Leupeptins
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Subject Areas on Research
- Agonist-induced internalization of the substance P (NK1) receptor expressed in epithelial cells.
- 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 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 B. Geller Professor for Research in Molecular Biology in the School of Medicine, Duke Cancer Institute
- McDonnell, Donald Patrick, Chair, Department of Pharmacology & Cancer Biology, Duke Innovation & Entrepreneurship