GATA3 antigen
- Known as:
- GATA3 antigenic
- Catalog number:
- 'H00002625-Q02-10
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3 antigen
Ask about this productRelated genes to: GATA3 antigen
- Gene:
- GATA3 NIH gene
- Name:
- GATA binding protein 3
- Previous symbol:
- -
- Synonyms:
- HDR
- Chromosome:
- 10p14
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2016-10-05
Related products to: GATA3 antigen
'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Anti_Tg)Thyroglobulin Antigen(Des-Asp187)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187)-ME20M_ME20S (185-193) (human, bovine, mouse), (Des-Asp187)-Melanocyte Lineage-Specific Antigen GP100 (185-193) (hu(Des-Asp187,Met186)-Melanocyte Protein PMEL 17 (185-193) (human, bovine, mouse)
(Des-Asp187,Met186)-Melanoma-Associated ME20 Antigen (185-193) (human, bovine, mouse), (Des-Asp187,Met186)-95 kDa Melano(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Des_Asp187,Met186)_Melanocyte Protein PMEL 17 (185_193) (human, bovine, mouse) Salt Trifluoroacetate Binding _ Synonym (Des_Asp187,Met186)_Melanoma_Associated ME20 Antigen (185_193) (human, bovine(Draxin) C1ORf187, Antigen blocking peptide(Val438)-Tyrosinase (432-444) (human)
(Val438)-LB24-AB (432-444) (human), (Val438)-Monophenol Monooxygenase (432-444) (human), (Val438)-SK29-AB (432-444) (human), (Val438)-Tumor Rejection Antigen AB (0x19 Antigen0x2 Antigen1,25-dihydroxyvitamin D3 Competitive ELISA, Coated with Antigen105 kDa islet cell antigen,BEM-3,Brain-enriched membrane-associated protein tyrosine phosphatase,ICA105,PTP IA-2,PTPLP,Ptprn,Rat,Rattus norvegicus,Receptor-type tyrosine-protein phosphatase-like N,R-P Related articles to: GATA3 antigen
- Higher prevalence of hepatocellular carcinoma (HCC) in men is largely attributed to the sex hormones and behavioral risk factors. This study investigated the effects of male (testosterone) and female (estradiol) hormones on Aurora-A/B kinases, GATA-3, and microRNAs (miR-3941, miR-4500, miR-4742) in HepG2 and Huh-7 cell lines. - Source: PubMed
Publication date: 2026/06/22
Rezaei TaranehAbidi MobinaMohammadi YaserFarzam FarnooshBahreini Elham - Hydrogen sulfide (HS) inhalation injures the respiratory, immune, and nervous systems, altering homeostasis and health, but the molecular mechanisms have been still unclear. In this study, we tested the effects of different concentrations of HS on immune index and enzyme activity of mouse tissues and measured differentially expressed genes (DEGs) in mouse lung tissues by transcriptome sequencing. The results showed that HS significantly increased tumor necrosis factor-alpha (TNF-α) (p < 0.05), catalase (CAT) (p < 0.01) and glutathione peroxidase (GSH-Px) (p < 0.05) activity levels; 80 and 100 ppm HS treatment significantly increased interleukin-1β(IL-1β), interleukin-10 (IL-10) (p < 0.01) and glutathione reductase activation coefficient (GRAC) (p < 0.01) but decreased malonaldehyde (MDA) and superoxide dismutase (SOD) levels (p < 0.05); 100 ppm HS treatment significantly increased glutathione S-transferase (GST) and reactive oxygen species (ROS) levels (p < 0.01). In addition, 963 DEGs were identified in different group. These genes were notably involved in immune responses, DNA modification, enzymatic activity, and cell cycle processes. FGFBP1, GATA3, KLRG1 and TBX21 may be crucial roles in the response to HS exposure. This study provides a reference and many differential genes for the study of hydrogen sulfide damage mechanism. - Source: PubMed
Publication date: 2026/06/22
Gao Jun LeiLi Bai HaoBan Zhi BinLi Li JiaLiang HaoYan Xiao GangXiao ChengZhang Fang Yu - Intervertebral disc degeneration (IVDD) is a major pathological basis of low back pain, but its molecular mechanisms remain incompletely understood. Identifying key genes and potential therapeutic compounds may provide new insights into the progression and treatment of IVDD. The GSE70362 bulk transcriptomic dataset was analyzed to identify 352 differentially expressed genes between IVDD and control nucleus pulposus samples. These DEGs were integrated with WGCNA, PPI network analysis, and LASSO regression to screen candidate hub genes, including ZEB2, COL6A2, CCND1, RAP1A, and GATA3. Functional enrichment, immune infiltration, and single-cell RNA-seq analyses were performed to characterize their biological relevance. Quercetin was selected as a candidate compound for molecular docking prediction and in vitro validation in LPS-induced nucleus pulposus cells. A total of 352 differentially expressed genes were identified, including 142 upregulated and 210 downregulated genes in IVDD samples. WGCNA identified five IVDD-related modules containing 454 genes, and 154 overlapping genes were obtained after intersection with differentially expressed genes. Further screening identified five hub genes: ZEB2, COL6A2, CCND1, RAP1A, and GATA3. Functional enrichment analysis indicated that these genes were mainly associated with cellular stress responses, extracellular matrix remodeling, cellular senescence, p53 signaling, focal adhesion, Rap1 signaling, and inflammatory pathways. Immune infiltration analysis showed decreased Tr1 and Th2 cells and increased macrophage infiltration in IVDD samples. Single-cell analysis revealed marked heterogeneity among nucleus pulposus cells and demonstrated that several hub genes were distributed across distinct degenerative cell states. Molecular docking provided preliminary computational evidence that quercetin may have potential binding affinities with the five hub proteins. In vitro experiments further showed that quercetin improved cell viability, reduced LPS-induced cell injury, reversed the abnormal expression of ZEB2, CCND1, RAP1A, GATA3, and partially restored COL6A2 expression. This study identified ZEB2, COL6A2, CCND1, RAP1A, and GATA3 as potential hub genes involved in IVDD progression. The integrated bioinformatics, single-cell, molecular docking, and experimental results suggest that quercetin may exert protective effects against IVDD-like nucleus pulposus cell injury, accompanied by partial reversal of abnormal hub gene expression and improvement of cell survival. These findings provide a potential molecular basis for further investigation of quercetin as a candidate therapeutic agent for IVDD. - Source: PubMed
Publication date: 2026/06/22
Zhang FuduoYang YingqiuGou XiaoyanYuan XiaolingZhu NianjunYin MingxiongHe Huaiyun - Mesonephric-like adenocarcinoma (MLA) is a rare and recently recognized subtype of endometrial and ovarian carcinoma characterized by distinctive morphology, immunophenotype, and aggressive clinical behavior. We report the case of a 60-year-old postmenopausal woman presenting with irregular vaginal bleeding. Imaging demonstrated a large uterine mass with deep myometrial invasion. Histopathological examination revealed diverse architectural patterns, including tubular, glandular, and slit-like structures, composed of cells with bland overlapping nuclei and occasional nuclear grooves. Immunohistochemical analysis showed positivity for GATA-3, TTF-1, EMA, and CK, and negativity for ER and PR, supporting the diagnosis of mesonephric-like adenocarcinoma of the uterine corpus. - Source: PubMed
Publication date: 2026/06/05
Wang TingYang WenlinGong XianglunXue Bing - Type II innate lymphoid cells (ILC2s) have been implicated in both tumor-promoting and tumor-suppressive functions, but the mechanism(s) underlying this functional heterogeneity is not clear. Here, we tested the hypothesis that signaling through β2-adrenergic receptor (β2-AR) drives the pro-tumor functions of ILC2s within the tumor microenvironment. Using global (β2AR/) and ILC2-specific conditional knockout (IL5β2AR) mouse models, we examined how β2-AR deficiency affects ILC2 function in breast cancer. We studied the impact of β2-AR function on ILC2 phenotype, gene profile, anti-tumor T cell response and breast tumor growth. β2AR inhibition resulted in an enrichment of KLRG1⁺ ILC2s with elevated GATA3 and ST2 expression in breast tumor. Loss of β2-AR signaling in ILC2s reduced their pro-tumorigenic activity and resulted in suppressed tumor growth. Additionally, β2-AR inhibition in ILC2s was associated with increased CD4⁺ T cell infiltration in breast tumors and a greater TNF-α CD8 T cell response. β2-AR deficiency reprograms ILC2s toward a more immunostimulatory phenotype, promoting T cell-mediated anti-tumor immunity. These findings identify activity of the β2-AR as a key regulator of ILC2 plasticity and suggest β2-AR blockade as a promising strategy to enhance cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/20
Choi Jee EunYan QiWang JianminSalgia Nicholas JMuhitch Jason BMacDonald Cameron RRoberts Nathan TJames Caitlin MMcCarthy Philip LMohammadpour HemnDaneshmandi SaeedRepasky Elizabeth A