TBX5 antibody - N-terminal region (ARP33403_P050)
- Known as:
- TBX5 (anti-) - N-terminal region (ARP33403_P050)
- Catalog number:
- arp33403_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TBX5 antibody - N-terminal region (ARP33403_P050)
Related genes to: TBX5 antibody - N-terminal region (ARP33403_P050)
- 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 - N-terminal region (ARP33403_P050)
Related articles to: TBX5 antibody - N-terminal region (ARP33403_P050)
- Atrioventricular block (AVB) represents a prevalent form of bradyarrhythmia in the pediatric population, broadly classified into congenital and acquired subtypes. Historically, the underlying mechanisms of AVB were predominantly attributed to structural cardiac anomalies, maternal autoantibody-mediated inflammatory processes, and pharmacological agents; however, the contribution of genetic factors remained largely underexplored. With the advent and progressive refinement of genetic sequencing technologies, a growing repertoire of arrhythmia-associated genes has been systematically identified. In this review, we comprehensively examine the genetic determinants implicated in pediatric AVB, encompassing genes encoding cardiac ion channels, including SCN5A, KCNQ1/KCNJ2 (KCN family), KCNH2 (HERG), TRPM4, and HCN4, as well as genes governing cardiac structural integrity (GJA5/GJA1, ZO-1, NKX2-5, TBX3/TBX5, HAND1/HAND2, and ID family members), metabolic regulation (PRKAG2, PPARA, and LAMP2), and immune-mediated pathways (TRIM21/TROVE2 and HLA class II loci). The genetic architecture underlying pediatric AVB demonstrates considerable complexity, characterized by notable genotypic heterogeneity and "multi-phenotypic" expressivity, wherein distinct mutations within a single gene may manifest across a spectrum of clinical phenotypes. Collectively, these findings establish a molecular framework for elucidating the pathogenesis of AVB, while simultaneously offering valuable insights to inform clinical diagnosis, facilitate precision-based intervention strategies, and guide the development of targeted therapeutic modalities. - Source: PubMed
Publication date: 2026/09/11
Pan ZhenhuiZhao WanlingLiu FuqiangLi Yifei - : In situ reprogramming of cardiac fibroblasts into induced cardiomyocytes (iCMs) holds great promise for myocardial infarction (MI) therapy by replenishing lost cardiomyocytes. A transcription factor cocktail consisting of Mef2c, Gata4, and Tbx5 (MGT) represents a widely used starting regimen for cardiac reprogramming, with numerous optimization efforts focused primarily on improving reprogramming efficiency. However, the effects of MGT exposure on non-target cardiac cell populations remain largely uncharacterized, and it remains unclear whether such unintended effects could pose safety concerns. : In this study, we introduced the widely used MGT cocktail into primary mouse bone marrow-derived macrophages (BMDMs) and the immortalized mouse macrophage cell line RAW 264.7. We first assessed cardiomyocyte-associated gene and protein expression. We then examined the polarization state of transduced RAW 264.7 cells. In BMDMs, we further assessed apoptosis- and necroptosis-associated markers to determine whether MGT delivery was accompanied by cell death. : (a) MGT introduction induced a transient increase in cardiomyocyte-associated Tnnt2/Myh6 transcripts and modest cTnT protein induction in macrophages, with cTnT immunofluorescence remaining elevated after two weeks in BMDMs and a small subset of cells displaying fibroblast-like morphology reminiscent of iCMs. (b) Transduced RAW 264.7 cells displayed elevated Cd206 transcript levels, accompanied by an increased proportion of spindle-like cells and enlarged nuclear area, collectively supporting an M2-like polarization shift. (c) Transduced primary BMDMs, but not RAW 264.7 cells, displayed elevated apoptosis- and necroptosis-associated responses, including increased YP1 fluorescence, PI staining, and p-MLKL immunofluorescence. : The classical MGT reprogramming regimen polarized RAW 264.7 cells toward an M2-like state, raising the possibility that, in the TGF-β-rich post-MI environment, this shift could increase the pool of macrophages susceptible to macrophage-to-myofibroblast transition and thereby potentially promote fibrosis. MGT-expressing LV elicited apoptosis-associated and necroptosis-associated changes in transduced BMDMs. These polarization and cell-survival effects highlight potential off-target and safety concerns for in situ direct cardiac reprogramming. Further investigations are warranted to determine whether and how such macrophage perturbations affect tissue remodeling and therapeutic outcomes in the post-MI setting. - Source: PubMed
Publication date: 2026/09/16
Chen TingzhenDing ShanshanZhang ZhongwenZhao LinCao KejunZhang GuannanWeng ChangyaGong GuangyuanXu LiangYang MinLi TianquanSheng ChengyuLi Yanxiu - The levels of human trophoblast surface antigen (Trop-2) and T-box protein 5 (TBX5) in the serum of patients with preeclampsia were detected, and their value in predicting adverse pregnancy outcomes was analysed. - Source: PubMed
Li YaoHuang SutongXuan YanShen HaoZhang WeiweiLi Jia - Partially anomalous pulmonary vein return (PAPVR) is a heterogeneous group of congenital heart defects. Here, we describe a 51-year-old patient with corrected PAPVR (cPAPVR) and atrioventricular canal defect who presented for AFL ablation. The right pulmonary veins were isolated, and the OP was heterogeneously fibrotic. Three left AFL and one cavo-tricuspid isthmus (CTI)-dependent AFL were induced and mapped using activation and Ablation at each site terminated the AFL. Subsequently, the entire OP was isolated. Post-ablation, she had no atrial arrhythmia at 6 months follow up. Genetic testing identified a pathological mutation in the TBX5 gene, consistent with Holt-Oram syndrome. - Source: PubMed
Publication date: 2026/09/23
Kosmopoulos MarinosAsatryan BabkenBarth AndreasDoshi AshishHale ZachariahCedars AriAronis Konstantinos N - Lung adenocarcinoma (LUAD) is the most common form of lung cancer and a leading cause of cancer-related mortality, underscoring the need for new chemopreventive strategies. α-Ketoglutarate (αKG), a tricarboxylic acid cycle metabolite and dioxygenase cofactor, links cellular metabolism to chromatin regulation. Here, we demonstrate that dietary calcium αKG (Ca-αKG) is associated with remodeling of LUAD in a sex-dependent manner. In female mice, Ca-αKG is associated with reduced tumor area, decreased repressive histone marks (H3K27me3 and H3K9me3), and upregulated TBX5 and myogenesis-associated genes. In male mice, Ca-αKG is associated with increased tumor area and elevated H3K27me3. Analysis of human LUAD revealed that TBX5 expression is enriched in female tumors and associated with improved survival, suggesting it may serve as a marker of favorable outcome. Together, these findings support Ca-αKG as an epigenetic modulator with potential chemopreventive activity in lung cancer and highlight the importance of incorporating sex as a biological variable in preclinical studies. - Source: PubMed
Publication date: 2026/09/23
Alcaraz MartínPandey AparamitaSantiago MiaDumitras CameliaPradis LeilaniGomez EstefanySoto AdrianaSaggese PasqualeKrall Abigail SLiu BinChristofk Heather RDubinett Steven MLi XueScafoglio Claudio