GATA3
- Known as:
- GATA3
- Catalog number:
- GTX11964
- Product Quantity:
- 50 µl
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3
Related genes to: GATA3
- 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
Related articles to: GATA3
- Augmented mucosal expression of the transcription factor GATA3 has been implicated in the pathogenesis of ulcerative colitis (UC). Here, we evaluated the efficacy and safety of SB012, an enema formulation of the DNAzyme hgd40 that specifically inactivates GATA3 messenger RNA, for induction therapy in patients with active UC. - Source: PubMed
Publication date: 2026/05/12
Atreya RajaKühbacher TanjaVieth MichaelJefremow AndreHirschmann SimonWaldner Maximilian JFischer SarahVetter MarcelDrvarov OliverWeigmann BennoMeyer MichaelMühl TanjaHomburg UrsulaSarigiannis GeorgiosGarn HolgerRenz HaraldNeurath Markus F - Innate lymphoid cells (ILCs) include T-bet-dependent NK and ILC1 cells, GATA-3-dependent ILC2 cells, and RORγt-dependent ILC3 cells. Their functional and developmental regulation at the posttranscriptional level remains elusive. The CCR4-NOT complex plays a central role in mRNA decay by mediating deadenylation. To explore the overall impact of mRNA decay on ILCs, we conditionally deleted Cnot3, an essential subunit of the CCR4-NOT complex. Loss of CNOT3 in ILC2 cells led to aberrant expression of T-bet and RORγt, accompanied by upregulation of type 1 and type 3 signature genes. Mechanistically, CNOT3 targeted the 3' untranslated regions of Tbx21 and Rorc mRNAs through interactions with Roquin and ZFP36L1, respectively. Elevated T-bet expression in CNOT3-deficient ILC2 cells suppressed GATA-3 levels, thereby impairing type 2 immune responses in models of airway allergy and helminth infection. Thus, our findings reveal that CNOT3 maintains ILC2 differentiation and function by restricting type 1 and type 3 transcriptional programs. - Source: PubMed
Publication date: 2026/05/12
Tatematsu MegumiTakasuga ShunsukeFuchimukai AkaneKimura YuumiIshii SatoshiTaniuchi IchiroIshiwata KenjiIkuta KoichiSexl VeronikaEberl GérardSawa ShinichiroKuba KeijiEbihara Takashi - While neuroendocrine markers such as chromogranin can be used to distinguish pheochromocytomas (positive) from adrenal cortical lesions (negative), other neuroendocrine markers such as synaptophysin can be positive in both entities. Insulinoma-associated protein 1 (INSM1) is a relatively novel marker often used in the diagnostic assessment of neuroendocrine tumors but with unexplored sensitivity/specificity in distinguishing between pheochromocytomas and adrenal cortical lesions. - Source: PubMed
Wu Douglas Jian-XianLobo AnandiMcKenney JesseSangoi Ankur R - Sepsis-induced cardiomyopathy represents a life-threatening complication arising from severe sepsis and septic shock. Hydroxysafflor yellow A (HSYA), a major quinone chalcone constituent, protects cardiac function in this disease. This study explored the detailed mechanisms of HSYA in mitigating sepsis-related cardiomyopathy. Potential targets of HSYA against sepsis-induced cardiomyopathy were identified by integrating sepsis-related genes (GSE131761), genes associated with myocardial damage (GeneCards), and potential targets of HSYA (CTD, GeneCards, SwissTargetPrediction). GO and KEGG pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were identified by machine learning and WGCNA. An in vitro cellular model was generated by stimulating AC16 cardiomyocytes with LPS. Cell viability and apoptosis were determined by CCK-8 assay and flow cytometry, respectively. KEGG pathway enrichment analysis revealed the potential involvement of NF-κB, TNF, IL-17, and MAPK signaling pathways in the protective role of HSYA against sepsis-induced cardiomyopathy. HSYA attenuated LPS-induced pro-inflammatory cytokine expression, ROS generation, and cell apoptosis in AC16 cardiomyocytes. Mechanistically, HSYA upregulated GATA3 expression in LPS-stimulated AC16 cardiomyocytes. Moreover, downregulation of GATA3 enhanced pro-inflammatory cytokine expression, ROS generation, and cell apoptosis in HSYA-treated AC16 cardiomyocytes under LPS. Our in vitro findings suggest that GATA3 may serve as a potential mediator through which HSYA attenuates LPS‑induced cardiomyocyte injury by concurrently dampening inflammation, oxidative stress, and apoptosis. - Source: PubMed
Publication date: 2026/05/09
Lou LihongYuan LinZeng ChunliHan YaoguoLu MingLei Ming - Vesicular cutaneous lupus erythematosus (VCLE) is a rare autoimmune disease in dogs and is considered the canine counterpart of human subacute cutaneous lupus erythematosus (SCLE). However, the molecular mechanisms underlying VCLE remain incompletely defined. - Source: PubMed
Publication date: 2026/05/11
Keating TreasaStranahan LaurenWiener DominiqueKeating M KellyLeon RenatoBanovic Frane