Leupeptins

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  Subject Areas on Research

  • Antigen-presenting cell lines internalize peptide antigens via fluid-phase endocytosis. 
  • Calpain-mediated AQP2 proteolysis in inner medullary collecting duct. 
  • Catalytic autoantibodies against myelin basic protein (MBP) isolated from serum of autistic children impair in vitro models of synaptic plasticity in rat hippocampus. 
  • Chaperone-mediated 26S proteasome remodeling facilitates free K63 ubiquitin chain production and aggresome clearance. 
  • Chemical Modulation of Endocytic Sorting Augments Adeno-associated Viral Transduction. 
  • Diversity in membrane binding sites of ankyrins. Brain ankyrin, erythrocyte ankyrin, and processed erythrocyte ankyrin associate with distinct sites in kidney microsomes. 
  • Effects of TNFalpha on expression of ICAM-1 in human airway epithelial cells in vitro: oxidant-mediated pathways and transcription factors. 
  • HDAC6 controls major cell response pathways to cytotoxic accumulation of protein aggregates. 
  • Interleukin-3-induced activation of the JAK/STAT pathway is prolonged by proteasome inhibitors. 
  • Merlin facilitates ubiquitination and degradation of transactivation-responsive RNA-binding protein. 
  • Nuclear factor-kappa B regulates pain and COMT expression in a rodent model of inflammation. 
  • Nuclear factor-kappaB is constitutively activated in primitive human acute myelogenous leukemia cells. 
  • Prevention of brefeldin A-induced resistance to teniposide by the proteasome inhibitor MG-132: involvement of NF-kappaB activation in drug resistance. 
  • Regulation of RIPK3- and RHIM-dependent Necroptosis by the Proteasome. 
  • Regulation of beta-catenin signaling by the B56 subunit of protein phosphatase 2A. 
  • Requirement of dendritic Akt degradation by the ubiquitin-proteasome system for neuronal polarity. 
  • Suppression of NF-kappaB-dependent proinflammatory gene expression in human RPE cells by a proteasome inhibitor. 
  • The bacterial effector HopM1 suppresses PAMP-triggered oxidative burst and stomatal immunity. 
  • The turnover of estrogen receptor α by the selective estrogen receptor degrader (SERD) fulvestrant is a saturable process that is not required for antagonist efficacy. 
  • VCP is essential for mitochondrial quality control by PINK1/Parkin and this function is impaired by VCP mutations. 
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  Keywords of People

  • Bennett, Vann, George Barth Geller Distinguished Professor of Molecular Biology, Duke Cancer Institute
  • McDonnell, Donald Patrick, Glaxo-Wellcome Distinguished Professor of Molecular Cancer Biology, in the School of Medicine, Duke Innovation & Entrepreneurship