GATA3 polyclonal antibody
- Known as:
- GATA3 pab (anti-)
- Catalog number:
- PAB18658
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- GATA3 polyclonal antibody
Related genes to: GATA3 polyclonal 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 polyclonal antibody
Related articles to: GATA3 polyclonal antibody
- This study aimed to investigate the role of miR-10a and its rs3809783 polymorphism in postoperative incisional pain among patients undergoing laparoscopic cholecystectomy for acute cholecystitis (ACC-LC). Levels of miR-10a and immune markers (CD68, CD19, CD3, T-bet, GATA-3, IL-17A, Bcl-6) were measured in gallstone mucosal tissue, and genotyping was performed via PCR and sequencing. An incisional pain mouse model was used for mechanistic exploration. The results showed that miR-10a expression was decreased in ACC-LC patients compared with controls and was negatively correlated with pain intensity. Patients carrying the rs3809783 AT genotype exhibited lower miR-10a levels and higher pain scores than AA carriers. Among the elevated immune markers, only Bcl-6/Tfh was associated with pain severity. Further analysis confirmed Bcl-6 as a direct target of miR-10a, with the A→T substitution at rs3809783 enhancing Bcl-6-mediated Tfh polarization. This genotype was also correlated with longer anal exhaust time, higher inflammatory markers, and more complications. In conclusion, miR-10a and its rs3809783 polymorphism may serve as biomarkers for postoperative pain in ACC-LC by regulating the Bcl-6/Tfh pathway. - Source: PubMed
Publication date: 2026/08/25
Sun YueZhao LanZhang ZengzhenLi HuiqingFu Xiaobo - Primary neuroendocrine carcinoma of the breast is a rare malignancy. Tumors demonstrating predominant neuroendocrine differentiation with focal squamous features are exceptionally uncommon, and metachronous contralateral development following previously treated invasive ductal carcinoma (IDC) has been reported only rarely. We present the case of a 68-year-old woman with a history of estrogen receptor-positive, HER2-negative left breast IDC treated with neoadjuvant chemotherapy, mastectomy, adjuvant radiation therapy, and endocrine therapy who developed a distinct contralateral high-grade breast carcinoma seven years later. Following the discovery of right axillary lymphadenopathy, imaging revealed a right breast mass with progressive axillary adenopathy. Histopathologic examination demonstrated a primary small-cell neuroendocrine carcinoma of the breast with focal squamous differentiation. Immunohistochemistry showed diffuse positivity for INSM1, synaptophysin, and p63, with negativity for estrogen receptor, progesterone receptor, HER2, TTF-1, CDX2, SOX10, and GATA3, supporting a primary breast origin. This case highlights the diagnostic complexity and therapeutic uncertainty surrounding a metachronous contralateral neuroendocrine breast carcinoma following treatment of a separate primary breast malignancy. This exceptionally rare entity underscores the importance of continued case reporting to improve understanding of its clinicopathologic features and guide future management strategies. - Source: PubMed
Publication date: 2026/08/24
Parkhurst Erik LHamad Amar - This study investigates relationships among the multi-omics features of ductal carcinoma in situ (DCIS) and provides evidence to support non-invasive classification and personalized treatment strategies. - Source: PubMed
Publication date: 2026/09/18
Zhao YajiePu ChunruiZhang ChongjianLiu Zhenzhen - Adipose tissue dysfunction drives obesity-associated metabolic disease, yet the transcriptional regulators of pathological adipose remodeling remain undefined. Here, we identify adipocyte as a diet-inducible regulator that is dispensable for basal adipogenesis but necessary and sufficient for diet-induced obesity and systemic metabolic dysfunction. Adipocyte-specific deletion redirects adipose expansion from hypertrophic to hyperplastic growth and improves glucose tolerance, insulin sensitivity, and adipose inflammation, whereas human GATA3 re-expression in adipocytes restores obesity and metabolic dysfunction, suggesting cross-species conservation and establishing both necessity and sufficiency for a causal driver. Multi-omic profiling, integrating proteomics, metabolomics, and single-cell mass cytometry, reveals that Gata3 loss suppresses a STAT3-anchored inflammatory myeloid program while enhancing mitochondrial oxidative capacity. Through further tracing of this adipocyte-intrinsic program to distal metabolic organs, systemic lipidomic and chemokine profiling identifies a two-pronged mechanism through which adipocyte Gata3 drives hepatic dysfunction: selective remodeling of lipoprotein-surface lipids and a coordinated CXCL5/CXCL2/CXCL9 chemokine axis. Collectively, these findings reposition Gata3 from a putative anti-adipogenic brake to a diet-inducible master regulator of pathological adipose remodeling and nominate adipocyte-targeted Gata3 inhibition as a strategy to uncouple adipose expansion from systemic metabolic disease. - Source: PubMed
Publication date: 2026/09/10
Qin MinghuiLi FuqiangYang MingjieWang LaiSharifi Behrooz GShah Prediman K - Extraembryonic lineages, specifically the trophectoderm (TE) and primitive endoderm (PrE), are indispensable for early embryogenesis and successful pregnancy. Expanded potential stem cells (EPSCs) can contribute to both embryonic and extraembryonic fates, providing a platform to model early lineage specification. - Source: PubMed
Publication date: 2026/09/09
Kim HaneulCai LianHyun Sang-HwanKim Eunhye