Research Topics
Genomes and Genes
| Yuzuru ImaiSummaryAffiliation: Tohoku University Country: Japan Publications
| Collaborators
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Detail Information
Publications
The loss of PGAM5 suppresses the mitochondrial degeneration caused by inactivation of PINK1 in DrosophilaYuzuru Imai
Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan
PLoS Genet 6:e1001229. 2010..These results suggest that PGAM5 negatively regulates the PINK1 pathway related to maintenance of the mitochondria and, furthermore, that PGAM5 acts between PINK1 and Parkin, or functions independently of Parkin downstream of PINK1...- Phosphorylation of 4E-BP by LRRK2 affects the maintenance of dopaminergic neurons in DrosophilaYuzuru Imai
Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan
EMBO J 27:2432-43. 2008..Our results suggest that chronic inactivation of 4E-BP by LRRK2 with pathogenic mutations deregulates protein translation, eventually resulting in age-dependent loss of DA neurons... 
Pael receptor is involved in dopamine metabolism in the nigrostriatal systemYuzuru Imai
Laboratory for Motor System Neurodegeneration, RIKEN Brain Science Institute BSI, Saitama, Japan
Neurosci Res 59:413-25. 2007..These results strongly suggest that the Pael-R signal regulates the amount of DA in the dopaminergic neurons and that excessive Pael-R expression renders dopaminergic neurons susceptible to chronic DA toxicity...- A product of the human gene adjacent to parkin is a component of Lewy bodies and suppresses Pael receptor-induced cell deathYuzuru Imai
Laboratory for Motor System Neurodegeneration, RIKEN Brain Science Institute, Saitama 351 0198, Japan
J Biol Chem 278:51901-10. 2003..These data suggest that Glup may play an important role in the formation of Lewy bodies and protection of dopaminergic neurons against Parkinson's disease... - Pael receptor, endoplasmic reticulum stress, and Parkinson's diseaseRyosuke Takahashi
Laboratory of Motor Neurodegeneration, RIKEN Brain Science Institute BSI, 2 1 Hirosawa, Wako, 351 0198, Saitama, Japan
J Neurol 250:III25-9. 2003..We found that CHIP enhanced parkinmediated ubiquitination of Pael-R. In concert with Hsp70, CHIP also enhanced the ability of parkin to inhibit cell death induced by Pael-R, indicating that CHIP and Hsp70 are both co-factors of parkin... 
Activation of FoxO by LRRK2 induces expression of proapoptotic proteins and alters survival of postmitotic dopaminergic neuron in DrosophilaTomoko Kanao
Institute of Development, Aging and Cancer, Tohoku University, 4 1 Seiryo machi, Aoba ku, Sendai 980 8575, Japan
Hum Mol Genet 19:3747-58. 2010..These data suggest that the cell death molecules regulated by FoxO are key factors during the neurodegeneration in LRRK2-linked PD...- [Frontier researches for the development of molecular-targeted therapies for familial Parkinson disease]Yuzuru Imai
Institute of Development, Aging and Cancer, Tohoku University, 4 1 Seiryo machi, Aoba ku, Sendai, Miyagi 980 8575, Japan
Brain Nerve 61:903-13. 2009.... - CHIP is associated with Parkin, a gene responsible for familial Parkinson's disease, and enhances its ubiquitin ligase activityYuzuru Imai
Laboratory for Motor System Neurodegeneration, RIKEN Brain Science Institute, Saitama 351 0198, Japan
Mol Cell 10:55-67. 2002..Furthermore, CHIP enhanced the ability of Parkin to inhibit cell death induced by Pael-R. Taken together, these results indicate that CHIP is a mammalian E4-like molecule that positively regulates Parkin E3 activity... - In vivo evidence of CHIP up-regulation attenuating tau aggregationNaruhiko Sahara
Laboratory for Alzheimer s Disease, RIKEN Brain Science Institute, Saitama, Japan
J Neurochem 94:1254-63. 2005..If confirmed, this would indicate that the quality-control machinery in a neuron might play an important role in retarding the pathogenesis of tauopathies... - Parkin and endoplasmic reticulum stressRyosuke Takahashi
Laboratory for Motor System Neurodegeneration, RIKEN Brain Science Institute, Saitama 351 0198, Japan
Ann N Y Acad Sci 991:101-6. 2003..In conclusion, we showed that the accumulation of unfolded Pael receptor (a substrate of parkin) may cause selective death of dopaminergic neurons in AR-JP... - How do Parkin mutations result in neurodegeneration?Yuzuru Imai
Motor System Neurodegeneration, RIKEN Brain Science Institute BSI, Saitama 351 0198, Japan
Curr Opin Neurobiol 14:384-9. 2004..Further investigation of Parkin knockout mice will hopefully provide new evidence in the search for Parkin's substrates and further clarify their role in Parkinson's disease... - [Parkin protein and molecular mechanism of Parkinson's disease]Yuzuru Imai
Nippon Ronen Igakkai Zasshi 41:619-21. 2004 - Pael-R is accumulated in Lewy bodies of Parkinson's diseaseTetsuro Murakami
Department of Neurology, Okayama University Graduate School of Medicine and Dentistry, 2 5 1 Shikata cho, Okayama 700 8558, Japan
Ann Neurol 55:439-42. 2004..The absence of Pael-R and Parkin in glial cytoplasmic inclusions (GCIs) in MSA implies a distinct pathway involved in the formation of LBs and GCIs... - [Dopaminergic neuronal death in Parkinson's disease: is accumulation of unfolded proteins a cause or effect?]Yuzuru Imai
Tanpakushitsu Kakusan Koso 49:1113-7. 2004 - Activation of PAR-1 kinase and stimulation of tau phosphorylation by diverse signals require the tumor suppressor protein LKB1Ji Wu Wang
Department of Pathology, Stanford University School of Medicine, and Geriatric Research, Education, and Clinical Center Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304, USA
J Neurosci 27:574-81. 2007..These results reveal a new function for the tumor suppressor protein LKB1 in a signaling cascade through which the phosphorylation and function of tau is regulated by diverse signals under physiological and pathological conditions... - Pael receptor induces death of dopaminergic neurons in the substantia nigra via endoplasmic reticulum stress and dopamine toxicity, which is enhanced under condition of parkin inactivationYasuko Kitao
Department of Neuroanatomy, Kanazawa University Medical School, 13 1, Takara machi, Kanazawa City, 920 8640 Ishikawa, Japan
Hum Mol Genet 16:50-60. 2007..These data suggest a model in which ER- and dopamine-related stress are major contributors to decreased viability of dopaminergic neurons in a setting relevant to Parkinson's disease... - Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by ParkinYufeng Yang
Department of Pathology and Geriatric Research, Education and Clinical Center Veterans Affairs Palo Alto Health Care System, Stanford University School of Medicine, Palo Alto, CA 94304, USA
Proc Natl Acad Sci U S A 103:10793-8. 2006..Together, these results implicate Pink1 and Parkin in a common pathway that regulates mitochondrial physiology and cell survival in Drosophila... - Inactivation of Drosophila DJ-1 leads to impairments of oxidative stress response and phosphatidylinositol 3-kinase/Akt signalingYufeng Yang
Department of Pathology, Stanford University School of Medicine, and Geriatric Research, Education and Clinical Center Veterans Affairs Palo Alto Health Care System, Palo Alto, CA 94304, USA
Proc Natl Acad Sci U S A 102:13670-5. 2005..Manipulation of PI3K/Akt signaling may therefore offer therapeutic benefits for the treatment of PD... - Parkin suppresses dopaminergic neuron-selective neurotoxicity induced by Pael-R in DrosophilaYufeng Yang
Laboratory of Developmental Neurobiology, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA
Neuron 37:911-24. 2003..Our study implicates Parkin as a central player in the molecular pathway of Parkinson's disease (PD) and suggests that manipulating Parkin expression may provide a novel avenue of PD therapy... - Pael-R transgenic mice crossed with parkin deficient mice displayed progressive and selective catecholaminergic neuronal lossHua Qin Wang
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
J Neurochem 107:171-85. 2008..parkin-ko/Pael-R-tg mice represents an AR-JP mouse model displaying chronic and selective loss of catecholaminergic neurons... - Rines/RNF180, a novel RING finger gene-encoded product, is a membrane-bound ubiquitin ligaseMiyuki Ogawa
Laboratory for Comparative Neurogenesis, RIKEN Brain Science Institute, Wako Shi, Saitama 351 0198, Japan
Genes Cells 13:397-409. 2008..These results suggest that Rines is a membrane-bound E3 ubiquitin ligase... - Cell type-specific upregulation of Parkin in response to ER stressHua Qin Wang
Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan
Antioxid Redox Signal 9:533-42. 2007..Luciferase assays failed to detect the transcriptional activation of 500 bp parkin/Glup promoter in response to ER stress. These results indicate that induction of parkin by ER stress represents a cell type-specific response... - Parkin phosphorylation and modulation of its E3 ubiquitin ligase activityAyako Yamamoto
Laboratory of Alzheimer s and Parkinson s Disease Research, Department of Metabolic Biochemistry, Ludwig Maximilians University, 80336 Munich, Germany
J Biol Chem 280:3390-9. 2005..Thus, complex regulation of the phosphorylation state of parkin may contribute to the unfolded protein response in stressed cells... - The neuropeptide head activator is a high-affinity ligand for the orphan G-protein-coupled receptor GPR37Meriem Rezgaoui
, , Martinistr. 52, 20246 Hamburg, Germany
J Cell Sci 119:542-9. 2006....