Pdx1 (zebrafish)
- Known as:
- Pdx1 (zebrafish)
- Catalog number:
- Y213738
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Pdx1 (zebrafish)
Related genes to: Pdx1 (zebrafish)
- Gene:
- PDX1 NIH gene
- Name:
- pancreatic and duodenal homeobox 1
- Previous symbol:
- IPF1
- Synonyms:
- IDX-1, STF-1, PDX-1, MODY4
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-30
- Date modifiied:
- 2016-10-05
Related products to: Pdx1 (zebrafish)
Related articles to: Pdx1 (zebrafish)
- Multiple signaling pathways and transcription factors (TFs) establish organ domains in the developing gastrointestinal tract. How these are integrated into spatial-temporal networks to regulate organogenesis and how disruptions to those networks lead to congenital syndromes remain poorly understood. Using human pluripotent stem cell cultures and Xenopus embryos, we demonstrate that retinoic acid (RA) from the lateral plate mesoderm directly activates expression of the TF rfx6 in posterior foregut endoderm. Rfx6 subsequently promotes posterior foregut identity while suppressing Wnt-dependent hindgut and Bmp-dependent pharyngeal fates through direct and indirect mechanisms. Rfx6 can directly activate the expression of several key foregut TFs (onecut1 and pdx1) and Wnt antagonists (sfrp2/5) while indirectly restricting expression of Wnt and Bmp ligands. Rfx6 also directly suppresses transcription of the Wnt-dependent hindgut TF cdx2 and the Bmp-dependent pharyngeal TFs nkx2-5 and nkx2-6. Thus, Rfx6 acts at multiple levels to integrate RA, Wnt, and Bmp activity into a network with lineage-promoting TFs to control gut tube patterning. These results provide insight into the molecular basis of Mitchell-Riley Syndrome congenital anomalies, which are caused by RFX6 mutations. - Source: PubMed
Publication date: 2026/09/01
Rankin Scott ABiesiada JacekMcCracken Kyle WPatel Riya KRana MehekLuedeke David MKechele Daniel OWells James MZorn Aaron M - The outcome of directed differentiation for cell-based therapies is profoundly influenced by the starting cell's intrinsic state, or cellular context. How pluripotent versus lineage-primed cells interpret the same developmental cues remains unclear. To address this, we performed a comparative transcriptomic analysis using two mouse cell lines engineered for episomal expression: a pluripotent embryonic stem cell line (PLT-ES) and a multipotent pancreatic stem cell line (PLT-PPPD). We introduced a core set of pancreatic transcription factors - PMN: Pdx1 (pancreatic and duodenal homeobox 1), MafA (MAF BZIP transcription factor A), and NeuroD1 (neurogenic differentiation 1) - into both cell types and analyzed global gene expression and insulin promoter activity. The two cell types exhibited strikingly divergent fates. In lineage-primed PLT-PPPD cells, PMN expression induced a mixed pancreatic/hepatic phenotype. In stark contrast, PMN expression in pluripotent PLT-ES cells failed to initiate an endodermal program, instead robustly driving differentiation towards mesodermal lineages. Intriguingly, reporter assays revealed that the PMN factors could activate the insulin promoter in both PLT-ES and PLT-PPPD cells, regardless of the overall differentiation outcome. Our findings demonstrate that cellular context is a paramount determinant of cell fate. The activation of a single promoter is insufficient to orchestrate a complete differentiation program. While pancreatic stem cells exhibit plasticity within the endodermal lineage, pluripotent cells are misdirected towards entirely different germ layers if not appropriately primed. This study underscores the critical importance of using lineage-committed cells for predictable therapeutic outcomes. - Source: PubMed
Publication date: 2026/08/31
Yamato Eiji - Esculetin, a coumarin derivative, exhibits diverse biological activities; however, its impact on pancreatic β-cell stress responses and survival remains poorly defined. In this study, we investigated the effects of esculetin on cellular stress signaling, apoptosis, and functional gene expression in INS-1 pancreatic β-cells. Following treatment with 3000 µM esculetin for 6 h, cell viability, proliferation, apoptosis, oxidative stress, endoplasmic reticulum (ER) stress markers, MAPK signaling components, cell cycle distribution, and β-cell-specific gene expression were assessed. In silico molecular docking was performed to explore putative interactions between esculetin and proteins involved in ER stress, MAPK signaling, and apoptosis. Treatment with 3000 µM esculetin for 6 h increased apoptotic cell death by approximately 32-fold and elevated total oxidation status and oxidative stress index. Intracellular insulin, Ca²⁺, and CA19-9 levels were increased, accompanied by cell cycle arrest characterized by G0/G1 phase accumulation and a reduction in the G2/M population. Expression of ER stress sensors ATF6, IRE1α, and CHOP was upregulated, whereas PERK expression was reduced. In parallel, MAPK/JNK pathway activation was evidenced by increased levels of p-ATF2, p-c-Jun, and HSP90, along with decreased p-Elk1. Gene expression analysis revealed marked downregulation of β-cell functional and identity-associated genes, including Ins1, Ins2, IR, Akt, MafA, Nkx6.1, Pdx1, NeuroD1, and Pax6, while FoxO1 expression was upregulated. Collectively, these findings suggest the involvement of ER stress-associated MAPK/JNK signaling in esculetin-induced apoptosis and functional impairment in INS-1 pancreatic β-cells, providing mechanistic insight into stress-associated β-cell dysfunction. - Source: PubMed
Publication date: 2026/08/29
Karatug Kacar Ayse - Neuroendocrine tumors (NETs) associated with the intrapancreatic bile duct are rare and poorly characterized. Their relationship to conventional pancreatic neuroendocrine tumors (PanNETs) and to neuroendocrine cells of the periampullary and peribiliary regions remains unclear. A total of 199 resected NETs from the pancreas were evaluated for anatomical location and intrapancreatic bile duct narrowing. Transcription factor and hormone expression were assessed by whole-slide immunohistochemistry. For comparison, 22 duodenal NETs, 6 ampullary NETs and non-neoplastic duodenal, ampullary, and bile duct tissues were examined. Nineteen tumors (10%) were associated with bile duct narrowing, including 11 lower (periampullary) and 8 upper bile duct lesions. Compared with NETs without bile duct narrowing, these tumors were exclusively non-functioning, occurred more frequently in women and exhibited higher Ki-67 indices. Lower bile duct-narrowing tumors were associated with shorter progression-free survival. All but one bile duct-narrowing tumor expressed PDX1 (18/19, 95%), whereas CDX2 expression was observed in 73% (8/11) of lower bile duct-narrowing tumors. These tumors frequently expressed gastrin (73%) and somatostatin (73%), occasionally serotonin (27%), and lacked glucagon and insulin expression. Their transcription factor and hormone expression profiles closely resembled those of duodenal NETs and neuroendocrine cells of periampullary and peribiliary glands and differed from those of conventional PanNETs. Bile duct-narrowing NETs from the pancreas, particularly those involving the lower bile duct, represent a distinct clinicopathological subgroup characterized by a PDX1-positive, frequently CDX2-positive phenotype and enrichment for gastrin and somatostatin expression. Their resemblance to duodenal NETs and periampullary/peribiliary neuroendocrine cells supports a shared differentiation program and suggests a possible non-islet cell origin. - Source: PubMed
Publication date: 2026/08/27
Kasajima AtsukoUra AyakoEvert KatjaEvert MatthiasMärkl BrunoMoser ElisaSteiger KatjaMogler CarolinDemir Ihsan EkinMartignoni MarcEiber Matthiasvon Werder AlexanderFriess HelmutKlöppel Günter - Large MAF transcription factors, including MafA and MafB, are essential for maintaining β-cell identity, function and survival. While MafA has been widely studied in pancreas development and type 2 diabetes, the extended roles of MafB in humans are still emerging. During embryogenesis, MafB promotes differentiation of β-cells. While MafB is downregulated in adult mouse β-cells, it remains active in adult human β-cells, indicating important species-specific functions. Mechanistically, MafB cooperates with other β-cell-specific transcription factors, including PDX1, NEUROD1 and NKX6.1, to regulate genes critical for β-cell differentiation and insulin expression. Loss of MafB in human β-cells is associated with hallmark features of diabetic pathology, such as dedifferentiation, impaired insulin production, and transdifferentiation under metabolic stress. In addition to its endocrine roles within islets, MafB regulates macrophage polarization and apoptotic cell clearance, suggesting immune-metabolic interactions that may contribute to islet inflammation and dysfunction. Translationally, MafB may be leveraged to enhance stem-cell-derived β-cell differentiation and maturation and support β-cell identity preservation under stress and potentially immune responses; however, these applications remain to be further studied and validated. In this review, we integrate findings from developmental biology, animal models, and human studies to clarify the overarching role of MafB in bridging β-cell development, immune regulation, and potential translational application in stem-cell therapy or as a biomarker target in diabetes research. - Source: PubMed
Publication date: 2026/07/23
Mu-U-Min Razik Bin AbdulDiane AbdoulayeAl-Siddiqi Heba Hussain