Rabbit polyclonal to GATA3, Host Rabbit
- Known as:
- Rabbit pab GATA3, Host Rabbit
- Catalog number:
- YF-PA11957
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Rabbit polyclonal GATA3 Host
Related genes to: Rabbit polyclonal to GATA3, Host Rabbit
- 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
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- 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 - Leucine-rich pentatricopeptide repeat-containing protein (LRPPRC) is a recently identified N6-methyladenosine (m6A) reader protein involved in a myriad of biological processes in cancer. However, its roles in glioma have not been reported. Both in vitro and in vivo studies were performed to examine the anti-glioma activity of LRPPRC silencing. Chromatin immunoprecipitation assay and RNA immunoprecipitation assay were used for the analysis of interaction between upstream and downstream molecules. Methylated RNA immunoprecipitation assay was conducted to examine m6A modification. Our results showed that LRPPRC expression was dramatically upregulated in glioma tissues and cell lines. LRPPRC regulated the m6A modification of protocadherin-7 (PCDH7) and affected its expression in glioma cell lines; LRPPRC silencing significantly inhibited glycolysis and induced ferroptosis in glioma cell lines; this was reversed by PCDH7 overexpression. Furthermore, GATA-binding protein 3 (GATA3) directly bound to the LRPPRC promoter and transcriptionally regulated LRPPRC. LRPPRC mediated the regulatory effects of GATA3 on glycolysis and ferroptosis in glioma cell lines. In vivo studies showed that LRPPRC silencing suppressed tumor growth. Taken together, our data demonstrate that LRPPRC expression was dramatically upregulated in gliomas and that inhibition of the GATA3/LRPPRC/PCDH7 axis exerted an anti-glioma effect by regulating glycolysis and ferroptosis. - Source: PubMed
Publication date: 2026/05/04
Sun YongJia YunlongBu XingyaoChen YushengWang Ruixing - Allergic rhinitis (AR) is a common chronic nasal mucosal inflammatory disorder driven by type 2 immunity, but the spatial stromal-immune cell interactions underlying its pathogenesis remain unclear. - Source: PubMed
Publication date: 2026/04/17
Zhao MiaoDuan JiaqiXie YongminHuang GuanYang GuiYang PingchangZeng Haotao - Gastric metastasis from breast cancer (GMBC) is a rare but diagnostically challenging condition, whose clinical and imaging features often mimic primary gastric cancer or treatment-related adverse effects. This study integrates a detailed case of a 54-year-old woman with Luminal B invasive lobular carcinoma who developed gastric metastasis during systemic therapy, with a systematic review of 35 recent cases (2019-2024) to delineate the clinical profile and management of GMBC. In the reported case, immunohistochemical analysis revealed phenotypic evolution, with hormone receptor expression shifting from ER 80%/PR 5% in the primary tumor to ER 30%/PR negative in the gastric metastasis. Literature synthesis identified invasive lobular carcinoma as the predominant histology (57.14%), abdominal pain as the most common symptom (54.29%), and highlighted the diagnostic utility of immunohistochemical markers-particularly GATA3 (positive in 71.43% of tested cases). Treatment remains primarily systemic, with endocrine therapy demonstrating survival benefit in hormone receptor-positive disease. We emphasize the need for heightened clinical suspicion in breast cancer patients with upper gastrointestinal symptoms and propose a structured diagnostic pathway centered on endoscopic deep biopsy and comprehensive immunohistochemical profiling. Re-biopsy to assess phenotypic evolution is crucial for guiding personalized therapy, while surgical intervention should be reserved for palliation of complications or selected cases of oligometastatic disease. - Source: PubMed
Publication date: 2026/04/16
Zhang XiaoyuLin XiangwuYang DunyaLin XianglanZhang YanLiu ShiyuChen XiYu NayingChen Qunxiang - Natural killer (NK) cells are effector cells of the innate immune system. The cytokine microenvironment influences NK cell function. Dysregulation of NK cell cytotoxicity can manifest in reproductive disorders and is also observed in tumor-transformed tissues. The search for immunotherapies capable of regulating NK cell activity is therefore relevant. This study aimed to evaluate the effect of the TGFβ signaling pathway inhibitor and the cyclin-dependent kinase (CDK) 7/12/13 inhibitor on the transcriptional profile of NK-92 cell line. In the study, the cytokines TGFβ1, IL-12, IL-15, IL-18, and TNFα, and the TGFβ receptor type 1 (TGFβR1) inhibitor LY3200882 and the CDK7/12/13 inhibitor THZ1 were used. The cells were cultured sequentially in the presence of inhibitors and cytokines, followed by assessment of the gene expression of , , , , , , , , , , and We observed direct effects of the inhibitors on NK cells. LY3200882 increased the expression of and , and reduced . THZ1 increased the expression of , , and , while it reduced and . IL-12, IL-15, IL-18, and TNFα modified the gene expression of some phenotypic and cytotoxic receptors and transcription factors. TGFβ1 increased the expression of , , and . Blocking TGFβ-dependent signaling with LY3200882 abolished TGFβ1 effects. We assessed CD56 presence on NK-92 cell membrane and found its increase in the presence of LY3200882. After LY3200882 treatment, in the presence of TGFβ1 and choriocarcinoma cell line JEG-3, the expression of CD56 receptor on NK cell membrane decreased. Pretreating NK cells with THZ1 decreased the expression of , , and in the presence of TGFβ1. Thus, LY3200882 partially neutralized TGFβ1 effects on the expression of NK cell receptor genes. THZ1 followed by TGFβ1 treatment promoted NK cell transcriptional profile characteristic for CD56dim NK cells. Both LY3200882 and THZ1 affected the NK cell transcription even without cytokine treatment. The independent effects of synthetic inhibitors on NK cells, as well as their influence in the presence of tumor cells, should be considered. - Source: PubMed
Publication date: 2026/04/17
Mikhailova ValentinaMarko OksanaMkrtchyan EdgarSokolov Dmitry