors, T and Tbx6, in the developing forelimb mesenchyme to examine how artificially changing the relative levels of T-box proteins affects forelimb formation. Skeletal, apoptotic, and gene expression assays were used to characterize the resulting phenotypes. While ectopic T and Tbx6 both affected the size and shape of the forearm bones and ossification, they differentially affected digit formation: T caused loss of digits and Tbx6 led to phalange bone duplications and extra digit formation. These dissimilar phenotypes suggest that these transcriptional activators differentially affect pathways critical for regulating forelimb development. - Source: PubMed
Denhart Mariah HChapman Deborah L - Sirtuin 1 () is known to regulate stem cell differentiation and cardiomyocyte function, yet its specific role and mechanism in human embryonic stem cell (hESC) differentiation into cardiomyocytes remain unclear. This study aimed to elucidate the functional contribution and molecular pathway of in cardiomyogenesis. : A knockout (/) hESC line was generated using CRISPR-Cas9 technology. The expression of key differentiation markers was analyzed by RT-qPCR at days 6, 8, and 9. The underlying mechanism was investigated through integrated RNA-sequencing (RNA-seq) analysis and dual-luciferase reporter assays. : deletion significantly downregulated the expression of mesodermal (TBX6, KDR), cardiac precursor (NKX2.5, TBX5), and mature cardiomyocyte (cTNT, Hand2) markers. Mechanistically, a competing endogenous RNA (ceRNA) axis, LncRNA XR_951230.1/miR-3663-3p/SMYD1, was identified. knockout reduced XR_951230.1 expression, which consequently elevated miR-3663-3p activity and suppressed its target gene SMYD1. : These findings indicate that is essential for promoting hESC differentiation into cardiomyocytes, potentially via the XR_951230.1/miR-3663-3p/SMYD1 pathway. This study provides new insights into the regulatory network of stem cell-based cardiomyogenesis and suggests potential targets for stem cell-based cardiac disease therapy. - Source: PubMed
Publication date: 2026/02/27
Li ChengyuMahemuti MairepatiMaimaiti YusupujiangWang TingZhang XinJiapaer Zeyidan