The Kunitz-protease inhibitor domain in amyloid precursor protein reduces cellular mitochondrial enzymes expression and function
Tài liệu tham khảo
Glenner, 1984, Alzheimer’s disease: initial report of the purification and characterization of a novel cerebrovascular amyloid protein, Biochem. Biophys. Res. Commun., 120, 885, 10.1016/S0006-291X(84)80190-4
Weidemann, 1989, Identification, biogenesis, and localization of precursors of Alzheimer’s disease A4 amyloid protein, Cell, 57, 115, 10.1016/0092-8674(89)90177-3
Golde, 1990, Expression of beta amyloid protein precursor mRNAs: recognition of a novel alternatively spliced form and quantitation in Alzheimer’s disease using PCR, Neuron, 4, 253, 10.1016/0896-6273(90)90100-T
Mattson, 1997, Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives, Physiol. Rev., 77, 1081, 10.1152/physrev.1997.77.4.1081
Johnson, 1990, Relation of neuronal APP-751/APP-695 mRNA ratio and neuritic plaque density in Alzheimer’s disease, Science, 248, 854, 10.1126/science.2111579
Preece, 2004, Amyloid precursor protein mRNA levels in Alzheimer’s disease brain, Brain Res. Mol. Brain Res., 122, 1, 10.1016/j.molbrainres.2003.08.022
Moir, 1998, Relative increase in Alzheimer’s disease of soluble forms of cerebral Abeta amyloid protein precursor containing the Kunitz protease inhibitory domain, J. Biol. Chem., 273, 5013, 10.1074/jbc.273.9.5013
Tanzi, 1988, Protease inhibitor domain encoded by an amyloid protein precursor mRNA associated with Alzheimer’s disease, Nature, 331, 528, 10.1038/331528a0
Hook, 1999, The Kunitz protease inhibitor form of the amyloid precursor protein (KPI/APP) inhibits the proneuropeptide processing enzyme prohormone thiol protease (PTP). colocalization of KPI/APP and PTP in secretory vesicles, J. Biol. Chem., 274, 3165, 10.1074/jbc.274.5.3165
Xu, 2009, AbetaPP/APLP2 family of Kunitz serine proteinase inhibitors regulate cerebral thrombosis, J. Neurosci., 29, 5666, 10.1523/JNEUROSCI.0095-09.2009
Salameh, 2010, The amyloid precursor protein/protease nexin 2 Kunitz inhibitor domain is a highly specific substrate of mesotrypsin, J. Biol. Chem., 285, 1939, 10.1074/jbc.M109.057216
Ho, 1996, The alternatively spliced Kunitz protease inhibitor domain alters amyloid beta protein precursor processing and amyloid beta protein production in cultured cells, J. Biol. Chem., 271, 30929, 10.1074/jbc.271.48.30929
Belyaev, 2010, The transcriptionally active amyloid precursor protein (APP) intracellular domain is preferentially produced from the 695 isoform of APP in a {beta}-secretase-dependent pathway, J. Biol. Chem., 285, 41443, 10.1074/jbc.M110.141390
Mattson, 2004, Pathways towards and away from Alzheimer’s disease, Nature, 430, 631, 10.1038/nature02621
Itoh, 2013, Mitochondrial dynamics in neurodegeneration, Trends Cell Biol., 23, 64, 10.1016/j.tcb.2012.10.006
Brooks, 2007, Gene expression profiles of metabolic enzyme transcripts in Alzheimer’s disease, Brain Res., 1127, 127, 10.1016/j.brainres.2006.09.106
Bubber, 2005, Mitochondrial abnormalities in Alzheimer brain: mechanistic implications, Ann. Neurol., 57, 695, 10.1002/ana.20474
Calkins, 2011, Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer’s disease, Hum. Mol. Genet., 20, 4515, 10.1093/hmg/ddr381
Liang, 2008, Alzheimer’s disease is associated with reduced expression of energy metabolism genes in posterior cingulate neurons, Proc. Natl. Acad. Sci. USA, 105, 4441, 10.1073/pnas.0709259105
Sheng, 2012, Impaired mitochondrial biogenesis contributes to mitochondrial dysfunction in Alzheimer’s disease, J. Neurochem., 120, 419, 10.1111/j.1471-4159.2011.07581.x
Wang, 2008, Amyloid-beta overproduction causes abnormal mitochondrial dynamics via differential modulation of mitochondrial fission/fusion proteins, Proc. Natl. Acad. Sci. USA, 105, 19318, 10.1073/pnas.0804871105
Tan, 2008, Effects of gamma-secretase cleavage-region mutations on APP processing and Abeta formation: interpretation with sequential cleavage and alpha-helical model, J. Neurochem., 107, 722, 10.1111/j.1471-4159.2008.05643.x
Mullan, 1992, A pathogenic mutation for probable Alzheimer’s disease in the APP gene at the N-terminus of beta-amyloid, Nat. Genet., 1, 345, 10.1038/ng0892-345
Mattson, 2002, Modification of brain aging and neurodegenerative disorders by genes, diet, and behavior, Physiol. Rev., 82, 637, 10.1152/physrev.00004.2002
Hilbich, 1993, Amyloid-like properties of peptides flanking the epitope of amyloid precursor protein-specific monoclonal antibody 22C11, J. Biol. Chem., 268, 26571, 10.1016/S0021-9258(19)74350-6
Hsiao, 1996, Correlative memory deficits, Abeta elevation, and amyloid plaques in transgenic mice, Science, 274, 99, 10.1126/science.274.5284.99
Mattson, 2002, Contributions of mitochondrial alterations, resulting from bad genes and a hostile environment, to the pathogenesis of Alzheimer’s disease, Int. Rev. Neurobiol., 53, 387, 10.1016/S0074-7742(02)53014-2
Anandatheerthavarada, 2003, Mitochondrial targeting and a novel transmembrane arrest of Alzheimer’s amyloid precursor protein impairs mitochondrial function in neuronal cells, J. Cell Biol., 161, 41, 10.1083/jcb.200207030
Devi, 2006, Accumulation of amyloid precursor protein in the mitochondrial import channels of human Alzheimer’s disease brain is associated with mitochondrial dysfunction, J. Neurosci., 26, 9057, 10.1523/JNEUROSCI.1469-06.2006
Wang, 2009, Impaired balance of mitochondrial fission and fusion in Alzheimer’s disease, J. Neurosci., 29, 9090, 10.1523/JNEUROSCI.1357-09.2009
Liesa, 2009, Mitochondrial dynamics in mammalian health and disease, Physiol. Rev., 89, 799, 10.1152/physrev.00030.2008
