GATA3 antigen

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899.25 €

Known as:: GATA3 antigenic
Catalog number:: 'H00002625-Q01-25
Product Quantity:: 25
Category:: -
Supplier:: ACR
Gene target:: GATA3 antigen

Related genes to: GATA3 antigen

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 antigen

Related articles to: GATA3 antigen

PTEN-low associated mismatch repair deficiency and nuclear PD-L1 expression in basal-type bladder cancer.
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
HuR Regulates GATA3-Driven Type 2 Inflammation in CD4⁺ T cells and ILC2 in Airway Inflammation.
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
Shaping Cell Identity: Global Transcriptome and Pathway Shifts during Mouse Mammary Epithelial Cell Differentiation.
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
Sensitive detection of somatic mutations in GC-rich cancer gene promoters.
Somatic mutations in protein-coding genes and noncoding regulatory regions are the major drivers of cancer. Only a relatively small number of somatic noncoding mutations that are likely drivers have been described to date, including those in the promoters of the , and genes. The impact of these alterations can be profound by initiating, increasing, or abolishing gene expression. Promoter mutations in particular have been difficult to identify even from whole tumor genomes due to their high content of G and C nucleotides, which leads to loss of sequencing coverage in these regions. Therefore, the landscape of somatic drivers in gene promoters remains incomplete. Here, we present a hybrid capture assay optimized for >3000 promoters of cancer genes. We show that this assay allows for deep sequencing of challenging GC-rich promoter regions, enabling discovery of reliable point mutations, short insertions and deletions, copy number variants, and mutational signatures in cell line models as well as formalin-fixed, paraffin-embedded archival tissue samples. Our assay nominated candidate noncoding driver mutations in , and in breast cancer for future functional follow-up. - Source: PubMed
Publication date: 2026/05/04
Qi MeifangDave Preshita SanjayFrancis NicoleDeFelice MatthewPollock SamCorbitt HollyMitsiades Irene RinWang GengchaoFrere PaulFox AlanKhitrov GregoryPetersen CarolineLarkin KatieHamilton SusannaEllisen Leif WGulhan Doga CHidalgo-Miranda AlfredoLennon NiallCibulskis CarrieRheinbay Esther
Immunohistochemical Evaluation of GATA3 Expression in Patch-Stage Mycosis Fungoides (MF) Compared With Benign Inflammatory Dermatoses (BID).
The histopathologic distinction between patch-stage mycosis fungoides (MF) and benign inflammatory dermatoses (BID) remains a persistent diagnostic challenge, often due to overlapping clinical and immunophenotypic features. GATA binding protein 3 (GATA3), a transcription factor critical in T-helper 2 cell differentiation, has emerged as a potential immunohistochemical marker in T-cell neoplasms. This study aimed to evaluate GATA3 expression in patch-stage MF compared with BID to assess its diagnostic value. Sixty formalin-fixed, paraffin-embedded skin biopsies were retrospectively analyzed, including 30 cases of patch-stage MF and 30 cases of BID (psoriasis, chronic dermatitis, and lichen planus). Immunohistochemical staining for GATA3 was performed, and lymphocytic nuclear staining was assessed in dermal and epidermal compartments. GATA3 expression > 50% in dermal lymphocytes was observed in 20% of MF cases and 6.7% of BID cases, yielding high specificity (93.3%) but low sensitivity (20%) for MF diagnosis. Epidermal GATA3 expression was uniformly low across both groups. No significant correlations were found between GATA3 expression and key histopathologic or immunophenotypic features of MF. Although elevated dermal GATA3 expression may support the diagnosis of MF in some cases, its substantial overlap with BID and low sensitivity limit its utility as a reliable standalone diagnostic marker for early-stage MF. GATA3 can be incorporated into broader immunohistochemical panels alongside more specific markers to improve diagnostic accuracy. - Source: PubMed
Publication date: 2026/05/04
Montazer FatemehMalekan MohammadAbedi Hamid

GATA3 antigen

Related genes to: GATA3 antigen

Related products to: GATA3 antigen

Related articles to: GATA3 antigen

PTEN-low associated mismatch repair deficiency and nuclear PD-L1 expression in basal-type bladder cancer.

HuR Regulates GATA3-Driven Type 2 Inflammation in CD4⁺ T cells and ILC2 in Airway Inflammation.

Shaping Cell Identity: Global Transcriptome and Pathway Shifts during Mouse Mammary Epithelial Cell Differentiation.

Sensitive detection of somatic mutations in GC-rich cancer gene promoters.

Immunohistochemical Evaluation of GATA3 Expression in Patch-Stage Mycosis Fungoides (MF) Compared With Benign Inflammatory Dermatoses (BID).