GATA3 Antibody
- Known as:
- GATA3 Antibody
- Catalog number:
- Y212708
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GATA3 Antibody
Ask about this productRelated genes to: GATA3 Antibody
- 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 Antibody
Related articles to: GATA3 Antibody
- Low birthweight increases chronic kidney disease (CKD) risk. Using a gestational low protein (LP) mouse model, we hypothesized that protein restriction would alter nephrogenesis and adult gene expression. Pregnant CD-1 dams received normal protein (NP) or LP diets. Pups were studied on postnatal days 2-7 to assess the nephron progenitor cell population. Adult mice underwent transdermal GFR measurement and histologic evaluation, bulk RNA sequencing, and cationic-ferritin-enhanced MRI. Nephrogenesis was protracted in LP mice compared with NP mice. Adult LP mice had fewer glomeruli. LP males had lower GFR and more atubular glomeruli without glomerular hypertrophy. LP males demonstrated down-regulated and LP females demonstrated down-regulation. LP offspring exhibited prolonged postnatal nephrogenesis with a lower glomerular number as adults, indicating an extended developmental window did not compensate for their reduced nephron endowment at birth. Suppression of the retinoic acid-GDNF signaling pathway was present in LP males. These findings identify a potential early life therapeutic window to mitigate CKD risk in growth-restricted offspring. - Source: PubMed
Publication date: 2026/09/23
Timberline SageDailey Rachel KJohnson WyattKameshwar Ayyappa Kumar SistaIsaac JayadeRonde KimberlyConaway MarkCwiek AleksandraBennett Kevin MBaldelomar Edwin JLi TengWu TeresaHoch Matthew RSchuh Meredith PIndugula ShaliniSeki YoshinoriSuzuki MasakoReidy Kimberly JCharlton Jennifer R - Type 2 innate lymphoid cells (ILC2) are a population of lineage-negative cells in the lung, gastrointestinal tract, and skin which have emerged as a significant component of type 2 allergic inflammation. The regulation of cyclooxygenase-2 (COX-2) metabolites is critical to the pathophysiology of many inflammatory disorders, including allergic asthma. While COX-2 regulates Th9 and Th17 cell differentiation and function during allergic lung inflammation, it remains unknown whether COX-2 also regulates ILC2 cell differentiation and function under similar conditions. To address this question, we examined lung ILC2 cells from COX-2+/+ and COX-2-/- mice after ovalbumin (OVA)- or Alternaria-induced allergic lung inflammation. ILC2 cells were significantly increased in COX-2-/- lungs compared with COX-2+/+ lungs after OVA exposure in vivo. The increase in ILC2 cells was accompanied by an increase in expression of the cytokines IL-5 and IL-13, and the transcription factor GATA3. Both genetic disruption and selective inhibition of COX-2 significantly increased ILC2 cell differentiation from isolated common lymphoid progenitor cells (CLP) in vitro. Furthermore, COX-2-derived PGE2 acting via EP2 receptors significantly reduced IL-33 and TSLP expression, and attenuated ILC2 cell differentiation in vitro and in vivo. Thus, during allergic lung inflammation, COX-2-derived PGE2 signals through the EP2 receptor to negatively regulate lung ILC2 cell differentiation and function. - Source: PubMed
Publication date: 2026/09/22
Li HongEdin Matthew LMenendez DanielBradbury J AlyceGraves Joan PGruzdev ArtiomWhitehead Gregory SSifre Maria IDeGraff Laura MZeldin Darryl C - Female adnexal tumor of probable Wolffian origin (FATWO) is an extremely rare gynecologic neoplasm derived from mesonephric duct remnants. It exhibits nonspecific clinical and imaging features, frequently leading to preoperative misdiagnosis. To date, ultrasound findings of FATWO remain poorly characterized, with limited systematic reports. This study summarizes the ultrasonic manifestations of four pathologically confirmed FATWO cases and reviews the literature, aiming to improve preoperative recognition and fill the gap in systematic ultrasound descriptions of FATWO. - Source: PubMed
Publication date: 2026/09/11
Xu LiYe LeiChu KetanWang Junmei - Salivary duct carcinoma is a rare, aggressive salivary gland malignancy that morphologically and immunophenotypically resembles breast ductal carcinoma. The rhabdoid variant is characterized by discohesive tumor cells with rhabdoid cytomorphology, frequent loss of E-cadherin expression, and morphologic overlap with pleomorphic invasive lobular carcinoma of the breast. We report a 74-year-old man who presented with an enlarging right buccal mass and trismus. Positron emission tomography-computed tomography demonstrated right cervical lymphadenopathy with no evidence of breast or lung primary. Resection revealed a discohesive, infiltrative tumor composed of pleomorphic rhabdoid cells, with scattered cells containing intracytoplasmic mucin imparting a signet-ring morphology, and prominent targetoid perineural invasion. Immunohistochemically, the tumor showed diffuse positivity for keratin 7, gross cystic disease fluid protein 15 (GCDFP15/PIP), androgen receptor, weak GATA3 expression, loss of E-cadherin, and cytoplasmic p120-catenin (CTNND1) staining, a profile closely resembling that of invasive lobular carcinoma. Extensive nodal metastases were identified. Despite multimodal therapy, the disease recurred. This report highlights the importance of recognizing salivary duct carcinoma with rhabdoid features to avoid misdiagnosis and guide appropriate management. - Source: PubMed
Publication date: 2026/09/19
Khalid Muhammad HassaanChristie-Nguyen Phuoc TAshfaq MaryamKakarala BhanupriyaIbrahim Nourhan GSaluja Karan - BackgroundMalignant serous effusions may be the first manifestation of an underlying malignancy, and accurate primary-site attribution is essential. However, distinguishing Müllerian carcinoma, breast carcinoma, and mesothelioma in effusion cytology remains a challenge because of overlapping immunophenotypes. We evaluated SOX17 and TRPS1 in this setting.Materials and MethodsA multicenter retrospective cohort including 650 tissue specimens (300 breast carcinomas, 300 Müllerian tumors, and 50 mesothelial lesions) and 150 malignant serous effusion cell blocks was analyzed. SOX17 and TRPS1 expression was assessed by immunohistochemistry and compared with established markers, including PAX8, GATA3, WT1, and calretinin. Sensitivity, specificity, and positive predictive value (PPV) were calculated according to the primary diagnosis.ResultsIn the tissue cohort, SOX17 showed 87% sensitivity and 100% specificity for Müllerian tumors, with no expression in breast carcinomas or mesothelial lesions, including tumors with PAX8/WT1 co-expression. This specificity was retained in cell blocks, yielding a PPV of 100%. TRPS1 showed 98% sensitivity for breast carcinoma and identified 84% of GATA3-negative breast carcinomas. However, TRPS1 expression was also observed in 48% of tubo-ovarian serous carcinomas, limiting its PPV for breast carcinoma in effusions to 55% despite a negative predictive value of 97%.ConclusionSOX17 is a highly specific confirmatory marker for Müllerian origin and may help resolve diagnostic pitfalls related to PAX8-positive mesothelial lesions. TRPS1 is a complementary marker for breast carcinoma, including GATA3-negative tumors, but its stand-alone diagnostic value is limited by cross-reactivity in Müllerian serous carcinomas. These findings support a panel-based approach for accurate primary-site attribution in malignant serous effusions. - Source: PubMed
Publication date: 2026/09/19
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