GATA4 Control Peptide antibody /CP
- Known as:
- GATA4 Control Peptide (anti-) /CP
- Catalog number:
- 'AP11353CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA4 Control Peptide antibody /
Related genes to: GATA4 Control Peptide antibody /CP
- Gene:
- GATA4 NIH gene
- Name:
- GATA binding protein 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-30
- Date modifiied:
- 2016-10-05
Related products to: GATA4 Control Peptide antibody /CP
Related articles to: GATA4 Control Peptide antibody /CP
- Lung organogenesis is orchestrated by dynamic epithelial-mesenchymal interactions during embryogenesis, yet the gene regulatory programs and signaling dynamics governing these processes in the pseudoglandular stage remain incompletely understood. In this study, we integrated spatial and single-cell transcriptomic data across embryonic developmental stages to systematically characterize epithelial and mesenchymal dynamics during lung development. To achieve more refined cell types at single-cell resolution in spatial transcriptomic data, we developed a bin-based deconvolution strategy that enabled high-precision cell-type assignment. We subsequently constructed a 3D spatiotemporal landscape of lung development and elucidated the molecular regulatory mechanisms underlying epithelial-mesenchymal maturation during lung morphogenesis. In addition, we analyzed transcription factor module activity, intercellular communication signaling, and predicted downstream target genes, while integrating public GWAS metadata to link developmental programs with lung cancer-related features. We observed pronounced stage-specific functional heterogeneity between the pseudoglandular and late embryonic stages. Notably, E13.5 emerged as a critical transition window, during which progenitor states shifted toward more mature cellular phenotypes. We reconstructed epithelial-mesenchymal interactions and uncovered coordinated rewiring of ligand-receptor signaling and transcriptional networks across developmental stages. Regulatory network analysis further identified temporally coordinated transcription factor modules centered on , , , , , and , which collectively orchestrated branching morphogenesis, epithelial patterning, and tissue stabilization. Integration with lung cancer genome-wide association data demonstrated that embryonic lung progenitor states exhibit strong associations with lung cancer-related transcriptional programs, particularly involving epithelial-mesenchymal plasticity and RNA-splicing pathways. Furthermore, TP53/HNRNP-mutant lung adenocarcinomas displayed embryonic-like molecular features associated with cytoskeletal remodeling and progenitor-state reactivation. Together, our study provided a spatiotemporally resolved framework of embryonic lung development and identifies a critical transition window linking lung morphogenesis, regulatory network remodeling, and cancer-associated epithelial plasticity. - Source: PubMed
Publication date: 2026/06/01
Zheng HuiwenLin JinpeiLi HanyiHao ShijieCheng Mengnan - Congenital heart disease (CHD) is a leading cause of neonatal morbidity and mortality, with a complex aetiology involving genetic and environmental factors. Cardiac transcription factors, such as , and , are essential for heart development, and their gene polymorphisms may contribute to CHD. Additionally, maternal periconceptional environmental exposures may influence CHD risk. Limited studies explore gene-gene and gene-environment interactions in CHD pathogenesis. - Source: PubMed
Publication date: 2026/06/18
Wei JianhuiHuang PengChen LetaoYang TubaoWang TingtingLi ZiyeChen LizhangQin Jiabi - Human induced pluripotent stem cell (hiPSC) technologies offer human-relevant cardiac models for biomedical applications. However, workflows for differentiation of cardiac stromal cells and fabrication of engineered heart tissue (EHT) commonly rely on animal serum, contrary to growing policy demands to reduce use of these products. Applying marker analysis via COL-I, DDR2 and GATA4 for cardiac fibroblasts or CD31, CD34 and CD144 for endothelial cells, we tailored Panexin, a defined serum substitute, to support high efficiency differentiation of cardiac stromal lineages to 85% purity without additional purification steps. We evaluated fabrication of EHTs using hiPSC-cardiomyocytes only (monoculture) or further combined with cardiac fibroblasts and endothelial cells (triculture; 70%:15%:15%, respectively). Panexin poorly supported fabrication and contractility of EHTs, a finding unaltered by modulating spontaneous cardiac myofibroblast activation via TGFβ inhibition. In contrast, human serum enabled fabrication of mono- and tri-culture EHTs, wherein constructs made without TGFβ signalling inhibition delivered the strongest contractile forces and exceeded comparator tissues engineered using animal serum. Our data show that iterative evaluation of serum substitutes, human serum, cell combinations and signalling pathway modulators can mitigate use of animal serum for functional EHT generation, aligning with the UK government's roadmap for alternative methods. - Source: PubMed
Publication date: 2026/06/16
Vo Nguyen T NChung KelvinNasir AishahPavlovic DavorDenning Chris - This study aimed to investigate the role of Sortilin in vascular smooth muscle cell (VSMC) senescence and the senescence-associated secretory phenotype (SASP) and to explore whether GATA4 promotes VSMC senescence and aortic atherosclerosis by transcriptionally regulating Sortilin. Furthermore, we examined the potential of resveratrol (Res) to alleviate vascular aging and atherogenesis via the GATA4/Sortilin pathway. Bioinformatics analysis and experimental validation revealed co-upregulation of GATA4 and Sortilin in senescent VSMCs. Sortilin overexpression promoted VSMC senescence and SASP secretion, whereas its silencing resulted in the opposite effects. GATA4 transcriptionally activated Sortilin expression via direct binding to the Sort1 promoter, as confirmed by dual-luciferase reporter and chromatin immunoprecipitation (ChIP)-qPCR assays. Although GATA4-induced VSMC senescence was enhanced by co-overexpression of Sortilin, Sortilin knockdown did not significantly reverse GATA4-driven senescence, suggesting the involvement of additional mechanisms. Res treatment suppressed GATA4 and Sortilin expression, thereby attenuating VSMC senescence and the SASP. In apolipoprotein E-deficient (ApoE) mice fed a high-fat diet, AAV-mediated GATA4 overexpression promoted Sortilin expression, vascular oxidative stress, inflammation and accelerated aortic aging and atherosclerosis. These effects were counteracted by either AAV-Sortilin shRNA or dietary Res supplementation, which also improved blood lipid and glucose metabolism. In summary, GATA4 transcriptionally upregulates Sortilin expression, thereby promoting VSMC senescence and vascular aging. Res inhibits the GATA4/Sortilin pathway, suggesting a potential therapeutic strategy for ameliorating atherosclerosis. - Source: PubMed
Publication date: 2026/06/16
Li HuijuanWang YunZhang ShaoxiangLi ShujunJiang LiujieLv Yuncheng - Generating mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) remains a major obstacle to accurate disease modeling and cardiac repair. As the transcription factor Irx3 is a key determinant of ventricular conduction system fate in mice, we hypothesized that suppressing IRX3 expression accelerates human working cardiomyocyte differentiation. Here, we demonstrate that depleting IRX3 enhances hiPSC-CM differentiation. IRX3-knockout (KO) hiPSCs generated a greater number of cardiomyocytes with elevated expression of TNNI1 and CX43. Notably, IRX3-KO cardiomyocytes exhibited improved electrophysiological properties, more uniform mitochondrial distribution, better sarcomere organization, and enhanced intercellular connectivity. We observed that IRX3 expression peaks during the early stages of cardiomyocyte differentiation, whereas IRX3-KO cardiac progenitors have increased expression of GATA4, NKX2-5, and TBX5, as well as enhanced cell proliferation. These integrative analyses indicate that IRX3 influences cardiomyocyte differentiation by modulating the gene regulatory networks driven by GATA4, NKX2-5, and TBX5, providing functional evidence linking gene regulatory networks to the structural and electrophysiological development of cardiomyocytes. Collectively, these findings identify IRX3 as a key regulator of early cardiac commitment and highlight the potential of IRX3 suppression to enhance the molecular and functional phenotype of hiPSC-derived cardiomyocytes. - Source: PubMed
Publication date: 2026/06/16
Ribeiro Kalthof AgathaFerreira Nikolas DreschSilva Caio MateusCordeiro Valadão IuriPinheiro de Sousa IguaracyBertoldi Ester Riserio MatosLima Vanessa MoraisTuraca Lauro ThiagoBarbosa Ana Beatriz Ruiz AfonsoFonseca-Alaniz Miriam HelenaConcordet Jean-PaulNeri Elida AdalgisaKrieger Jose E