GATA4 Lysate
- Known as:
- GATA4 Lysate
- Catalog number:
- NBL1-10983
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA4 Lysate
Related genes to: GATA4 Lysate
- 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 Lysate
Related articles to: GATA4 Lysate
- : Myocardial fibrosis (MF) is a prevalent pathological endpoint in various heart diseases, characterized by extracellular matrix (ECM) dysregulation and oxidative stress. Hyperoside (Hyp) plays a role in regulating cardiac oxidative stress and fibrosis. This study aimed to elucidate whether Hyp regulates isoproterenol (ISO)-induced MF in mice by modulating the GATA4/HIF-1α signaling pathway and reducing oxidative stress. : The binding affinity of Hyp to GATA4 and HIF-1α was assessed through molecular docking and dynamics simulation. The MF model of mice was established by subcutaneous injection of ISO. Cardiac function was measured by echocardiography. Myocardial injury and collagen deposition were examined using H&E and Sirius red staining. Levels of fibrosis markers, oxidative stress indicators, and GATA4/HIF-1α pathway indicators in serum and heart tissue were quantified by ELISA, Western blot, RT-qPCR and flow cytometry. The distribution of myocardial marker proteins was visualized by immunofluorescence and immunohistochemistry. : Molecular docking revealed high binding affinity of Hyp to GATA4 and HIF-1α (binding energies < -5.0 kcal·mol), and dynamics simulation showed that the complex's structure remained stable over 100 nanoseconds (RMSD < 0.1 nm). High-dose Hyp (36 mg/kg) significantly improved cardiac function, myocardial injury, collagen deposition, and inflammatory infiltration in MF mice. Molecularly, Hyp effectively reduces oxidative stress and fibrosis through upregulating GATA4 and downregulating HIF-1α. : Hyp suppresses oxidative stress by activating the GATA4/HIF-1α pathway, presenting a promising therapeutic target for the treatment of MF. - Source: PubMed
Publication date: 2026/05/12
Dou XiaotongWan HaofangChen TianxueZhou HuifenYu LiWan Haitong - : Lung adenocarcinoma (LUAD) is the most common type of lung cancer and a major cause of cancer death. Zinc finger proteins (ZNFs) have been implicated in LUAD progression, functioning either as oncogenes or tumor suppressors. Therefore, an in-depth investigation of ZNFs may contribute to the development of novel diagnostic and therapeutic strategies for LUAD. : Transcriptomic and clinical data were obtained from the TCGA and GEO databases. Prognosis-related ZNF genes were identified using univariate Cox, LASSO, and multivariate Cox regression analyses. An eight-gene ZNF-based prognostic signature was constructed and validated in two independent external cohorts (GSE50081 and GSE26939). A nomogram integrating independent prognostic factors was developed. Immune infiltration, somatic mutation profiles, and drug sensitivity were systematically analyzed. We further focused on FGD3, a key gene from the signature, examining its expression in LUAD cells and tissues, including lorlatinib-resistant models. : The prognostic signature comprising TRIM6, TRIM29, CTCFL, FGD3, GATA4, CASZ1, TRAF2, and ZNF322 effectively stratified patients into distinct risk groups with significantly different overall survival ( < 0.05). The risk score, together with T and N stage, served as independent prognostic predictors ( = 500, < 0.05). High-risk patients exhibited an immune-desert phenotype, increased tumor mutational burden, and distinct drug sensitivity patterns. Notably, FGD3 expression was downregulated in LUAD tissues ( = 14, < 0.0001) and lorlatinib-resistant cells, and its restoration suppressed resistant cell proliferation and partially reversed drug resistance. : This study establishes a promising ZNF-based prognostic model for LUAD, providing a potential tool for risk stratification and individualized therapeutic decision-making. The identification of FGD3 as a potential mediator of drug resistance highlights its promise as a candidate biomarker and therapeutic target in LUAD. - Source: PubMed
Publication date: 2026/05/14
Sun JiayueYang YueHuang XiaoyiXue DinglongLi JiazhuangHuang YaruMeng Qingwei - Hyperlipidemia is a major risk factor for atherosclerosis and other serious cardiovascular diseases, yet it often presents without obvious symptoms in the absence of comorbidities, complicating early detection and management. Given the high heritability of lipid traits, genome-wide association studies (GWAS) have identified numerous loci associated with serum lipids; however, pinpointing the causal variants remains a challenge. Here, we investigated the 5q33.3 locus and identified HAVCR1 as a likely effector gene influencing lipid metabolism. By integrating functional genomics and experimental validation, we identified two non-linked variants, rs6882076 and rs17573010, that modulate HAVCR1 via allele-specific binding by IRF2 and GATA4, respectively. rs6882076 was refined from prior GWAS findings, while rs17573010 emerged from ancestry-specific analysis. These findings highlight the complexity of genetic regulation across populations and establishes a mechanistic link between lipid metabolism and inflammation, offering insights into the genetic basis of hyperlipidemia and its potential translational relevance. - Source: PubMed
Publication date: 2026/05/25
Chen Wei-TingHsiung Chia-NiJou Yuh-ShanWang Hui-ChunShen Chen-YangChou Wen-Cheng - Despite the expression of multiple transcript isoforms from a gene, conventional gene expression analyses assume that a single transcript is expressed from each gene. We analyzed the transcript isoforms expressed in gonadotropin-induced mouse mural and cumulus granulosa cells (mGCs and cGCs) isolated from antral follicles to elucidate the potential mechanism of differentiation. Considering that either a single transcript or multiple isoforms are expressed from genes, we identified differential expression of about 70% of transcripts between mGCs and cGCs. Although the differential expressions were similar, the single-transcript-wise differentially expressed genes did not correlate with their corresponding differentially expressed transcript isoforms. We identified transcript isoforms of key transcriptional regulators in ovaries, including Chd1, Ezh2, Kdm5a/5b, Gata4, Esr2, Fos, Myc, and Ybx1, that were not identified in single-transcript-based analyses. Further analysis revealed a transcript switch in more than 30% of the differentially expressed isoforms. While one or more transcript isoforms of Cebpa, Dnmt3a, Pgr, Rest, Runx1, and Sirt1 were switched off, those of Brd7, Chd1, Med21, Nfkbia, Rbm39, Suv39h2, Tcf12, Xist, and Ybx3 were switched on in cGCs. Interestingly, several genes, including Dab2, Ezh2, Gata4, Gnas, Gtf2i, Klf10, Setdb1, and Sp3, exhibited at least one isoform that was switched off and another that was switched on in cGCs. Transcript switching was primarily due to alternative splicing, followed by alternative transcription start sites and polyadenylation sites. We also identified differential expression of the potential regulators of such transcript switching in cGCs. Our results suggest that transcript switching may play an important role in mural and cumulus granulosa differentiation, a key insight that would remain unknown without mRNA isoform analysis. - Source: PubMed
Publication date: 2026/05/23
Shila SharminPei Grace JBahadursingh ElizabethPeramsetty NikiDahiya VineshMarsh Courtney AThiyagarajan RamkumarZhang MeijiaFields Patrick ERumi M A Karim - Hyperoside, a common flavonoid glycoside, was evaluated for developmental toxicity in zebrafish embryos (6-96 hpf). Hyperoside reduced hatchability and survival (96-h LC50 170.9 μM; LC10 118.3 μM) and caused prominent cardiac defects, including tachycardia, pericardial edema, and atrioventricular malformation, along with altered expression of cardiac markers (nppa, vmhc, sox9b, and gata4). Transcriptomic and phenotypic assays indicated the activation of oxidative stress and apoptosis pathways. Hyperoside increased ROS and MDA, decreased antioxidant enzyme activities (SOD and CAT), and induced apoptosis in the cardiac region (AO staining; baxa/caspase-3/p53 upregulated, bcl2a downregulated). Co-treatment with N-acetyl-L-cysteine (NAC) reduced ROS, attenuated apoptosis, and rescued cardiotoxicity, supporting ROS-driven injury as a key mechanism. - Source: PubMed
Publication date: 2026/05/19
Zhou ZhuoShuoYang YilinLi GuisenGuo HongpengZhang XuGuo XinliLv SimianZhou HairuiBei LeiWu Dongmei