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)
- Fatty pancreas and pancreatitis are increasingly linked to Western dietary patterns and pancreatic cancer risk, yet intrinsic molecular mechanisms that preserve pancreatic identity under metabolic stress remain insufficiently defined. Heparanase-2 (Hpa2), a homolog of heparanase that lacks heparan sulfate-degrading activity, is clinically associated with favorable cancer outcomes, but its role in pancreatic homeostasis remains poorly defined. We fed wild-type (WT) and conditional Hpa2 knockout (Hpa2-KO) mice with a high-fat diet (HFD) and integrated histopathologic, transcriptomic, and proteomic analyses to define diet-dependent pancreatic responses. HFD elicited profound pancreatic remodeling selectively in Hpa2-KO mice, marked by massive fatty infiltration (fatty pancreas), extensive acinar-to-ductal metaplasia, β-islet hyperplasia, fibrosis, and pancreatic intraepithelial neoplasia (PanIN). These changes coincided with a decrease in acinar lineage identity, as reflected by marked suppression of GATA4, GATA6, MIST1, and PDX1. Systems-level analyses identified mTORC1 as a dominant signaling hub linking Hpa2 deficiency to metabolic reprogramming, with unanticipated effects on mitochondrial oxidative phosphorylation and ribosomal function. The results strongly imply that Hpa2 functions critically in preserving exocrine pancreatic identity and suppressing Western diet-driven pancreatic injury and neoplastic progression. Loss of Hpa2 advances diet-induced pancreatic disease, positioning Hpa2 as a key regulator of fatty pancreas, pancreatitis, and pancreatic cancer risk. - Source: PubMed
Publication date: 2026/05/01
Kayal YasminFarhoud MalikOdeh MaaliBarash UriNaroditsky InnaBassal RawanNishioka YasuhikoSanderson Ralph DIlan NetaVlodavsky Israel - () L. (Berberidaceae), deeply rooted in Iranian traditional medicine, exhibits significant antidiabetic potential attributed to its berberine content. This plant has been historically used for its glucose-lowering, anti-oxidant, and anti-inflammatory properties. This research investigated berberine's capacity to regenerate pancreatic β-cells in type 1 diabetic rats, specifically examining its dose-dependent effects on metabolic recovery, histopathological restoration, and molecular mechanisms underlying β-cell regeneration. - Source: PubMed
Salmanizadeh HosseinYazdanparast RaziehGhanadian Mustafa - Pancreatic ductal adenocarcinoma (PDAC) frequently invades adjacent peripancreatic adipose tissue, yet the role of tumour-infiltrating adipocytes (TIAs) in shaping antitumour immunity remains unclear. - Source: PubMed
Publication date: 2026/05/28
Luo YanYang JiayiLiu XinyuanZhang BinruYu TianhangGuan JianSong YiqinLi QiyuanLu TianqiLiu WeiZou LinzhuLin YongmingWu JiawenHan YunchengLi GuanqunYang XinleiZhang YingmeiTan HongtaoBai XueweiChen HuaHu JishengKong RuiSun Bei - Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer marked by dense stroma, immune suppression, and therapy resistance. While canonical NF-κB signaling has been extensively studied in PDAC, the non-canonical pathway and its key kinase, NF-κB-inducing kinase (NIK), remain less characterized. Here, we employed genetically engineered mouse models, including Pdx1-Cre; KRAS (KC), Pdx1-Cre; KRAS; p53 (KPC), and their NIK-deficient counterparts (KNiC and KPNiC). To mimic inflammation-driven tumorigenesis observed in human PDAC, we administered cerulein in the KC and KNiC mice to induce pancreatitis and promote lesion progression. We found that NIK deletion accelerated lesion formation, progression to high-grade PanINs and invasive carcinoma in both KC and KPC backgrounds. Despite similar tumor grade and burden at endpoint, KPNiC mice exhibited shortened survival compared to controls, indicating that NIK acts as a tumor-suppressor and limits early-stage tumor progression. Mechanistically, NIK loss was associated with elevated ERK signaling that increased lesion cell proliferation, and also reduced acinar cell death following pancreatitis. In the tumor microenvironment, NIK deletion promoted myofibroblast activation and enrichment of myCAF-associated gene expression, likely through secondary activation of canonical NF-κB and pro-fibrotic signaling pathways such as TGF-β, Wnt, and FGF. Finally, increased IL6-STAT3 signaling and neutrophil infiltration were observed, suggesting broader immunostromal remodeling in the absence of NIK. Consistent with these findings, analysis of TCGA-PAAD data showed that low NIK expression correlates with poor overall survival in human PDAC. These findings reveal a tumor-suppressive role of NIK in pancreatic cancer and underscore the need for caution in targeting NF-κB signaling, as balanced pathway activity appears critical for regulating early tumor progression and microenvironmental interactions in PDAC. - Source: PubMed
Publication date: 2026/05/27
Du ZiweiBüttner Ulrike F GWirth Hannah LeaGerstenlauer MelanieManfras UtaLoidl RikardaBahçeci DoğaSteiger KatjaMetzler ThomasChan Lap KwanTsesmelis MiltiadisWirth Thomas - Recent studies have identified ATRX/DAXX and PDX1/ARX as biomarkers defining novel pancreatic neuroendocrine tumor (PanNET) subtypes, while the clinical significance of somatostatin receptors (SSTRs) remains incompletely understood. - Source: PubMed
Publication date: 2026/05/11
Ciobanu Oana AMartin Carmen SorinaFica SimonaHerlea VladTudose IrinaVasilescu FlorinaSandra IrinaBarbu Carmen G