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pancreatic cells

MMP-7 Marks Severe Pancreatic Cancer and Alters Tumor Cell Signaling by Proteolytic Release of Ectodomains

[Biochemical Society Transactions] Proteolytic shedding of multiple protein ectodomains by matrix metalloproteinase 7 (MMP-7) from pancreatic cancer cell surfaces influence apoptosis, proliferation, migration, and invasion.

Lundquist Institute Investigator Dr. Eiji Yoshihara Receives Internationally Prestigious Award for Research on Type 1 Diabetes

[The Lundquist Institute (Cision US, Inc.)] The Lundquist Institute's investigator Dr. Eiji Yoshihara has received a five-year $749,995.50 Career Development Award from the Juvenile Diabetes Research Foundation for his proposed study on how human β cells gain immune evasive function by environmental cues.

β-Cell-Specific Deletion of PFKFB3 Restores Cell Fitness Competition and Physiological Replication under Diabetogenic Stress

[Communications Biology] To discriminate the role of PFKFB3 from HIF1α in vivo, scientists generated mice with conditional β-cell specific disruption of the Pfkfb3 gene on a human islet pancreatic polypeptide background and a high-fat diet.

Opposing Effects on Regulated Insulin Secretion of Acute vs Chronic Stimulation of AMP-Activated Protein Kinase

[Diabetologia] Mouse lines that expressed a gain-of-function mutation in the γ1 AMP-activated protein kinase (AMPK) subunit D316a were generated to examine the effects of chronic AMPK stimulation in the whole body, or selectively in the beta cell.

Major Histocompatibility Complex Class I Molecule Expression by Pancreatic Cancer Cells Is Regulated by Activation and Inhibition of the Epidermal Growth Factor Receptor

[Immunologic Research] In this current study, the authors discovered that epidermal growth factor receptor affected major histocompatibility complex class I mRNA and protein expression by human pancreatic cancer cell lines.

Calcineurin/NFATc2 and PI3K/AKT Signaling Maintains β-Cell Identity and Function during Metabolic and Inflammatory Stress

[iScience] Scientists showed that intracellular Ca2+ and reactive oxygen species signals generated by high glucose and cytokine-induced endoplasmic reticulum stress activated calcineurin/NFATc2 and PI3K/AKT to maintain β-cell identity and function.

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