ArticleDevelopmental biology2012
Ongoing Notch signaling maintains phenotypic fidelity in the adult exocrine pancreas.
Article in Developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 84 citations in OpenAlex.
- Translating the blueprint of cell fate: eIF5A-mediated translation regulates cellular identity in the pancreas.Molecular metabolism · 2026Article
- NADPH-producing enzymes restrict the formation of pancreatic precancerous lesions.Nature metabolism · 2026Article
- Defensive tolerance drives the reprogramming and dysfunction of infiltrating pathogenic B cells assuring the maintenance of tolerance.Research square · 2025Article
- Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer.Developmental cell · 2025Article
- Lfng-expressing centroacinar cell is a unique cell-of-origin for p53 deficient pancreatic cancer.Oncogene · 2025Article
- Suppression of dystroglycan function accompanies pancreatic acinar-to-ductal metaplasia and favours dysplasia development.The Journal of pathology · 2024Article
- Muscle inflammation is regulated by NF-κB from multiple cells to control distinct states of wasting in cancer cachexia.Cell reports · 2024Article
- Dysfunction of infiltrating cytotoxic CD8+ T cells within the graft promotes murine kidney allotransplant tolerance.The Journal of clinical investigation · 2024Article
- Activin A signaling stimulates neutrophil activation and macrophage migration in pancreatitis.Scientific reports · 2024Article
- Radiolabeled NGR-Based Heterodimers for Angiogenesis Imaging: A Review of Preclinical Studies.Cancers · 2023Review
- Heterodimeric RGD-NGR PET Tracer for the Early Detection of Pancreatic Cancer.Molecular imaging and biology · 2022Article
- Dysregulated insulin secretion is associated with pancreatic β-cell hyperplasia and direct acinar-β-cell trans-differentiation in partially eNOS-deficient mice.Physiological reports · 2022Article
- Dendritic Inhibition by Shh Signaling-Dependent Stellate Cell Pool Is Critical for Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Molecular signaling in pancreatic ductal metaplasia: emerging biomarkers for detection and intervention of early pancreatic cancer.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Murine Models for Lineage Tracing Cancer Initiating Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Notch1 Has an Important Role in β-Cell Mass Determination and Development of Diabetes.Diabetes & metabolism journal · 2021Article
- Single-cell transcriptomes of pancreatic preinvasive lesions and cancer reveal acinar metaplastic cells' heterogeneity.Nature communications · 2020Article
- Acinar transformed ductal cells exhibit differential mucin expression in a tamoxifen-induced pancreatic ductal adenocarcinoma mouse model.Biology open · 2020Article
- Adult Pancreatic Acinar Progenitor-like Populations in Regeneration and Cancer.Trends in molecular medicine · 2020Review
- PRDM3 attenuates pancreatitis and pancreatic tumorigenesis by regulating inflammatory response.Cell death & disease · 2020Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The Notch signaling pathway regulates embryonic development of the pancreas, inhibiting progenitor differentiation into exocrine acinar and endocrine islet cells. The adult pancreas appears to lack progenitor cells, and its mature cell types are maintained by the proliferation of pre-existing differentiated cells. Nonetheless, Notch remains active in adult duct and terminal duct/centroacinar cells (CACs), in which its function is unknown. We previously developed mice in which cells expressing the Notch target gene Hes1 can be labeled and manipulated, by expression of Cre recombinase, and demonstrated that Hes1(+) CACs do not behave as acinar or islet progenitors in the uninjured pancreas, or as islet progenitors after pancreatic duct ligation. In the current study, we assessed the function of Notch signaling in the adult pancreas by deleting the transcription factor partner of Notch, Rbpj, specifically in Hes1(+) cells. We find that loss of Rbpj depletes the pancreas of Hes1-expressing CACs, abrogating their ongoing contribution to growth and homeostasis of more proximal duct structures. Upon Rbpj deletion, CACs undergo a rapid transformation into acinar cells, suggesting that constitutive Notch activity suppresses the acinar differentiation potential of CACs. Together, our data provide direct evidence of an endogenous genetic program to control interconversion of cell fates in the adult pancreas.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.