hes1-protein--human and Pancreatitis

hes1-protein--human has been researched along with Pancreatitis* in 2 studies

Other Studies

2 other study(ies) available for hes1-protein--human and Pancreatitis

ArticleYear
MicroRNA-361-5p Aggravates Acute Pancreatitis by Promoting Interleukin-17A Secretion
    Journal of medicinal chemistry, 2021, 11-25, Volume: 64, Issue:22

    This study set out to explore the potential role of microRNA-361-5p (miR-361-5p) in acute pancreatitis through regulation of interleukin-17A (IL-17A). We first identified the expression of miR-361-5p, IL-17A, nuclear factor IA (NFIA), and hes family bHLH transcription factor 1 (Hes1) in serum samples collected from patients with acute pancreatitis, caerulein-induced mice, and a Th17 cell model. The predicted binding of miR-361-5p to NFIA was confirmed

    Topics: Animals; Case-Control Studies; Disease Models, Animal; Down-Regulation; Humans; Interleukin-17; Mice; MicroRNAs; NFI Transcription Factors; Nuclear Proteins; Pancreatitis; Th17 Cells; Transcription Factor HES-1

2021
Hes1 Controls Exocrine Cell Plasticity and Restricts Development of Pancreatic Ductal Adenocarcinoma in a Mouse Model.
    The American journal of pathology, 2016, Volume: 186, Issue:11

    Perturbation of pancreatic acinar cell state can lead to acinar-to-ductal metaplasia (ADM), a precursor lesion to the development of pancreatic ductal adenocarcinoma (PDAC). In the pancreas, Notch signaling is active both during development and in adult cellular differentiation processes. Hes1, a key downstream target of the Notch signaling pathway, is expressed in the centroacinar compartment of the adult pancreas as well as in both preneoplastic and malignant lesions. In this study, we used a murine genetic in vivo approach to ablate Hes1 in pancreatic progenitor cells (Ptf1a

    Topics: Acinar Cells; Animals; Carcinogenesis; Carcinoma, Pancreatic Ductal; Cell Differentiation; Cell Plasticity; Ceruletide; Disease Models, Animal; Female; Humans; Male; Metaplasia; Mice; Pancreas; Pancreas, Exocrine; Pancreatic Neoplasms; Pancreatitis; Regeneration; Signal Transduction; Stem Cells; Transcription Factor HES-1

2016