Gata3
- Known as:
- Gata3
- Catalog number:
- 049888A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- 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
- Craniofacial development requires precise coordination of epithelial patterning and morphogenesis. However, the molecular mechanisms governing olfactory epithelium development remain incompletely understood. Retinoic acid (RA) signaling and Gata3 have each been independently implicated in craniofacial morphogenesis, particularly in the formation of the primitive choanae, which constitute the opening between the nasal cavity and the oral cavity. Here, we generated a tamoxifen-inducible, genetically controlled compound mutant mouse model to simultaneously disrupt Rdh10, a rate-limiting enzyme for RA signaling, and Gata3 during early craniofacial development. We show that while deletion of Rdh10 following tamoxifen administration at E8.5 does not result in obvious craniofacial abnormalities, combined loss of Rdh10 and Gata3 leads to fully penetrant bilateral choanal atresia and severe defects in olfactory epithelium morphogenesis. Immunohistochemical analyses revealed a marked reduction in PAX6 and SIX1 positive cells and a concomitant expansion of SOX2 positive cells in compound mutant embryos. These results demonstrate that RA-Gata3 signaling cooperatively regulates olfactory epithelium development by controlling the balance between progenitor maintenance and lineage specification. We propose that the RA-Gata3 signaling pathway orchestrates a transcriptional network involving Pax6, Six1, and Sox2 to ensure proper epithelial patterning, branching morphogenesis, and choanae formation during early craniofacial development. - Source: PubMed
Matsushita AyakaTsujimoto TakayukiXiuping NieOmi-Sugihara MaikoXu LinMithun SahaNatsuyama ShotaOhara HarukaKoga SatoshiInubushi ToshihiroSandell Lisa LTrainor Paul AYamashiro TakashiKurosaka Hiroshi - Multiple pools of developmental progenitors are needed for kidney regeneration, but directing differentiation of each of these independently is rate limiting and disruptive to the process. We demonstrate that a mere 4 days of differentiation generates an induced metanephric mesenchyme (iMM) containing both nephron progenitor cells and renal stromal progenitor cells. When implanted beneath the kidney capsule of immunodeficient mice, iMM differentiates into podocytes, mesangial cells, and tubules that recruit host blood vessels to form glomeruli and peritubular capillaries. In contrast, mature organoids rapidly lose differentiated features after implantation and fail to become productively vascularized by the host. By examining morphological changes and gene expression patterns, we demarcate a window of opportunity for successful implantation during which iMM exists . Young organoid cultures containing epithelial and stromal progenitor cells thus provide a rapid, one-pot starting material for nephron regeneration, a concept that may be broadly applicable to many organ systems. - Source: PubMed
Publication date: 2026/01/29
Vincent ThomasNademi SameraNamestnikov MichaelCohen-Zontag OsnatDekel BenjaminFreedman Benjamin S - Molecular subtyping is critical for prognostic stratification and treatment in bladder cancer (BCa). However, few studies have combined immunohistochemistry (IHC)-based subtyping with spatial immune profiling and predictive biomarker evaluation. In this study, we retrospectively analyzed 109 BCa patients using a three-part profiling strategy: (1) molecular classification into basal, luminal, double-positive (DP), and double-negative (DN) subtypes with basal (CK5/6, CD44) and luminal (CK20, GATA3) markers, merging DP tumors with basal for analysis; (2) assessment of tumor biology by evaluating p53, PTEN, PD-L1, and mismatch repair (MMR) proteins; (3) multiplex IHC and digital pathology-assisted spatial quantification of immune cells. Basal-subtype tumors showed frequent PTEN loss (P = 0.032) and a novel nuclear PD-L1 pattern (P = 0.043) linked to chemoresistance and recurrence (P = 0.049). MMR profiling revealed reduced PMS2 expression (P < 0.0001) and coordinated downregulation of MMR proteins in PTEN-low tumors. Immune analysis indicated an immune-hot phenotype, but nuclear PD-L1 positivity did not correlate with T-cell density. This study highlights the significance of PTEN loss and nuclear PD-L1 expression in basal subtype BCa, contributing to improved risk stratification and potential precision treatments in bladder cancer. - Source: PubMed
Publication date: 2026/05/02
Zheng QiaoliZhao TingLiao EnyiCao ZhixingWang Shuang - Type 2 high asthma is driven by coordinated GATA3 dependent programs in CD4 T cells and group 2 innate lymphoid cells (ILC2). Although biologics targeting IL4, IL5, or IL13 benefit subsets of patients, many remain symptomatic, suggesting that upstream regulatory mechanisms may sustain type 2 inflammation. We investigated whether HuR (ELAVL1), an RNA-binding protein that stabilizes GATA3 and Th2 cytokines mRNA, regulates type 2 inflammatory programs in allergic asthma. Using a house dust mite (HDM) model in vivo, HuR inhibition with the small molecule KH3 reduced lung inflammation, suppressed Th2 cytokine expression, accelerated Gata3 mRNA decay in lung CD4 T cells, and attenuated airway hyperresponsiveness toward control levels. In ex vivo activated human lung CD4 T cells, KH3 accelerated GATA3 mRNA decay with minimal effects on RORC or TBX21 and selectively reduced Th2 cytokine secretion, while IL10 and IL2 were unchanged. Similarly, ILC2s isolated from peripheral blood mononuclear cells (PBMCs) of type 2 high asthmatic donors showed reduced GATA3 mRNA stability and diminished Th2 cytokine production following KH3 treatment. Single-cell transcriptomic analysis of bronchoalveolar lavage fluid after allergen challenge demonstrated co-enrichment of ELAVL1 and GATA3 within Th2 clusters in human airways. Together, these findings identify HuR as a post-transcriptional regulator of GATA3 driven type 2 inflammation in allergic asthma. - Source: PubMed
Publication date: 2026/04/27
Atasoy UlusFattahi FatemehYaekle LauraHolden JuliaTepper BrandonHussein KareemMeier JoshuaXu LiangNerella SrilaxmiLei JingBentley KelleyHershenson MarcHuang Steven K - Mouse mammary epithelial cells possess a remarkable ability to regenerate the entire mammary gland through precisely regulated differentiation, involving complex molecular, morphological, and functional changes. Here, we performed comprehensive transcriptomic profiling of HC11 mouse mammary epithelial cells undergoing lactogenic differentiation using RNA sequencing and integrative bioinformatics. We identified 566 differentially expressed genes, reflecting extensive transcriptional reprogramming and activation of biosynthetic, metabolic, and secretory programs. Strong up-regulation of terminal and lactogenic differentiation markers, including Wap, Csn2, Lpl, Cd36, Lalba, Btn1a1, Xdh, Gata3, and Cebpb, signified maturation into a secretory phenotype. Functional evaluation via gene set enrichment analysis revealed transcriptional enrichment of mTOR, prolactin, insulin, ErbB, and autophagy-associated pathways, consistent with anabolic readiness and terminal differentiation. Conversely, p53, Wnt, and FoxO pathways were down-regulated, marking a transition from proliferation to differentiation. Transcription factors (FoxO1, Zbtb16, and Srebf1) and epigenetic regulators (Gadd45a and Hist1h1e) exhibited dynamic changes, underscoring coordinated transcriptional and chromatin remodeling. Gene set enrichment and protein-protein interaction analyses identified 10 hub genes, Agt, Ccnd1, Igf1, Mki67, Myc, Calm4, Rasgrp1, Cd69, Il6, and Pecam1, as central drivers of differentiation. Clustering of uniquely regulated genes further implicated roles in milk synthesis, protease activity, and lineage stabilization. Together, these findings define a transcriptional framework for lactogenic differentiation in the HC11 cell line model and provide a basis for future mechanistic studies. - Source: PubMed
Publication date: 2026/05/04
Ahmad WaqarPanicker Neena GopinathanRizvi Tahir AMustafa Farah