GATA3 antibody Host Mouse
- Known as:
- GATA3 (anti-) Host Mouse
- Catalog number:
- 'H00002625-B01P
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GATA3 antibody Host Mouse
Related genes to: GATA3 antibody Host Mouse
- 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 antibody Host Mouse
Related articles to: GATA3 antibody Host Mouse
- Birt-Hogg-Dubé (BHD) syndrome is an autosomal dominant disorder caused by germline inactivation of the folliculin gene (FLCN). Approximately 25% of BHD syndrome patients are diagnosed with renal tumors, which can be multifocal and/or bilateral. These tumors have been reported to span a broad histologic spectrum; however, the majority exhibit a distinctive histology characterized by intermingled cytologic features similar to that seen in oncocytoma and chromophobe renal cell carcinoma. Accordingly, such tumors were previously termed 'hybrid oncocytic chromophobe tumor' (HOCT). To date, most studies have characterized tumors arising in BHD syndrome patients without molecular confirmation of FLCN biallelic inactivation; accordingly, the clinicopathologic characterization of molecularly confirmed FLCN biallelic inactivated tumors remains limited. This study evaluates a multi-institutional cohort of 18 renal tumors from different individuals, including integrated histologic, immunohistochemical, and targeted next-generation sequencing analyses. While all patients exhibited clinical characteristics raising suspicion for BHD syndrome, germline status was not available in 5 patients. Nevertheless, molecular analysis demonstrated findings supportive of FLCN biallelic inactivation in all patients, and there were no other candidate driver alterations or recurrent molecular findings. Histologically, most tumors showed 'conventional' histology consisting of solid or nested growth with a characteristic mosaic population of eosinophilic and clear cells and low-grade nuclear features, including frequent perinuclear halos and binucleation. Two cases showed 'non-conventional' histology including tubulocystic and tubulopapillary architecture. Immunohistochemistry revealed consistent GPNMB expression and a distinctive mosaic staining pattern for KRT7, L1CAM, and GATA3, aiding distinction from other eosinophilic renal neoplasms. Follow-up was available for 17 patients (median 37 months, range 1-110 months). Both patients with non-conventional morphology demonstrated advanced stage at presentation, including one with metastatic disease. Collectively, these findings define one of the largest molecularly-confirmed cohorts of FLCN biallelic inactivated tumors to date and support recognition of FLCN-driven tumors as a distinct, molecularly defined entity. - Source: PubMed
Publication date: 2026/05/21
Siegmund Stephanie EWobker Sara EHarik Lara RTretiakova MariaKandukuri ShivaniTrpkov KirilMaclean FionaOdintsov IgorAlchoueiry MichelAron ManjuPicken Maria MMahlow JonathonAdeniran Adebowale JHumphrey Peter AMoch HolgerTsai HarrisonHenske Elizabeth PHirsch Michelle S - Peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS) rarely occurs in pediatric and young adult populations, where little is known about its clinicopathologic and molecular features. We characterized 16 cases of PTCL, NOS diagnosed in patients ≤21 years old. Seven (44%) cases demonstrated SMARCB1/INI1 loss by immunohistochemistry and SMARCB1/INI1 alterations by next-generation sequencing, including biallelic SMARCB1/INI1 deletion (n=4), stop codon variant with 1-copy deletion (n=1) or copy-neutral loss-of-heterozygosity (CN-LOH; n=1), and frameshift variant (n=1). One case demonstrated biallelic SMARCE1 alterations (a nonsense variant and CN-LOH), which, to our knowledge, has not been previously described in a hematopoietic neoplasm. The SWI/SNF-intact group harbored pathogenic TET2, PTEN, EZH2, or TP53 variants. CDKN2A deletions were present in 3/7 SWI/SNF-deficient and 0/4 SWI/SNF-intact cases. 22q11.2 alterations were present on karyotype of 2/3 SMARCB1/INI1-deficient cases. SWI/SNF-deficiency was associated with intermediate-to-large cell cytomorphology, frequent mitotic (88%; p=0.041) and apoptotic (88%) activity, Reed-Sternberg-like cells (63%), necrosis (50%), and fibrosis (50%). All cases expressed CD45 and CD43 at initial diagnosis. SWI/SNF-deficient cases predominantly demonstrated a CD4+/CD8-, TCRab, and PTCL-GATA3 phenotype, whereas SWI/SNF-intact cases predominantly demonstrated a CD8+/CD4-, TCRgd, and PTCL-TBX21 phenotype. A PTCL-TBX21 phenotype was more common in SWI/SNF-intact than SWI/SNF-deficient cases (p=0.041). Cytotoxic markers were expressed in 71% of SWI/SNF-deficient and 88% of SWI/SNF-intact cases. Decreased or absent CD3 expression characterized 88% of SWI/SNF-deficient and 13% of SWI/SNF-intact cases (p=0.01). 63% of SWI/SNF-deficient cases demonstrated decreased/absent expression of ≥3 pan-T-cell antigens, compared to 13% of SWI/SNF-intact cases. Treatment was heterogeneous. Primary treatment failure or relapse occurred in 4/8 SWI/SNF-deficient and 4/7 SWI/SNF-intact cases. The median OS and EFS were 48.7 and 47.5 months for the SWI/SNF-deficient, and 16.4 and 8.9 months for the SWI/SNF-intact groups, respectively (p=NS). Death due to disease or therapy-related complications occurred in 4/8 (50%) cases in the SWI/SNF-deficient group and 6/7 (86%) of cases in the SWI/SNF-intact group. Our findings expand the knowledge of the clinicopathologic and molecular features of pediatric PTCL and highlight SWI/SNF-deficient T-cell lymphoma as a biologically distinct type of PTCL that is associated with characteristic clinicopathologic features. - Source: PubMed
Publication date: 2026/05/19
Bledsoe Jacob RFerry Judith ALi JingweiSassoon AaronStonhill Miekan ASiegele BradfordLiang XiayuanDalton JustinMochel Mark CIvashkevich YanaJohari VanditaSadigh SamSelove WilliamSood SadhikaWard NicholasWoda BruceDegar BarbaraFeraco Angela MRowe JaredDavies KimberlyAl-Ibraheemi AlyaaAmador CatalinaKovach Alexandra EFleming Mark DHarris Marian HTsai Harrison K - Current therapies for diabetic kidney disease (DKD) targeting hyperglycemia and hypertension fail to halt progression, urging exploration of additional drivers. Renal lipotoxicity and chronic inflammation form a self-perpetuating cycle driving DKD, yet multitarget interventions remain underexplored. We hypothesized that simultaneous inhibition of ANGPTL3 and IL-33, two key regulators of lipid metabolism and the inflammatory-fibrotic axis, would ameliorate DKD, and that integrating both antagonistic activities into a single bifunctional molecule offers translational advantages. We engineered a bifunctional fusion protein, FD03-sST2, comprising an anti-ANGPTL3 nanobody fused to the IL-33 decoy receptor sST2. In high-fat diet-fed db/db mice, FD03-sST2 significantly improved renal function (ACR, BUN, urine volume), reduced serum/hepatic lipids, and attenuated renal lipid accumulation. Mechanistically, it suppressed renal inflammation via NF-κB/NLRP3 inhibition and ameliorated fibrosis by suppressing the IL-33/ST2/ILC2 axis (reducing renal IL-33/GATA3 signals and inhibiting IL-33-induced profibrotic factors from ILC2s). Transcriptomic and metabolomic analyses confirmed attenuation of DKD-associated dysregulation. This study identifies a DKD cascade wherein lipotoxicity triggers IL-33 release, amplifying injury through inflammation and fibrosis. By targeting ANGPTL3 and IL-33 simultaneously, FD03-sST2 interrupts this vicious cycle at two nodes-improving lipid metabolism while suppressing downstream inflammatory and fibrotic signaling-providing an integrated alternative to separate biologics. - Source: PubMed
Publication date: 2026/05/19
Li ZhuojinCao ZhonglianZhou RongruiCheng XuHu XiaozhiXu ShuwenDou ZihanDu LingJu Dianwen - Secretory breast carcinoma (SBC) is an extremely rare subtype, accounting for ~1% of breast cancers but representing the most common malignant breast tumor in pediatric patients. Although generally indolent, SBC carries a risk of local recurrence even decades after treatment. Its defining molecular hallmark is the ETV6-NTRK3 fusion. - Source: PubMed
Publication date: 2026/05/14
Vlahović ANikolić SDjuričić S MDunđerović DIlić NSarajlija ADenčić Fekete MCvetinović AVasić M - Aberrant activation of , a key oncogenic driver, defines a major subgroup comprising ∼30% of childhood T-lineage acute lymphoblastic leukemias (T-ALLs). We and others have shown that somatic non-coding mutations within upstream and intronic -regulatory regions of contribute to transformation by creating binding sites for MYB and other transcription factors. Here we investigated -regulatory mechanisms mediated by somatic mutations occurring in an intergenic region located 29 kilobase pairs downstream of the canonical transcription initiation site, implicated in 6% of -expressing T-ALLs. These somatic variants include i) complex indels resulting in MYB transcription factor binding sites (TFBSs) and ii) internal tandem duplications (ITDs) encompassing canonical MYB TFBSs. Chromatin immunoprecipitation sequencing (ChIP-seq) revealed binding of the TAL1 core regulatory circuit (CRC) transcription factors MYB, GATA3, and RUNX1, resulting in enhancer activity mediated by sequences with the mutant allele. Strikingly, ChIP-seq peaks for the repressive H3K27me3 mark and the active H3K27ac mark co-existed across regulatory sequences but enriched for different haplotypes. transcription from the mutant haplotype initiated from a promoter located within exon 4 of the canonical transcript, resulting in a short isoform normally expressed by hematopoietic stem cells (HSC). Interestingly, neither the isoform expression nor the enhancer activity could be predicted by the sequence-to-function deep learning artificial intelligence (AI) model AlphaGenome, emphasizing the importance of experimental validation. Our findings indicate that selection for -regulatory, non-coding variants leads to reactivation of enhancers normally active in HSC but silenced in differentiated lineages during normal hematopoietic cell development. - Source: PubMed
Publication date: 2026/05/06
Terekhanova Nadezhda VChen XiaolongChow Kin-HoeLiu YuShao YingDong LiJu BenshengVinayachandran VineshZubair HaseebHagiwara KoheiYang WentaoMa XiaotuNatarajan SivaramanEaston JohnTeachey David TLook A ThomasZhang Jinghui