Human GATA4 ELISA Kit
- Known as:
- Human GATA4 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- orb51868
- Product Quantity:
- 96 well
- Category:
- Peptides
- Supplier:
- Biorb
- Gene target:
- Human GATA4 ELISA Kit
Related genes to: Human GATA4 ELISA Kit
- 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: Human GATA4 ELISA Kit
Related articles to: Human GATA4 ELISA Kit
- 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 - The zig-zag eel () exhibits sexual dimorphism in growth patterns. Identifying the genes involved in sex differentiation is a crucial step toward achieving single-sex breeding and serves as a vital foundation for elucidating the XY sex determination mechanism in . This study measured the morphological characteristics of male and female and found that males were significantly superior to females in body weight and nearly all morphological indices. Subsequently, whole-transcriptome sequencing was performed on the gonads of adult males and females, identifying 11,714 DEmRNAs, 3442 DElncRNAs, 416 DEcircRNAs, and 620 DEmiRNAs, including male sex differentiation genes such as , , , and , and female sex differentiation genes like , , and . Functional enrichment analysis identified pathways associated with sex differentiation, including the TGF-beta signaling pathway, the steroid hormone biosynthesis, the Hippo signaling pathway, and the Wnt signaling pathway, etc. A ceRNA network was constructed based on differentially expressed mRNAs and ncRNAs, revealing that the sex differentiation-related genes , , , , and are regulated by one or multiple pairs of lncRNA/circRNA-miRNA pairs. The study results will provide molecular targets for research on sex-controlled breeding in and lay an important theoretical foundation for clarifying its sex differentiation mechanisms. - Source: PubMed
Publication date: 2026/06/05
Zhu JunxianJia XianghuiJi LiqinChen ChenGao CaixiaHong XiaoyouLiu XiaoliWei ChengqingZhu XinpingLi Wei - Efficient differentiation of pluripotent stem cells (PSCs) into functional cells is critical for regenerative medicine and biomanufacturing, yet is often hampered by apoptosis. Ginkgolide A (GA) is a diterpene lactone derived from Ginkgo biloba leaves and a member of the ginkgolide family, compounds known for diverse biological activities including neuroprotection and cardiovascular regulation. However, the mechanism by which ginkgolides influence the directed differentiation of stem cells remains unclear. Here, using a CRISPR-Cas9-engineered TNNT2-mCherry reporter PSC line and a defined cardiac differentiation protocol, we screened ginkgolides for their effects on cardiomyocyte production. Results demonstrated that GA significantly enhanced cardiomyocyte induction efficiency and accelerated the onset of spontaneous beating. Concurrently, GA effectively inhibited apoptosis during differentiation and RNA-seq results also revealed that GA orchestrates stage-specific upregulation of anti-apoptotic genes (e.g., MCL1, XIAP) and core cardiogenic transcription factors (NKX2-5, GATA4). Molecular docking predictions suggested a high binding potential between GA and cytochrome c, suggesting GA might inhibit the intrinsic mitochondrial apoptosis cascade by interfering with cytochrome c's binding to Apoptotic Peptidase Activating Factor-1 (APAF-1). These data demonstrate that GA enhances the differentiation of pluripotent stem cells into cardiomyocytes, potentially through its anti-apoptotic effect. This mechanism highlights its potential as a safe culture additive to boost cell survival and yield for large-scale biomanufacturing and tissue engineering applications. - Source: PubMed
Publication date: 2026/06/05
Xu WenjieWu XiaolongLei ZuoDang XiaoyuShi HongzhaoLi JiannanYuan LimingZhao YayaLi WenhaoChen JingLi NaHua Jinlian