GATA2 Luciferase Reporter Vector
- Known as:
- GATA2 Luciferase Reporter Vector
- Catalog number:
- LR0030
- Product Quantity:
- 10 ug
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- GATA2 Luciferase Reporter Vector
Related genes to: GATA2 Luciferase Reporter Vector
- Gene:
- GATA2 NIH gene
- Name:
- GATA binding protein 2
- Previous symbol:
- -
- Synonyms:
- NFE1B
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2019-04-23
Related products to: GATA2 Luciferase Reporter Vector
Related articles to: GATA2 Luciferase Reporter Vector
- GATA1 and GATA2 are zinc-finger transcription factors essential for normal hematopoiesis. As genetic testing becomes more widely integrated into clinical practice, -related disorders are increasingly recognized, making it important for clinicians to understand their diagnosis and management. - Source: PubMed
Publication date: 2026/04/24
Karr MatthewPalmisiano NeilChen Xiaoyi - Postpartum depression (PPD) is a common and serious mental disorder after childbirth, imposing a heavy burden on mothers, infants, and families. Abnormalities in the tryptophan-kynurenine (TRP-KYN) metabolic pathway are considered to be involved in its pathogenesis, but the role of quinolinic acid phosphoribosyltransferase (QPRT), a key downstream enzyme in this pathway, remains unclear. This study aims to explore the association between PPD in women undergoing cesarean section and gene polymorphisms, as well as other risk factors for PPD. - Source: PubMed
Zhao ShanshanLin GuoxinLi ZiyuanPing AnqiWang SaiyingDuan Kaiming - Invasive plants pose a major threat to global biodiversity, yet the molecular and genomic mechanisms underlying their success remain poorly understood. Here, we investigate the invasion of the common reed Phragmites australis, a grass species that became invasive in North America after its introduction from Europe, to elucidate the molecular mechanisms potentially underlying its invasion process. - Source: PubMed
Publication date: 2026/04/22
Wang CuiOrd JamesYan MengxiaoCai YunfeiShao HongjinLin LeleSalojärvi JarkkoLiu LeleGuo Weihua - The rising incidence and mortality of lung adenocarcinoma (LUAD) present a significant public health challenge. Histidine, an essential amino acid, plays a pivotal role in metabolic processes, yet its specific contribution to LUAD pathogenesis remains to be elucidated. This study obtained bulk and single-cell RNA sequencing (scRNA-seq) data for LUAD from UCSC Xena and Code Ocean platforms, respectively. By integrating differential expression analysis, univariate/multivariate Cox analysis, and LASSO regression analysis, prognostic genes for LUAD were identified, and a prognostic risk model was constructed. Algorithms including ESTIMATE, ssGSEA, and CIBERSORT were employed to investigate immune heterogeneity across different groups. Furthermore, molecular subtypes of LUAD were identified through consensus clustering. This study, through the integration of bulk and scRNA-seq data, identified epithelial cells as the key effector cell population in LUAD, which can be further subdivided into four functionally heterogeneous subpopulations. Seven histidine metabolism-related epithelial cell-specific genes with prognostic significance in LUAD were identified (WIF1, GATA2, CD69, ID1, C4BPA, WFDC2, and CCL20), enabling the construction of a robust prognostic risk model. Immune infiltration analysis revealed that low-risk patients exhibited more robust immune infiltration and activity. Furthermore, cross-cancer exploratory evidence suggested potential sensitivity to CTLA-4 and PD-L1 inhibitors in this group. Furthermore, consensus clustering analysis successfully partitioned LUAD into two molecular subtypes exhibiting immune heterogeneity. The prognostic model constructed based on epithelial cell-specific genes associated with histidine metabolism effectively distinguishes LUAD patients and their immune characteristics, revealing epithelial cells as a key cell population regulating LUAD histidine metabolism. - Source: PubMed
Publication date: 2026/04/28
Mao ChaofanZhou Lin - A 52-year-old man presented with sarcomatoid diffuse pleural mesothelioma that had relapsed at an isolated site after a complete response to dual-immune checkpoint inhibition (ICI). Targeted sequencing exhibited amplification of chromosome 9p24, encompassing JAK2, PD-L1, PD-L2, and PTPRD in the relapsed (post-ICI) tumor, compared with baseline (pre-ICI). On multiplex immunofluorescence, tumor-associated macrophages (TAMs) and CD8 cytotoxic T lymphocytes (CTLs) made up most of the cells in baseline and relapsed tumor (59% and 47%, respectively). Baseline tumor cells expressed genes linked to extracellular matrix remodeling and epithelial-mesenchymal transition, intermixed with M2-like TAMs and tissue-resident, effector-like CTLs. Relapsed tumor cells shifted to a growth factor-driven phenotype (NT5E, NOD1, GATA2, FN1, PDCD1LG2) that is known to cause functional impairment of CTLs, which then transitioned to an exhausted state (FCRL3, CST7, GPR171, TRAT1, LAG3); exhausted CD8 and CD4 T cells are seen in the peripheral blood at relapse. TAMs were enriched in antigen-presentation (CD80, CD86, CXCL10), extracellular matrix-degradation (MMP9, CTSL), and CTL-suppression (ARG1, PLA2G7) pathways. Our analyses revealed that regional immunosuppression mediated by adaptive reprogramming of tumor-cell and immune-cell (TAMs, CTLs)-intrinsic changes-rather than by immune evasion or stromal exclusion-served as a mechanism of acquired resistance to dual-ICI therapy. - Source: PubMed
Publication date: 2026/04/15
Ollila HelyKulkarni PrateekKim HyojinAnkola PratitiChintala Navin KThomas CarlosSauter Jennifer LOffin MichaelAdusumilli Prasad S