GATA3 (Human) Recombinant Protein (Q02)
- Known as:
- GATA3 (Human) Recombinant Protein (Q02)
- Catalog number:
- H00002625-Q02-25
- Product Quantity:
- 25 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GATA3 (Human) Recombinant Protein (Q02)
Related genes to: GATA3 (Human) Recombinant Protein (Q02)
- Gene:
- DDX47 NIH gene
- Name:
- DEAD-box helicase 47
- Previous symbol:
- -
- Synonyms:
- DKFZp564O176, FLJ30012, HQ0256, RRP3
- Chromosome:
- 12p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-13
- Date modifiied:
- 2016-10-05
- 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 (Human) Recombinant Protein (Q02)
Related articles to: GATA3 (Human) Recombinant Protein (Q02)
- Herbal extract formulations have attracted increasing interest as immunomodulatory agents in veterinary medicine. This study evaluated the immunomodulatory potential of three herbal extracts, namely Extract A (Boswellia serrata, Commiphora myrrha, and propolis), Extract B (Nypa fruticans), and Extract C (Boswellia serrata, Commiphora myrrha, Scutellaria baicalensis, Gardenia jasminoides, and propolis), using a bovine peripheral blood mononuclear cell (PBMCs) in vitro model. Cytotoxicity assessment via WST-1 assay confirmed that all three extracts were non-cytotoxic at concentrations of 50, 100, and 200 μg/mL. RT-qPCR analysis demonstrated that all three extracts significantly modulated the expression of cytokines and transcription factors associated with Th1 (IFN-γ, TBX21), Th2 (IL-4, GATA3), Th17 (IL-17, RORC), and regulatory T cell (CTLA4, Foxp3) pathways. Extract A induced sustained upregulation across multiple targets, Extract B elicited rapid but transient responses, and Extract C produced broad and progressive modulation. These findings provide experimental evidence for the immunomodulatory activity of these herbal formulations in bovine immune cells, supporting their further evaluation as candidate agents for veterinary immunotherapy. - Source: PubMed
Publication date: 2026/07/06
Xiang Xi-RuiLee Eun-SeoLee Jun HoKyung Su MinYoo Han Sang - To investigate the clinical, histopathological, and immunohistochemical features of penile median raphe cysts and to further characterize their epithelial phenotypes and possible histogenesis. We performed a multicenter retrospective analysis of 45 patients with penile median raphe cysts diagnosed between January 2015 and March 2026. Clinical records, histopathological findings, and immunohistochemical profiles were reviewed. Formalin-fixed, paraffin-embedded specimens were evaluated using a panel of epithelial and lineage-associated markers. The patients had a mean age of 35.6 years (range, 10-80 years). It generally presents as a translucent, skin-colored cyst located under the foreskin or on the frenulum just below the urethral opening on the glans. Histopathologically, all cysts were centered in the dermis and showed no connection with the epidermis or urethra. Nineteen cysts (42.2%) were lined entirely by like urethral transitional epithelium, 17 (37.8%) by squamous epithelium, and 9 (20.0%) showed mixed epithelial lining. Immunohistochemically, both epithelial types expressed P63 and AR. Like urethral transitional epithelium cells expressed CK7, CK20, CK19, 34βE12, and GATA3, with focal P504S positivity and negative NKX3.1 staining. The squamous epithelium expressed CEA and EMA and was negative for 34βE12 and NKX3.1. All patients underwent surgical excision, and no recurrence was observed during the available follow-up. Penile median raphe cysts are uncommon developmental lesions with heterogeneous epithelial linings. Many lesions show a urothelial-/urethral-type immunophenotype, whereas others demonstrate squamous or mixed differentiation, supporting histogenetic heterogeneity rather than a single uniform origin. Surgical excision appears to be an effective treatment. - Source: PubMed
Publication date: 2026/07/04
Huang YishunWang LixinXu FengAo JunwenLi XiaohongZhang Guangping - Congenital heart disease (CHD) represents the most prevalent and life-threatening birth defect. The identification of underlying factors contributing to abnormal cardiac development can offer valuable insights for the comprehensive medical management of affected pediatric patients. This study aimed to investigate the role and underlying mechanisms of GATA3-AS1 in the progression of CHD. The proliferation ability and apoptosis level of AC16 cardiomyocytes overexpressing GATA3-AS1 were detected by CCK-8 assay and flow cytometry. The downstream target miRNAs and mRNAs of GATA3-AS1 were validated using qPCR and western blot to elucidate the GATA3-AS1-associated ceRNA regulatory network. The interaction between GATA3-AS1 and its downstream target genes was validated using the dual-luciferase reporter assay. Finally, the expression patterns of GATA3‑AS1 and its downstream target genes were validated in clinical samples. Cellular functional assays demonstrated that the overexpression of GATA3-AS1 significantly suppressed the proliferation of AC16 cardiomyocytes while inducing apoptosis in these cells. The qPCR analysis revealed that, in AC16 cells overexpressing GATA3-AS1, the expression levels of NR2F2 were significantly upregulated, whereas the expression levels of miR-149-3p and miR-6769b-5p were significantly downregulated. Additionally, Western blot analysis further validated the significant upregulation of NR2F2 protein expression. The dual-luciferase reporter gene assay confirmed that GATA3-AS1 regulated cellular biological behavior by competitively binding to miR-149-3p with NR2F2. Finally, qPCR confirmed that the expression of GATA3-AS1, miR-149-3p, and NR2F2 in clinical samples were consistent with cytological experiments. GATA3-AS1 regulates the proliferation and apoptosis of AC16 cells via the GATA3-AS1/has-miR-149-3p/NR2F2 axis, potentially contributing to the formulation of more personalized and effective medical management strategies for patients with CHD. - Source: PubMed
Publication date: 2026/07/08
Wang HuamingLin XiGu QiuyangXu XiangWei LinglinLiu Xinxiu - Transcription factor (TF) dosage represents an overlooked aspect of developmental regulation. While Gata3 has traditionally been viewed as a determinant of trophectoderm (TE), its potential role in primitive endoderm (PE) has remained unclear. Here, we demonstrate that Gata3 functions as a dosage-sensitive regulator directing mutually exclusive lineage programs in mouse embryonic stem (ES) cells. Low levels of Gata3 (Gata3-L) promote PE-like transcriptional states, while high levels (Gata3-H) drive TE identity by rapidly repressing pluripotency and inducing TE markers. Genome-wide binding analysis reveals a dose-dependent redistribution of Gata3 across enhancers, with chromatin engagement consistent with pioneer factor-like activity. Functional 3D blastoid assays combined with single-cell transcriptomics further establish that Gata3 dosage alone is sufficient to instruct the spatial segregation of PE- versus TE-like compartments. These findings redefine Gata3 not merely as a TE determinant but as a central dosage-sensitive switch in lineage specification. More broadly, our results position TF dosage as a fundamental regulatory parameter that integrates enhancer selection, chromatin engagement, and spatial patterning, providing new opportunities to refine stem cell-based models and engineer developmental outcomes. - Source: PubMed
Publication date: 2026/07/06
Jang YeejinKim MijeongChoi JoonhyukKim Jonghwan - Small cell carcinoma of the bladder (SCCB) is a rare aggressive cancer, representing less than 1% of bladder cancers. Similar to small cell lung cancer (SCLC), it progresses rapidly, metastasizes early, and has a poor prognosis, complicating treatment. Unlike more common bladder cancers, SCCB often resists localized treatments and responds better to chemotherapy. However, its management generally relies on protocols for SCLC due to limited specific research. - Source: PubMed
Publication date: 2026/07/03
AbuHaweeleh Mohannad NElfaieg AmroAlhyari AbdelkareemAbuhayeh NadaKhalil Ibrahim AMahmood NabilAkhtar MohammedAl-Rumaihi Khalid