GATA3 Lysate
- Known as:
- GATA3 Lysate
- Catalog number:
- NBL1-10981
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3 Lysate
Related genes to: GATA3 Lysate
- 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 Lysate
Related articles to: GATA3 Lysate
- 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 - Tumor recurrence is a major clinical challenge in low-risk non-muscle invasive bladder cancer (NMIBC). Molecular studies have identified two main subtypes with distinct genetic pathways: papillary, low-grade tumors, often with FGFR3 mutations and favorable outcomes, and nonpapillary, high-grade tumors, which are linked to higher rates of progression and muscle invasion. This study evaluates the prognostic value of immunohistochemical (IHC) markers- cluster of differentiation 44 (CD44), cytokeratin 5/6 (CK5/6), cytokeratin 20 (CK20), GATA-binding protein 3 (GATA3), human epidermal growth factor receptor 2 (Cerb-B2), E74-like factor 3 (ELF-3), and tuberous sclerosis complex 1 (TSC-1)-for recurrence in patients with low-risk NMIBC. - Source: PubMed
Publication date: 2026/06/20
Altın EnesDoğan ÇağrıArslan Ayşegül İsalTopkaç Erdem CanYazıcı Cenk MuratÖzcan RıdvanAkgül Hacı MuratŞahin Mehmet Fatih - Urothelial carcinoma arising in a mature cystic teratoma of the ovary is a rare event with only 13 cases reported thus far. In this article, we present the clinicopathologic features of one such case and a review of the literature. The patient was a 76-yr-old African American postmenopausal woman who presented with a painful abdominal mass and weight loss. The left ovarian tumor was 36 cm in greatest dimension and contained several papillary areas, the largest being 10 cm. The patient underwent a total abdominal hysterectomy, bilateral salpingo-oophorectomy, omentectomy and pelvic washings. Microscopically, the papillary excrescences represented an invasive, high-grade papillary urothelial carcinoma, while the cyst in the background was a mature cystic teratoma. Immunohistochemically, the urothelial carcinoma was positive for CK7, CK20, GATA-3, uroplakin II, p40, p63, and ER (20%, weak intensity), while negative for WT1 and PR; p53 expression was aberrant (nuclear overexpression). Next-generation sequencing (NGS) showed a microsatellite-stable tumor with low tumor mutational burden, and molecular alterations typically seen in urothelial carcinomas, including KRAS gain of function, ARID1A loss of function, RB1 loss of function, and two TP53 loss of function mutations. In addition, PDL1 positivity was present, representing a clinically actionable target. The tumor was FIGO stage 1A. No adjuvant therapy was given, and the patient is alive with no evidence of disease after a follow-up of 7 mo. - Source: PubMed
Publication date: 2026/06/22
Repollet Otero Patricia ARamalingam PreethaBevers Michael WMalpica Anais