GATA3
- Known as:
- GATA3
- Catalog number:
- AP30358PU-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3
Ask about this productRelated 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
- Colonic immune homeostasis is critically maintained by regulatory T (Treg) cells. Here, we identify SUMO-specific peptidase 1 (SENP1) as an important regulator of colonic Treg function and intestinal immune homeostasis. Treg-specific Senp1 deletion does not impair thymic Treg development, but selectively disrupts the homeostasis of colonic Treg subset without affecting Treg maintenance in other peripheral tissues. Mechanistically, SENP1 deficiency reduces CD25 expression on Tregs, blunting IL-2 responsiveness and compromising their expansion and survival. This is associated with a selective reduction in the proportion of tissue-adapted Gata3 Tregs and accumulation of CD25 precursor-like Tregs in the intestinal lamina propria. Senp1 depletion also downregulates core effector Treg signature genes including Gata3, Klrg1, and Il1rl1, correlating with dysregulated Th2 response control. Single-cell RNA sequencing analysis reveals transcriptional alterations consistent with impaired colonic Treg tissue adaptation after SENP1 ablation. Functionally, with adoptive transfer experiments we found that Senp1-deficient Tregs show impaired accumulation in vivo and are associated with weaker control of pathogenic T cell expansion in the colon. Consistently, Treg-specific Senp1-deficient mice display heightened susceptibility to DSS-induced colitis, highlighting a critical role of SENP1 in sustaining functional Treg programs and limiting pathogenic intestinal inflammation. - Source: PubMed
Publication date: 2026/05/16
Hao YanyunLiu HongzhiLiang QiuliFan QiujuWang TianshiCheng Jinke - Gastric cancer (GC) remains a major global health burden, often diagnosed at advanced stages with poor prognosis. Helicobacter pylori (H. pylori) infection promotes GC development through inflammation and altered signaling. Collagen triple helix repeat containing 1 (CTHRC1), a secreted ECM protein, is upregulated in several cancers and may be involved in H. pylori-related gastric tumorigenesis, though the mechanism is unclear. - Source: PubMed
Publication date: 2026/05/17
Ma MengdiZhang ChaoyangYu KexunWang HuizhenLi Yongxiang - Renal imaging suggests that congenital anomalies of the kidney and urinary tract (CAKUT) affect one in 200 of the population, and 20% have a monogenic cause. This study determined the population frequency of predicted pathogenic variants in six commonly affected CAKUT genes. - Source: PubMed
Publication date: 2026/05/16
Huang MarySavige Judy - 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