Midnolin is a novel regulator of parkin expression and is associated with Parkinson’s Disease
暂无分享,去创建一个
[1] M. Brini,et al. Emerging (and converging) pathways in Parkinson's disease: keeping mitochondrial wellness. , 2017, Biochemical and biophysical research communications.
[2] A. Nairn. Faculty of 1000 evaluation for GDNF, NGF and BDNF as therapeutic options for neurodegeneration. , 2016 .
[3] W. Nemoto,et al. ERK5 induces ankrd1 for catecholamine biosynthesis and homeostasis in adrenal medullary cells. , 2016, Cellular signalling.
[4] H. Ariga. Common mechanisms of onset of cancer and neurodegenerative diseases. , 2015, Biological & pharmaceutical bulletin.
[5] Y. Obara,et al. Phosphorylation of ERK5 on Thr732 Is Associated with ERK5 Nuclear Localization and ERK5-Dependent Transcription , 2015, PloS one.
[6] S. Baltrusch,et al. Identification of the Ubiquitin-like Domain of Midnolin as a New Glucokinase Interaction Partner* , 2013, The Journal of Biological Chemistry.
[7] N. Patel,et al. GDNF, NGF and BDNF as therapeutic options for neurodegeneration. , 2013, Pharmacology & therapeutics.
[8] L. Greene,et al. ATF4 Protects Against Neuronal Death in Cellular Parkinson's Disease Models by Maintaining Levels of Parkin , 2013, The Journal of Neuroscience.
[9] P. Maher,et al. Mutation of ATF4 mediates resistance of neuronal cell lines against oxidative stress by inducing xCT expression , 2011, Cell Death and Differentiation.
[10] S. Koyama,et al. Authentically Phosphorylated α-Synuclein at Ser129 Accelerates Neurodegeneration in a Rat Model of Familial Parkinson's Disease , 2011, The Journal of Neuroscience.
[11] David S. Park,et al. Parkin is transcriptionally regulated by ATF4: evidence for an interconnection between mitochondrial stress and ER stress , 2011, Cell Death and Differentiation.
[12] W. Nemoto,et al. Basic fibroblast growth factor promotes glial cell-derived neurotrophic factor gene expression mediated by activation of ERK5 in rat C6 glioma cells. , 2011, Cellular signalling.
[13] David S. Park,et al. Neuronal Apoptosis Induced by Endoplasmic Reticulum Stress Is Regulated by ATF4–CHOP-Mediated Induction of the Bcl-2 Homology 3-Only Member PUMA , 2010, The Journal of Neuroscience.
[14] Y. Obara,et al. The Signaling Pathway Leading to Extracellular Signal-Regulated Kinase 5 (ERK5) Activation via G-Proteins and ERK5-Dependent Neurotrophic Effects , 2010, Molecular Pharmacology.
[15] Keiji Tanaka,et al. Does impairment of the ubiquitin-proteasome system or the autophagy-lysosome pathway predispose individuals to neurodegenerative disorders such as Parkinson's disease? , 2010, Journal of Alzheimer's disease : JAD.
[16] W. Nemoto,et al. ERK5 Activity Is Required for Nerve Growth Factor-induced Neurite Outgrowth and Stabilization of Tyrosine Hydroxylase in PC12 Cells* , 2009, The Journal of Biological Chemistry.
[17] R. Takahashi,et al. Pael‐R transgenic mice crossed with parkin deficient mice displayed progressive and selective catecholaminergic neuronal loss , 2008, Journal of neurochemistry.
[18] Giovanni Coppola,et al. ATF4 is an oxidative stress–inducible, prodeath transcription factor in neurons in vitro and in vivo , 2008, The Journal of experimental medicine.
[19] P. Coussens,et al. Differential expression of genes for transcription factors in theca and granulosa cells following selection of a dominant follicle in cattle , 2008, Molecular reproduction and development.
[20] Joseph T. Glessner,et al. PennCNV: an integrated hidden Markov model designed for high-resolution copy number variation detection in whole-genome SNP genotyping data. , 2007, Genome research.
[21] P. Stork,et al. The requirement of Ras and Rap1 for the activation of ERKs by cAMP, PACAP, and KCl in cerebellar granule cells , 2007, Journal of neurochemistry.
[22] W. Scheper,et al. Activation of the unfolded protein response in Parkinson's disease. , 2007, Biochemical and biophysical research communications.
[23] T. Iwatsubo,et al. The Role of G-Protein-Coupled Receptor Kinase 5 in Pathogenesis of Sporadic Parkinson's Disease , 2006, The Journal of Neuroscience.
[24] P. Stork,et al. PKA phosphorylation of Src mediates Rap1 activation in NGF and cAMP signaling in PC12 cells , 2004, Journal of Cell Science.
[25] Bryan L Roth,et al. Parkin-deficient Mice Exhibit Nigrostriatal Deficits but Not Loss of Dopaminergic Neurons* , 2003, Journal of Biological Chemistry.
[26] Santiago Canals,et al. Parkin gene inactivation alters behaviour and dopamine neurotransmission in the mouse. , 2003, Human molecular genetics.
[27] E. Kandel,et al. Rap1 Couples cAMP Signaling to a Distinct Pool of p42/44MAPK Regulating Excitability, Synaptic Plasticity, Learning, and Memory , 2003, Neuron.
[28] P. Lockhart,et al. Identification of a novel gene linked to parkin via a bi-directional promoter. , 2003, Journal of molecular biology.
[29] A. Markus,et al. Neurotrophic factors and axonal growth , 2002, Current Opinion in Neurobiology.
[30] A. Mungall,et al. The genomic structure and promoter region of the human parkin gene. , 2001, Biochemical and biophysical research communications.
[31] N. Hattori,et al. An Unfolded Putative Transmembrane Polypeptide, which Can Lead to Endoplasmic Reticulum Stress, Is a Substrate of Parkin , 2001, Cell.
[32] H. Suemori,et al. Novel nucleolar protein, midnolin, is expressed in the mesencephalon during mouse development. , 2000, Gene.
[33] E. Mccleskey,et al. Rap1 mediates sustained MAP kinase activation induced by nerve growth factor , 1998, Nature.