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X-box-binding protein 1 (XBP1) is a protein containing the basic leucine zipper structure. It belongs to the cAMP-response element binding protein (CREB)/activating transcription factor transcription factor family. As the main transcription factor, spliced XBP1 (XBP1s) participates in many physiological and pathological processes and plays an important role in embryonic development. Previous studies showed that XBP1-knockout mice died because of pancreatic exocrine function deficiency, indicating that XBP1 plays an important role in pancreatic development. However, the exact role of XBP1 in pancreatic development remains unclear. This study aimed to investigate the role of XBP1 in the pancreatic development of Xenopus laevis embryos. Whole-mount in situ hybridization and quantitative real-time PCR results revealed that the expression levels of pancreatic progenitor marker genes pdx1, p48, ngn3, and sox9 were downregulated in XBP1s morpholino oligonucleotide (MO)-injected embryos. The expression levels of pancreatic exocrine and endocrine marker genes insulin and amylase were also downregulated. Through the overexpression of XBP1s, the phenotype and gene expressions were opposite to those in XBP1s MO-injected embryos. Luciferase and chromatin immunoprecipitation assays showed that XBP1s could bind to the XBP1-binding site in the foxa2 promoter. These results revealed that XBP1 is required in the pancreatic development of Xenopus laevis and might function by regulating foxa2.
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http://dx.doi.org/10.1093/abbs/gmaa114 | DOI Listing |
J Clin Invest
September 2025
Department of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter, United Kingdom.
Understanding the genetic causes of diseases affecting pancreatic β cells and neurons can give insights into pathways essential for both cell types. Microcephaly, epilepsy and diabetes syndrome (MEDS) is a congenital disorder with two known aetiological genes, IER3IP1 and YIPF5. Both genes encode proteins involved in endoplasmic reticulum (ER) to Golgi trafficking.
View Article and Find Full Text PDFWorld J Pediatr
September 2025
Department of Hepatobiliary and Pancreatic Surgery, the First Affiliated Hospital, Zhejiang University School of Medicine, No. 79 Qingchun Road, Hangzhou 310003, China.
Background: Carbapenem-resistant Enterobacteriaceae (CRE) infections can pose a significant risk following pediatric liver transplantations. This study aimed to identify risk factors for CRE infections and develop prediction models for pediatric recipients.
Methods: This study enrolled pediatric patients who underwent liver transplantation between 2017 and 2023.
Khirurgiia (Mosk)
September 2025
Kuban State Medical University, Krasnodar, Russia.
Objective: To validate and assess clinical efficacy of a prognostic model for predicting severe acute pancreatitis (SAP) based on inflammatory markers (IL-6, ΔIL-22), thromboelastography parameters (K-time) and the BISAP score.
Material And Methods: A prospective observational cohort study enrolled 181 patients with acute pancreatitis. Serum IL-6 and IL-22 were measured in 24 and 48 hours after clinical manifestation, respectively.
Int J Surg
September 2025
Department of Ultrasound, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou 310003, China.
Background: Pancreatic cancer (PC) presents a significant therapeutic challenge due to its immunosuppressive tumor microenvironment (TME). Emerging evidence supports the efficacy of high-voltage electrical pulses (HVEPs) in PC treatment, leveraging dual benefits of pancreatobiliary duct integrity maintenance and immunogenicity activation.
Objective: PubMed, Embase, Cochrane Library, and Web of Science were searched from January 2000 to January 2025.
J Obes
September 2025
School of Natural Sciences, University of Lincoln, Lincoln, UK.
To investigate the genetic determinants of fat distribution across anatomical sites and their implications for health outcomes. We analyzed neck-to-knee MRI data from the UK Biobank ( = 37,589) to measure fat at various locations and used Mendelian randomization to assess effects on 26 obesity-related diseases and 94 biomarkers from FinnGen and other consortia. We identified genetic loci associated with 10 fat depots: abdominal subcutaneous adipose tissue ( = 2 loci), thigh subcutaneous adipose tissue (25), thigh intermuscular adipose tissue (15), visceral adipose tissue (7), liver proton density fat fraction (PDFF) (8), pancreas PDFF (11), paraspinal adipose tissue (9), pelvic bone marrow fat (28), thigh bone marrow fat (27), and vertebrae bone marrow fat (5).
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