NKX6-3 Blocking Peptide
- Known as:
- NKX6-3 Blocking Peptide
- Catalog number:
- 33r-8015
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- NKX6-3 Blocking Peptide
Related products to: NKX6-3 Blocking Peptide
Related articles to: NKX6-3 Blocking Peptide
- Presently, we investigated hypothesized roles and mechanisms of cell type-specific, selective activation of different vascular NOX (NADPH oxidase) isoforms in obesity and metabolic syndrome. - Source: PubMed
Publication date: 2026/04/23
Huang KaiHuang YuanliZhang YuhanZhang YixuanHatch Nicholas WFreed Julie KCai Hua - infection is the main risk factor for gastric cancer. easily develop antibiotic resistance and evade host defenses. In-depth knowledge of the first barrier that encounter, the gastric surface mucus-producing epithelial cells (SMCs), may enable improved treatment and prevention. This study aimed to characterize SMC gene expression, mucus glycosylation, and identify how colonization affects these parameters. The glycosylation of eight -infected and eight sham control mice was characterized by mass spectrometry. SMCs from five infected and five sham control mice were extracted with laser microdissection (LCM) and sequenced with RNA sequencing (RNA-Seq). SMCs were characterized by high gene expression for proteins secreted into mucus (, , , , and , mitoribosome RNA, and cytoskeleton proteins. Mucin glycans were large, complex, heavily fucosylated, and dense with H-antigen motifs. Two main glycosylation pathways ending in H-antigen glycans were identified and corroborated with glycosyltransferase expression. Glycosylation was consistent between -infected and sham control mice. RNA-Seq data was analysed for differential gene expression, gene set enrichment analysis, and network analysis of functionally-related genes. The analyses revealed that genes required for protein synthesis and oxidative phosphorylation were down-regulated in infected mice. Most up-regulated genes were either interferon-stimulated genes or able to induce interferon production themselves. Depletion of Nkx6-3 occurred in the infected mice, indicating initiation of a pre-cancerous cascade. LCM RNA-Seq of SMCs was thus feasible and enabled characterization of the SMC and definition of a gene set showing how infection affects SMCs. - Source: PubMed
Publication date: 2026/03/25
Erhardsson MattiasSantos LicíniaBenktander JohnSharba SinanThorell KaisaLindén Sara - Genome-wide association studies (GWAS) identified over 600 loci containing single-nucleotide polymorphisms (SNPs) associated with type 2 diabetes (T2D), most of which reside in non-coding regions. Among the set of T2D SNPs, linking causal genome variants to disease risk experimentally has remained a challenge; however, advances in synthetic mammalian genome writing techniques now enable the delivery of multiple haplotypes to human induced pluripotent stem cells (hiPSCs) to create a series of isogenic cell lines that can be differentiated and phenotyped . Here, to begin efforts in dissecting a T2D GWAS locus, we engineered an gene cluster knockout hiPSC line and introduced a landing pad facilitating the delivery of synthetic haplotype payloads. We built four haplotypes, including several that are not observed in nature, containing risk SNPs spanning the gene cluster using a method called "variant Switching Auxotrophic markers for Integration" (vSwAP-In), and integrated them precisely into hiPSCs. deletion blocked pancreatic progenitor and skeletal muscle differentiation, suggesting that and are required for early pancreatic and skeletal muscle development, and perhaps related to the existence of two nonoverlapping sets of SNPs in linkage disequilibrium that associate with the expression of the two adjacent genes. When / T2D "Risk" haplotypes were reintroduced, skeletal muscle and pancreatic progenitor differentiation capabilities were restored. expression was elevated in the Risk and All-Risk haplotypes compared to the Risk and Non-Risk haplotypes, establishing a functional experimental platform to examine risk SNP clusters in their native contexts. Overall, this work establishes a platform for the dissection of GWAS loci using synthetic haplotype genomics in hiPSCs. - Source: PubMed
Publication date: 2026/01/04
Chalhoub NoorVarshney ArushiZhang WeiminUhl SkylerLaurent Jon MMcLoughlin ColleenAshe HannahMou XingruiDale NathanRamnarine KiranPaull DanielGoldberg JordanMaurano Matthew TBrosh RanFenyö DavidCipriani FilippoParker Stephen C JBoeke Jef D - Early B-cell development is primarily regulated at the transcriptional level and comprises the consecutive differentiation stages B-cell progenitor, pro-B-cell and pre-B-cell. These entities provide the cells of origin in B-cell precursor acute lymphoid leukemia (BCP-ALL) that show aberrations of developmental transcription factors (TFs), representing major oncogenic drivers. Analysis of physiological TFs in these developmental entities helps us to understand their normal and disturbed activities and regulatory connections. Here, we focused on NKL-subclass homeodomain TF NKX6-3, which is active in both normal B-cell progenitors and TCF3::PBX1 fusion gene-positive BCP-ALL cases. By performing siRNA-mediated knockdown and forced expression experiments in BCP-ALL model cell lines, we established a gene regulatory network for NKX6-3 together with TALE-class homeodomain TFs IRX1 and MEIS1, as well as ETS-TF SPIB. Importantly, NKX6-3 was activated by TCF3::PBX1, underlying their co-expression in BCP-ALL. Furthermore, comparative expression profiling analysis of public BCP-ALL patient data revealed TGFb-pathway in-hibitor CD109 as a downregulated target gene of NKX6-3. TGFb-signalling, in turn, enhanced NKX6-3 expression, indicating mutual activation. Finally, RNA-seq analysis of BCP-ALL cell line RCH-ACV after NKX6-3 knockdown revealed MPP7 as an upregulated target gene of both NKX6-3 and TCF3::PBX1, revealing a role for the HIPPO-pathway in B-cell progenitors and TCF3::PBX1-positive BCP-ALL. Collectively, our data introduce novel players and regulatory connections to normal and aberrant TF-networks in B-cell progenitors to serve as potential diagnostic markers or therapeutic targets. - Source: PubMed
Publication date: 2025/10/14
Nagel StefanMeyer CorinnaPommerenke Claudia - The fatty acid composition of meat, which affects both its quality and the consumer's health, is a complex trait influenced by genetic and environmental factors. Identification of the genes influencing the fatty acid composition of meat is very important for the selection and breeding of chickens with desirable and healthier fatty acid profiles. The objective of this study was to identify functional candidate genes for fatty acid profiles of the breast meat of the Korean native chicken-red-brown line (KNC-R) through genome-wide association studies. We genotyped 382 KNC-R chickens (190 males, 192 females) using the Illumina chicken 60K single nucleotide polymorphism (SNP) chip (Illumina, San Diego, CA, USA), and association tests were performed by mixed linear model in the Genome-wide Complex Trait Analysis (GCTA) software, based on mixed linear model analysis-leave-one-chromosome-out (MLMA-LOCO). We detected one SNP each on chromosomes 2 (rs13667281), 10 (rs14011157), and 22 (rs10731996) that were significantly (p < 0.05) associated with nervonic (C24:1), linoleic (C18:2), and eicosadienoic (C20:2) acids, respectively. We found 13 protein-coding genes related to lipid metabolism, including IGF2BP3, GPNMB, NPY, OSBPL3, IL6, NR2F2, GPAT4, NKX6-3, ANK1, SFRP1, ERLIN2, STAR, and PPP1R3E. Interestingly, two candidate genes (GPNMB and SFRP1) were reported to regulate the expression of genes known to be involved in fatty acid synthesis, such as the FASN, ACACA, ACLY, ELOVL, and SCD genes. Identification of functional candidate genes for fatty acid profiles might facilitate the selection and breeding of chickens with desirable and healthier fatty acids. - Source: PubMed
Publication date: 2025/03/31
Munyaneza Jean PierreKim MinjunCho EunjinJang AeraChoo Hyo JunLee Jun Heon