Nkx6.1
- Known as:
- Nkx6.1
- Catalog number:
- 000716A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Nkx6.1
Related products to: Nkx6.1
Related articles to: Nkx6.1
- Diabetes mellitus, characterized by β-cell dysfunction and loss, results in impaired insulin secretion and chronic metabolic complications. Mesenchymal stem cells represent a promising source for β-cell regeneration owing to their endodermal differentiation potential. This study optimized the differentiation of human tonsil-derived mesenchymal stem cells (TMSCs) into pancreatic β-like cells through the comparative evaluation of two signaling-based protocols. - Source: PubMed
Publication date: 2026/04/22
Yang JiinKim Ha YeongKim So JeongKim Han Su - Impairment of pancreatic β-cell function is a primary etiology of type 2 diabetes mellitus (T2DM). The sulfated manno-glucuronan (GMn) was found to possess a backbone structure consisting of interspersing 1, 3-linked β-D-GlcpA residues and alternating 1, 2-linked α-D-Manp residues and 1, 4-linked β-D-GlcpA residues. Additionally, random sulfation occurs at the C6 position of the Man residues. GMn demonstrated no detectable cytotoxicity in MIN6 cells and attenuated palmitic acid (PA)-induced decreases in cell viability in a dose-dependent manner. Furthermore, GMn effectively reversed PA-impaired glucose-stimulated insulin secretion (GSIS) in a dose-dependent manner in both MIN6 cells and primary mouse islets. In vivo, GMn treatment significantly attenuated glycemic levels in high-fat diet/streptozotocin-induced type 2 diabetic mice, elevated β-cell insulin content, and decreased the proportions of α-, δ-, and pancreatic polypeptide (PP)-cells. Mechanistically, GMn significantly suppressed aldehyde dehydrogenase 1A3 (ALDH1A3)-mediated retinol metabolism and increased the expression of key β-cell identity/function markers, including PDX1, NKX6.1, MAFA, and NeuroD1, in pancreatic islets. Consistently, in vitro studies demonstrated that GMn counteracted PA-induced upregulation of ALDH1A3, while promoting the expression of the same set of β-cell transcription factors. Collectively, these findings indicate that GMn may enhance β-cell proliferation and reduces β-cell differentiation by downregulating ALDH1A3 expression. - Source: PubMed
Publication date: 2026/03/19
Zhang WenjingZhang FumingZou XiaotingWu NanHe SunyueLu LusiXu ChunyiXu WeiyingJin WeihuaZhou Jiaqiang - Tissue-engineered scaffolds are increasingly important for improving pancreatic islet transplantation, as conventional transplantation disrupts the pancreas's native vasculature and extracellular matrix, reducing islet viability and function. This underscores the need to develop a three-dimensional porous microencapsulation scaffold system that can replicate a supportive microenvironment, providing both mechanical stability and biological cues vital to preserving islet viability and function. This study investigated the potential of two freeze-dried and crosslinked gelatin-based scaffolds: Gelatin vinyl acetate copolymer (GeVAc) and gelatin with oxidized dextran dialdehyde (GELDEX), for supporting pancreatic islet culture. Their physicochemical properties, architecture, and wettability were analyzed using scanning electron microscopy and contact angle measurements. Both scaffolds exhibited hydrophilic, biocompatible, and structurally stable characteristics. Mouse pancreatic MIN6 cells were cultured on the scaffolds for 7 days to evaluate islet viability, extracellular matrix deposition and functionality through immunocytochemistry, glucose-stimulated insulin secretion (GSIS), and gene expression analysis. MIN6 cells adhered well to both scaffolds, forming dense monolayers and multicellular spheroids that resembled native islet clusters. GeVAc scaffolds showed significantly higher glucose sensitivity and glucose stimulation index (GSI) compared to GELDEX. While INS1 and PDX1 expression levels were comparable in both scaffolds, NKX6.1 expression was significantly higher in GeVAc. These findings indicate that scaffold architecture and surface characteristics play a crucial role in creating a supportive microenvironment for islet cluster formation, highlighting the potential of gelatin-based scaffolds as microencapsulation platforms for clinical islet transplantation in diabetes therapy. - Source: PubMed
Salim RukhiyaUnnikrishnan P SArya D AThomas Lynda V - - Source: PubMed
Publication date: 2026/04/14
Carty Senegal - Forkhead Box A2 (FOXA2) is a transcription factor essential for endodermal development and the formation and function of several metabolic organs, including the liver and pancreas. Within the pancreatic lineage, FOXA2 plays a crucial role in orchestrating islet development, maintaining β-cell identity, and regulating genes central to glucose sensing and insulin secretion. This review provides a comprehensive overview of FOXA2's dual role in both developmental and mature stages of pancreatic islets, highlighting its function as a gatekeeper of lineage specification and metabolic homeostasis. We describe FOXA2's dynamic expression patterns during embryogenesis, its regulatory interactions with other key transcription factors, such as PDX1 and NKX6.1, and its influence on chromatin accessibility during islet cell differentiation. Furthermore, we discuss the consequences of FOXA2 dysregulation, including impaired α- and β-cell maturation, loss of functional identity, and contributions to the pathogenesis of diabetes. Insights from mouse models, human stem cell-derived islets, and patient genetics underscore the clinical relevance of FOXA2 in monogenic and complex forms of diabetes. By integrating developmental biology, genomics, and disease modeling approaches, this review highlights FOXA2 as a central regulator connecting pancreatic organogenesis with long-term metabolic control. Understanding FOXA2's regulatory networks may open new avenues for therapeutic strategies aimed at restoring or preserving β-cell function in diabetes. - Source: PubMed
Publication date: 2025/12/09
Elsayed Ahmed KManzoor YusraAbdelalim Essam M