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
- : 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 - Unbalanced Notch signaling in liver sinusoidal endothelial cells (LSEC) leads either to vascular malformations or MASH-like liver fibrosis. Here, we investigated this dual reaction pattern for interactions of Notch signaling with Alk1 and Gata4 pathways which we hypothesized to contribute to aberrant angiogenesis or to liver fibrosis, respectively. - Source: PubMed
Publication date: 2026/09/24
Schmid Christian DTuo YangKürschner-Zacharias Sina WGreco AlessandroSchüler JuliaHoffmann JohannesHardt Marius RolandTrogisch Felix AWeyer VanessaSticht CarstenDooley StevenReiners-Koch Philipp-SebastianOlsavszky VictorGoerdt SergijWinkler Manuel - Extraembryonic lineages, specifically the trophectoderm (TE) and primitive endoderm (PrE), are indispensable for early embryogenesis and successful pregnancy. Expanded potential stem cells (EPSCs) can contribute to both embryonic and extraembryonic fates, providing a platform to model early lineage specification. - Source: PubMed
Publication date: 2026/09/09
Kim HaneulCai LianHyun Sang-HwanKim Eunhye - Post-myocardial infarction (MI) ventricular arrhythmia (VA) remains a leading cause of sudden cardiac death. Current antiarrhythmic drugs often fail to target the core metabolic-structural remodeling underlying arrhythmias. The transcriptional repressor ID2, which has been implicated in cardiovascular development, remains poorly characterized regarding its role and contribution to VA pathogenesis. This study investigated the role of the transcriptional repressor ID2 in post-myocardial infarction ventricular arrhythmia. - Source: PubMed
Publication date: 2026/09/22
Pan GangHuang ShihaoWang XuewenLiu MingxinXu Yuanhua - Radiation-induced heart disease is a well-recognized complication of thoracic radiotherapy, with atrial fibrillation (AF) being a particularly notable sequela. The mechanisms by which ionizing radiation (IR) heightens susceptibility to AF remain inadequately understood. This study seeks to elucidate the role of cellular senescence and the GATA4-NF-κB signaling pathway in radiation-induced atrial remodeling and the pathogenesis of AF. An in vivo mouse model was developed through localized cardiac irradiation using 20 Gy X-rays. The irradiated mice demonstrated dose-dependent atrial structural and electrophysiological remodeling. Transcriptomic analysis revealed significant enrichment in DNA damage response (DDR), NF-κB signaling, and aging-related pathways. IR exposure induced substantial DNA damage, activated ATM/ATR pathways, and enhanced autophagic flux. These responses culminated in the accumulation of GATA4 and phosphorylation of NF-κB, which drove the expression of the senescence-associated secretory phenotype (SASP), coinciding with increased senescence-associated β-galactosidase (SA-β-gal) activity. In vitro, these crucial findings were recapitulated using irradiated HL-1 atrial cardiomyocytes, whereas the knockdown of GATA4 effectively suppressed both cellular senescence and SASP expression. Notably, treatment with the senolytic combination of dasatinib and quercetin (D/Q) alleviated DNA damage, inhibited excessive autophagy, and suppressed the GATA4-NF-κB pathway in irradiated mice, thereby reducing SASP levels. These improvements resulted in the reversal of atrial structural and electrophysiological remodeling and a marked reduced susceptibility to AF. Overall, our findings demonstrate that IR promotes atrial remodeling by inducing DNA damage-mediated cellular senescence via the GATA4-NF-κB-SASP axis. Targeting this pathway with senolytics such as D/Q thus identifies a promising therapeutic strategy for preventing radiation-induced atrial fibrillation. - Source: PubMed
Publication date: 2026/09/15
Zhang ChaoLan HuaiYu LimingZhao JikaiHuang TaoSun BoxuanMeng ShanDuan JinfengLiu JingZhou ZijunWang ZhishangLi JiahuiHuang XinyiWang Huishan