GATA6 antibody - middle region (ARP31859_P050)
- Known as:
- GATA6 (anti-) - middle region (ARP31859_P050)
- Catalog number:
- arp31859_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GATA6 antibody - middle region (ARP31859_P050)
Related genes to: GATA6 antibody - middle region (ARP31859_P050)
- Gene:
- GATA6 NIH gene
- Name:
- GATA binding protein 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 18q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-11
- Date modifiied:
- 2016-10-05
Related products to: GATA6 antibody - middle region (ARP31859_P050)
Related articles to: GATA6 antibody - middle region (ARP31859_P050)
- The differences in egg production performance among hens are closely linked to the efficiency of follicle selection, which is characterized by granulosa cell differentiation and progesterone production. In this study, by integrating ATAC-seq and mRNA-seq analyses on granulosa cells from pre-hierarchical (Pre-GCs) and hierarchical (Post-GCs) follicles, we set out to identify key regulatory factors involved in chicken follicle selection. - Source: PubMed
Publication date: 2026/04/17
Li DandanQi ChaoSun YiKang LiWei QingqingJiang Yunliang - Epithelial cell adhesion molecule (EpCAM) is a tumor-associated antigen that marks pluripotent embryonic stem cells (ESCs). Regulation of Epcam expression yields a spatiotemporal patterning during embryogenesis that is thoroughly mimicked in a 3D model of spontaneous differentiation of embryoid bodies (EBs). Here, we present a role of EpCAM in exit from pluripotency of murine ESCs (mESCs) to establish cardiomyocytes in EBs. Comparative transcriptomic analysis of wildtype and Epcam-knockout mESCs at strategic time points of spontaneous differentiation uncovered molecular deficiencies of Epcam-knockout ESCs in "Wnt signaling" and "Heart development". Multi-level bioinformatic analyses revealed central lineage-defining transcription factors Eomes, Foxa2, and Gata6 as differentially expressed genes (DEGs) that are misregulated in Epcam-knockout mESCs. Gene expression association of Epcam with Eomes, Foxa2, and Gata6 was prominent at day three of spontaneous differentiation, representing primitive streak formation in EBs. Interrogation of public single-cell RNA sequencing (scRNAseq) datasets supported a co-expression of Epcam and Eomes at early stages of murine embryogenesis in epiblast, primitive streak, nascent mesoderm, extraembryonic ectoderm and endoderm. Newly generated scRNAseq of wildtype mESCs in spontaneous differentiation delineated the formation of epiblast, primitive streak, endo- and mesoderm cells, and cardiomyocytes. Expression and pseudotime analysis positioned Epcam expression slightly ahead of Eomes at the transition of early to late primitive streak, along with rising Wnt signaling. Accordingly, conditional re-expression of Epcam or Eomes but not of Foxa2 or Gata6 complemented differentiation defects of Epcam-knockouts and confirmed an involvement of Wnt signaling in the EpCAM-dependent activation of Eomes. Hence, defective exit of pluripotency in Epcam-deficient ESCs is linked to Eomes regulation via Wnt signaling. - Source: PubMed
Publication date: 2026/04/11
Gong NingyueGouda MaheshBalaz Ana MarijaSong JiahangKranz GiselaHess JuliaBaumeister PhilippUnger KristianKatalina VeraCanis MartinGires Olivier - High recurrence rates, significant metastatic potential, and limited overall survival make triple-negative breast cancer (TNBC) the most challenging subtype among breast cancers. Previous studies have indicated that the downregulation of TGFB2-AS1 can enhance the stem-like properties of tumor cells, thereby promoting TNBC progression. Bioinformatics analysis has revealed the regulatory role of GATA6 in TGFB2-AS1 transcription, providing insights into the transcriptional regulation of TGFB2-AS1 by GATA6 and offering potential prognostic biomarkers and therapeutic strategies for TNBC. - Source: PubMed
Publication date: 2026/04/01
Liu ChangYu QianruWang DifeiDuan ZhengZhang XinWang JiaoQi XiaoyuYe JiayinZhao QianHe JianrongZhou Cixiang - - Source: PubMed
Publication date: 2026/03/28
Kalenderoglou NikolettaDimitri FedericaGonzález Carmen NavarroVidal-Puig AntonioHobbs JacobYounis AwaisChristodoulides ConstantinosCarobbio StefaniaChristian Mark - Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies, with a 5-year survival of only ∼13%. Despite incremental advances through combination chemotherapy, most patients relapse rapidly due to profound molecular heterogeneity and intrinsic resistance. Recent genomic and transcriptomic studies have defined distinct PDAC molecular subtypes, classical and basal-like, which differ in differentiation state, prognosis, and therapeutic vulnerability. Classical tumors, marked by GATA6 and hepatocyte nuclear factors, exhibit epithelial identity and relative chemosensitivity, whereas basal-like tumors driven by ΔNp63 and MYC display mesenchymal and inflammatory programs associated with resistance and poor outcome. Importantly, these subtypes are dynamic, with single-cell and spatial analyses revealing frequent coexistence and therapy-induced transitions, highlighting cellular plasticity as a major determinant of treatment response. Subtype identity is governed by lineage-defining transcription factors, chromatin regulators, and stromal cues that integrate to form reversible epigenetic states. Targeting these mechanisms with inhibitors of EZH2, BET proteins, or CDK9 can restore differentiation programs and resensitize tumors to chemotherapy. Integrating molecular subtyping with epigenetic modulation thus offers a rational path toward biomarker-guided therapy. Continued efforts combining spatially resolved profiling, organoid modeling, and liquid-biopsy monitoring will be essential to capture tumor evolution in real time. Understanding and therapeutically exploiting the transcriptional and epigenetic plasticity in PDAC may ultimately enable reprogramming of resistant states and improve clinical outcomes in this intractable disease. - Source: PubMed
Publication date: 2026/03/23
Parassiadis ChristinaJohnsen Steven A