GATA3
- Known as:
- GATA3
- Catalog number:
- NBP1-39915
- Product Quantity:
- 0.05 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3
Related genes to: GATA3
- 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
Related articles to: GATA3
- Distinguishing epithelioid malignant mesothelioma (EMM) from poorly differentiated lung adenocarcinoma (PD-LUAD) remains challenging, particularly when 21.7% of PD-LUADs lack lineage-specific markers (thyroid transcription factor-1 (TTF-1)/Napsin A), creating a diagnostic blind spot. While GATA-binding protein 3 (GATA3) is established in sarcomatoid mesothelioma, its complementary diagnostic value and prognostic relevance in EMM are not well defined. - Source: PubMed
Publication date: 2026/05/14
Thabit Dina MoustafaThabet Dalia M - Trophoblasts, integral to placental function, are pivotal in implantation and in establishing the maternal-fetal interface. Abnormal proliferation and invasion of trophoblasts can significantly contribute to the onset and progression of recurrent spontaneous miscarriage. Tumor necrosis factor ligand superfamily member 3B (TNFSF13B) is a classical B-cell activating factor that plays an important role in regulating the proliferation, growth, differentiation and invasion of a variety of cells, and is involved in the pathogenesis of multiple human diseases. However, its role in unexplained recurrent miscarriage (URM) remains unclear. In the present study, we found that TNFSF13B expression was significantly decreased in trophoblast cells of villous tissue from unexplained recurrent miscarriage(URM) patients. TNFSF13B promoted the proliferation and invasion of HTR-8 cells. Using dual luciferase reporter and chromatin immunoprecipitation assays, we identified GATA-binding protein 3 (GATA3) as a key transcription factor that binds to the core promoter region of TNFSF13B and regulates TNFSF13B expression. Overexpression of F-box and WD-repeat domain-containing protein 7 (FBXW7) ubiquitin-degraded GATA3, resulting in decreased TNFSF13B expression. TNFSF13B regulates the proliferation and invasion of trophoblast cells through PI3K/Akt signaling pathway, which is inhibited and eventually leads to abortion. Taken together, our findings suggest that TNFSF13B, GATA3 and FBXW7 may be involved in the pathogenesis of URM and may serve as potential therapeutic targets. - Source: PubMed
Publication date: 2026/04/28
Zhou HuipingUskenbayeva NurayXu YangYan HongchaoLi DengfengZhang KunFang LishaWang Jing - Gata3 is an essential transcription factor for the development of several distinct immune cell lineages such as T cells, natural killer (NK) cells, and innate lymphoid cells (ILCs). As such, the levels and timing of expression are critical for directing lineage fate decisions. The locus has a complex and dynamic distal regulatory enhancer landscape. Recently, we identified a non-coding RNA, , located immediately upstream of the classic +280 kb T/NK cell enhancer (Tce1). To test its function, we excised the locus in mice and observed a selective reduction of group 2 ILCs (ILC2) across multiple tissues, but mature T, NK, and other ILC lineages remained unchanged. In bone marrow, common innate lymphoid cell progenitors (ILCPs) increased while ILC2 progenitors (ILC2P) decreased, with a modest reduction of in upstream progenitors consistent with an early developmental bottleneck. Chromatin profiling showed the Dreg1 locus is accessible in early lymphoid progenitors and became decorated with H3K27ac in ILCP in a Tcf1-dependent manner. Furthermore, Tcf1-deficient cells did not express and showed alterations in the epigenetic landscape of the locus. Finally, we discovered that potential homologues of harboured in a syntenic enhancer of are also highly expressed in human ILC2. Taken together, we conclude that is a Tcf1-dependent non-coding RNA critical for fine tuning the high level of required for the optimal development of the ILC2 lineage. - Source: PubMed
Publication date: 2026/05/13
Quon SaraTang AdelynnIannarella NadiaSchoffer KaelChan Wing FukJohanson Timothy MVasanthakumar AjithkumarAllan Rhys - The greatest cause of death from breast cancer is metastasis, yet little is known about the molecular mechanisms behind this phenomenon. Using four publically accessible datasets, we conducted a thorough transcriptome analysis of 187 samples from seven breast cancer metastatic sites: the brain, bone, lung, liver, lymph nodes, skin, and local-regional skin (skinlr). Of the 12,005 genes that were found to be shared by all samples in this investigation, 604-885 differentially expressed genes (DEGs) were unique to each metastatic location. Pathways including PI3K-Akt signaling, prolactin signaling, complement, and coagulation cascades were identified by functional enrichment analysis as important metastasis drivers with unique functions in different locales. The results of regulatory analysis revealed 77 upstream factors, including 14 kinases (like EPHB3, PAK3) and 63 transcription factors (like ESR1, FOXA1, and GATA3), some of which were discovered for the first time in breast cancer metastases (like TCF4, HOXA10). It was shown that hub genes including MMP9, SPP1, and PDGFRB are essential for the survival and development of metastases, offering new information on site-specific biology. Crucially, by identifying site-specific molecular markers, these discoveries pave the way for personalized medicine techniques and allow tumor-specific therapy tactics, such as targeting Central Carbon Metabolism in lung and skin metastases. This work provides actionable options for tumor-specific treatment and tailored interventions by highlighting new molecular candidates and signaling pathways for metastatic breast cancer. - Source: PubMed
Publication date: 2026/05/12
Salari AliMikaeili Namini ArshamAlipour AramFarahani FatemehSalehi FarnazShafiei Tehrani Zahra SadatBagherpour GhasemYosefy FatemehJafari DelaramShahbazi AliMirzaei Chegeni MasoumehKhodadad Hossyni Mohammad AminSafari Kharkheshi MahboubehBakhshi Manjili Monire - Augmented mucosal expression of the transcription factor GATA3 has been implicated in the pathogenesis of ulcerative colitis (UC). Here, we evaluated the efficacy and safety of SB012, an enema formulation of the DNAzyme hgd40 that specifically inactivates GATA3 messenger RNA, for induction therapy in patients with active UC. - Source: PubMed
Publication date: 2026/05/12
Atreya RajaKühbacher TanjaVieth MichaelJefremow AndreHirschmann SimonWaldner Maximilian JFischer SarahVetter MarcelDrvarov OliverWeigmann BennoMeyer MichaelMühl TanjaHomburg UrsulaSarigiannis GeorgiosGarn HolgerRenz HaraldNeurath Markus F