Human Polyclonal GATA2 Ab
- Known as:
- Human Polyclonal GATA2 Antibody
- Catalog number:
- a0677
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal GATA2
Related genes to: Human Polyclonal GATA2 Ab
- 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: Human Polyclonal GATA2 Ab
Related articles to: Human Polyclonal GATA2 Ab
- Erythropoiesis is a highly coordinated process governed by lineage-defining transcription factors. While several master regulators have been characterized, many additional factors expressed in erythroid progenitors remain poorly understood. Here, we identify the epithelial-to-mesenchymal transition (EMT)-associated transcription factor ZEB1 as a previously unrecognized regulator of erythroid maturation. ZEB1 is expressed in murine and human erythroid progenitors, and its loss impairs proliferation and disrupts the erythroid transcriptional network. Mechanistically, ZEB1 interacts with KLF1 and governs both its expression dynamics and nuclear localization. In ZEB1-deficient cells, GATA2 silencing is delayed due to failure of KLF1 to properly accumulate in the nucleus, impairing KLF1-mediated repression of GATA2 and perturbing the GATA2-KLF1 regulatory switch that drives late-stage erythropoiesis. Consistent with these findings, ZEB1 downregulation hampers maturation of primary human CD34⁺-derived erythroid cells. Together, our findings establish KLF1 as a repressor of GATA2, and ZEB1 as a critical enforcer of erythroid transcriptional circuitry, and demonstrate that erythroid cells recruit EMT-associated factors to ensure lineage completion. - Source: PubMed
Kinoo AlexiaDeleuze VirginieSalma MohammadLegoff NoémieCandotti JérémieGonzalez-Menendez PedroJoly AxelGaltier JérémyCharmeaux-Goulot JulieChahar SanjayRaynaud PeggyZheng HaoyangRouaisnel BettyBouvier QuentinFaux CélineVerdier FrédériqueHelmlinger DominiqueEl Hoss SaraMaciel Thiago TrovatiTaylor NaomiHermine OlivierKinet SandrinaAndrieu-Soler CharlotteSoler Eric - CD8⁺ T cells mediate host defense and tumor immunity through specialized differentiation states, yet the regulatory programs that guide these states may also limit their functional potential. Loss-of-function studies have defined many regulators required for T cell differentiation, but they do not readily reveal regulatory activities that emerge only when transcription factors are ectopically expressed outside their native lineage, dosage, or temporal context. Here, we developed single-cell gain-of-functon(GOF) sequencing (scGOF-seq), a multiplexed platform for in vivo mapping of transcription factor overexpression in antigen-specific CD8⁺ T cells across immunocompetent models of infection and cancer. By enforcing expression of canonical T cell regulators, lineage-silenced developmental factors, and temporally restricted transcription factors, scGOF-seq uncovered unexpected in vivo activities. Developmental regulators normally silenced in T cells, including NANOG, SOX2, OCT4 and GATA2, reshaped T cell differentiation in context-dependent ways, with NANOG promoting stemness-associated phenotypes and accumulation during chronic infection. In parallel, sustained cMyc expression outside its native temporal window generated a stem-like, effector-featured state with enhanced metabolic fitness, reduced terminal exhaustion, and profound antigen-dependent expansion exceeding 5,000-fold. Importantly, cMyc GOF maintained cell-cycle checkpoint signatures and demonstrated a strong dependence on antigen presence for proliferation across the tested conditions. scGOF-seq further identified cooperating transcription factor modules that complemented cMyc-driven programs and improved T cell responses in solid tumors. These findings establish systematic GOF perturbation as a framework for uncovering latent and temporally constrained regulatory activities in CD8⁺ T cells and guiding immune-state engineering. - Source: PubMed
Publication date: 2026/06/11
Milner J JustinPratt BrandonMullins GenevieveBrown Nolanvan Rooyen LaraGreen WilliamXie FucongZhabotynsky VasylModliszewski Jenniferde Vries NicholasJambor AlexanderCannon GabrielleGreen JarredSyed ZaidPlotkin AlecKennedy AndrewPaunto Coral Del Mar AliceaShi HuitongMerritt EmilyEgawa TakeshiSomasundaram AswhinWang WeiThaxton JessicaDotti GianpietroChung H Kay - Ovarian cancer is one of the deadliest female gynaecological cancers, known to have high metastatic ability and telomerase reactivation. The current study aims to explore the influence of exogenous Kisspeptin-10 (KP-10) on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using both in vitro and computational techniques. KP-10 significantly inhibited SKOV-3 proliferation, migration, and invasion at a dose-dependent level with an IC₅₀ of 72.28 nM. The molecular mechanisms showed the ability of KP-10 to affect the regulation of important transcriptional factors such as SP1, CDX2, GATA2, FLI1, and ZEB1 and hTERT expression, indicating telomerase-related oncogenic signaling modulation. Besides, KP-10 influenced the expression of tumor suppressive microRNAs, including miR-200, miR-345, and miR-577 which are known to inhibit epithelial-mesenchymal transition, invasion, and development of cancer. The bioinformatics analysis of the KISS1 promoter showed multiple binding sites of SP1, CDX2, GATA2, FLI1, among others, indicating the transcription network in KISS1 regulation. Taken together, this paper shows the KP-10-mediated modulation of transcriptional factors involved in the SP1-ZEB1-hTERT pathway, inhibiting proliferative and metastatic phenotypes of ovarian cancer cells. - Source: PubMed
Publication date: 2026/06/11
Shah HetviThomas AbinPandya Parth - Not available. - Source: PubMed
Publication date: 2026/06/11
Kotmayer LiliWlodarski Marcin W - Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) refers to liver cancer caused by chronic HBV infection and is the leading cause of liver cancer globally. Although aurora kinase A (AURKA) has been reported to be highly expressed in HBV-associated HCC, its specific mechanisms of action remain unclear. Through bioinformatics analysis (Gene Expression Omnibus (GEO)) and experimental validation (Western blot), the expression levels of AURKA, hepatitis B virus X protein (HBX), and GATA binding protein 2 (GATA2) were assessed. A HepG2.2.15 cell model was established. Functional assays (colony formation, flow cytometry, mouse xenograft tumor model) and mechanistic studies (dual-luciferase reporter assay, JASPAR database analysis, and chromatin immunoprecipitation (ChIP)) were conducted to investigate the mechanism of AURKA in HBV-associated HCC. Bioinformatics analysis identified AURKA as a core gene in HBV- associated HCC. AURKA was highly expressed in HBV-associated HCC. Knockdown of AURKA inhibited the proliferation of HepG2.2.15 cells, induced apoptosis, and reduced the protein level of the autophagy substrate P62 as well as the ratio of the autophagy marker LC3BII/LC3BI. By forming a complex with GATA2, HBX enhanced the transcriptional activity of the AURKA promoter, thereby promoting the malignant phenotypes of HepG2.2.15 cells. Additionally, in vivo experiments demonstrated that knockdown of GATA2 inhibited tumor growth. In conclusion, GATA2-regulated AURKA promotes the development of HBV-associated HCC, underscoring its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/06/09
Di LiangGuo QingliangZhao XiaofeiDing Jing