GATA3 Monoclonal Antibody [1C1] 100 µg
- Known as:
- GATA3 Monoclonal Antibody [1C1] 100 µg
- Catalog number:
- ABB-2238-100
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- EpigenTek
- Gene target:
- GATA3 Monoclonal Antibody [1C1] 100 µ
Related genes to: GATA3 Monoclonal Antibody [1C1] 100 µg
- Gene:
- C1orf174 NIH gene
- Name:
- chromosome 1 open reading frame 174
- Previous symbol:
- -
- Synonyms:
- RP13-531C17.2
- Chromosome:
- 1p36.32
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-21
- Date modifiied:
- 2017-07-11
- Gene:
- CBR1 NIH gene
- Name:
- carbonyl reductase 1
- Previous symbol:
- CBR
- Synonyms:
- SDR21C1
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-20
- Date modifiied:
- 2016-10-05
- Gene:
- DLG1 NIH gene
- Name:
- discs large MAGUK scaffold protein 1
- Previous symbol:
- -
- Synonyms:
- SAP97, SAP-97, hdlg, DLGH1, dJ1061C18.1.1
- Chromosome:
- 3q29
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-04
- Date modifiied:
- 2016-05-24
- Gene:
- DNAAF4 NIH gene
- Name:
- dynein axonemal assembly factor 4
- Previous symbol:
- DYX1C1
- Synonyms:
- EKN1, FLJ37882, CILD25
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-10-10
- Date modifiied:
- 2017-03-20
- Gene:
- DNAAF4-CCPG1 NIH gene
- Name:
- DNAAF4-CCPG1 readthrough (NMD candidate)
- Previous symbol:
- DYX1C1-CCPG1
- Synonyms:
- -
- Chromosome:
- 15q21.3
- Locus Type:
- readthrough
- Date approved:
- 2011-09-23
- Date modifiied:
- 2017-03-23
Related products to: GATA3 Monoclonal Antibody [1C1] 100 µg
Related articles to: GATA3 Monoclonal Antibody [1C1] 100 µg
- Group 2 innate lymphoid cells (ILC2s) play critical roles in type 2 airway inflammation. 17,18-epoxyeicosatetraenoic acid (17,18-EpETE), an eicosapentaenoic acid metabolite, is generated from dietary omega-3 fatty acids, and may have anti-inflammatory activities. We evaluated the effect of 17,18-EpETE and its metabolite, 17,18-dihydroxy-eicosa-5,8,11,14-tetraenoic acid (17,18-diHETE), on IL-33-induced airway inflammation involving ILC2s. We evaluated the in vitro effects of 17,18-EpETE and 17,18-diHETE on the IL-33-induced production of IL-5 and IL-13 by human ILC2s (isolated from peripheral blood) using ELISA. Expression of the corresponding fatty acid receptors and the GATA-3 transcription factor were examined using flow cytometry and quantitative RT-PCR. Additionally, we examined the in vivo effects of 17,18-EpETE or 17,18-diHETE in a mouse model of type 2 airway inflammation induced by intranasal (i.n.) instillation of IL-33. 17,18-EpETE or 17,18-diHETE inhibited IL-33-induced production of IL-5 and IL-13, and IL-33-induced expression of GATA-3 in human ILC2s. GW1100, an antagonist of G protein-coupled receptor (GPR) 40, or GW9662, an antagonist of peroxisome proliferator-activated receptor γ (PPARγ), counteracted the inhibitory effects of 17,18-EpETE or 17,18-diHETE on the IL-33-induced production of IL-5 and IL-13 by ILC2s. I.n. administration of 17,18-EpETE or 17,18-diHETE attenuated IL-33-induced eosinophil infiltration and mucus production in mouse nasal mucosa, and production of IL-5 and IL-13 in lung tissue and bronchoalveolar lavage fluid. The present study demonstrated the anti-inflammatory effects of 17,18-EpETE and 17,18-diHETE on IL-33-induced airway inflammation involving ILC2s. I.n. administration of 17,18-EpETE may be a new therapeutic approach for the treatment of intractable type 2 airway inflammation. - Source: PubMed
Publication date: 2026/06/03
Tojima IchiroNishiguchi TatsujiKawakita KentoKubo YoshihitoMurao TakuyaNakamura KeigoMatsumoto KojiKouzaki HideakiShimizu ShinoShimizu TakeshiTakenaka Yukinori - Extramammary Paget Disease (EMPD) is a rare cutaneous adenocarcinoma. While localized disease has an excellent prognosis, metastatic EMPD is aggressive with no standardized systemic therapy. This study characterizes the clinicopathologic and molecular landscape of metastatic/recurrent EMPD to identify therapeutic vulnerabilities. - Source: PubMed
Publication date: 2026/06/02
Suleiman RihamGuo RayLohman Mary EThome Stephan DPagliaro Lance CMarkovic Svetomir NHalfdanarson Thorvardur RFuentes Bayne Harry E - Despite therapy advances, better solutions for refractory bladder cancer remain an unmet need. Human cell-based models may aid in better treatment translation. We introduce 3D-UHU-TU, a bladder cancer microtissue model which incorporates spheroids derived from low- and high-grade human bladder cancer cell lines (RT112 and T24 respectively) into a healthy human urothelium. - Source: PubMed
Publication date: 2026/06/02
Murray Benjamin OGao JinhuiPasquina-Lemonche LaiaSwarbrick KatherineSimpson GuyChambers Mark APandha HardevFreeman AlexRohn Jennifer L - Early embryogenesis features rapid cell cycles that impose substantial replication stress (RS). How RS shapes lineage potential remains unclear. Using mouse embryonic stem cells (ESC) as an inner cell mass model, we show that RS rapidly and durably induces trophoectoderm (TE) regulators, including Cdx2, Gata3, Eomes, Elf5, Hand1 and Tfap2c. This program requires ATR checkpoint signaling as ATR inhibition suppresses RS-induced TE gene expression without restoring pluripotency markers, indicating an active, checkpoint-driven fate response rather than passive identity loss. Additionally, RS activates JNK, increasing c-JUN abundance and phosphorylation. Blocking JNK attenuates TE induction, placing AP-1 as a cooperating pathway. The TE bias persists after stress withdrawal, promoting acquisition of a TE-like phenotype and enhancing ESC contribution to extraembryonic compartments in embryo-like structures. Quantitative chromatin proteomics reveals eviction of nucleosomes and condensin along with enrichment of DNA repair factors and ATR cofactors, consistent with a chromatin-competent and checkpoint-responsive state, permissive for lineage rewiring. These findings define an ATR- and JNK/c-JUN-dependent stress response axis that redirects embryonic cell identity toward TE, linking RS to developmental plasticity. If reactivated in the adult, this pathway could lead to somatic fate shifts that may predispose to malignancy. - Source: PubMed
Publication date: 2026/06/02
Gnocchi AndreaEl Kai ChristelleCastellan CristinaSantorelli LuciaArghavanifard NegarBachi AngelaCostanzo Vincenzo - To explore the status of peripheral blood immunological markers and gene mutations in patients with myelodysplastic syndrome (MDS) and the correlation between them. - Source: PubMed
Sun Da-XiangMa YunHan Qiu-HongChen ZhuoLiu Wei-YiWang De-XiuLi Rui-BaiLyu YanXiao Hai-YanLiu ChiLi LiuTang Xu-Dong