Research Topics
Genomes and Genes
| Hoon RyuSummaryAffiliation: Boston University Country: USA Publications
Research Grants
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Detail Information
Publications
Mitochondrial cyclic AMP response element-binding protein (CREB) mediates mitochondrial gene expression and neuronal survivalJunghee Lee
Neurology Department, Boston University School of Medicine, Boston, Massachusetts 02118, USA
J Biol Chem 280:40398-401. 2005....- Ibuprofen reduces Abeta, hyperphosphorylated tau and memory deficits in Alzheimer miceAnn C McKee
Department of Neurology, Boston University School of Medicine, Boston, MA, USA
Brain Res 1207:225-36. 2008..These findings provide further support for intraneuronal Abeta as a cause of cognitive impairment, and suggest that pathological alterations of tau are associated with intraneuronal oligomeric Abeta accumulation... - Differential expression of c-Ret in motor neurons versus non-neuronal cells is linked to the pathogenesis of ALSHoon Ryu
Department of Neurology and Pathology, Boston University School of Medicine, VA Boston Healthcare System, Boston, MA 02130, USA
Lab Invest 91:342-52. 2011..Furthermore, the induction of c-Ret expression in microglia may contribute to non-cell autonomous cell death of motor neurons by available GDNF in ALS... - ESET/SETDB1 gene expression and histone H3 (K9) trimethylation in Huntington's diseaseHoon Ryu
Geriatric Research Education and Clinical Center, Bedford Veteran s Affairs Medical Center, Bedford, MA 01730, USA
Proc Natl Acad Sci U S A 103:19176-81. 2006..Our data suggest that modulation of gene silencing mechanisms, through regulation of the ESET gene is important to neuronal survival and, as such, may be a promising treatment in HD patients... - Antioxidants modulate mitochondrial PKA and increase CREB binding to D-loop DNA of the mitochondrial genome in neuronsHoon Ryu
Geriatric Research Education and Clinical Center, Veteran s Affairs Medical Center, Bedford, MA 01730, USA
Proc Natl Acad Sci U S A 102:13915-20. 2005..These results suggest that the regulation of mitochondrial function via the mitochondrial PKA and CREB pathways may underlie some of the salutary effects of DFO in neurons... - Modulation of lipid peroxidation and mitochondrial function improves neuropathology in Huntington's disease miceJunghee Lee
Department of Neurology and Pathology, Boston University School of Medicine, Boston, MA 02118, USA
Acta Neuropathol 121:487-98. 2011..The present findings suggest that further therapeutic studies using NDGA are warranted in HD and other neurodegenerative diseases characterized by increased oxidative stress and altered mitochondrial function... 
Histone deacetylase inhibition by sodium butyrate chemotherapy ameliorates the neurodegenerative phenotype in Huntington's disease miceRobert J Ferrante
Geriatric Research Education and Clinical Center, Bedford Veterans Affairs Medical Center, Bedford, Massachusetts 01730, USA
J Neurosci 23:9418-27. 2003....- Combination therapy using minocycline and coenzyme Q10 in R6/2 transgenic Huntington's disease miceEdward C Stack
Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford, MA 01730, USA
Biochim Biophys Acta 1762:373-80. 2006..These data suggest that combined minocycline and CoQ10 treatment may offer therapeutic benefit to patients suffering from HD... - Sodium phenylbutyrate prolongs survival and regulates expression of anti-apoptotic genes in transgenic amyotrophic lateral sclerosis miceHoon Ryu
Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford, Massachusetts, USA
J Neurochem 93:1087-98. 2005..Phenylbutyrate may therefore provide a novel therapeutic approach for the treatment of patients with ALS... - Modulation of nucleosome dynamics in Huntington's diseaseEdward C Stack
Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford, MA 01730, USA
Hum Mol Genet 16:1164-75. 2007..These data show the ability of anthracycline compounds to rebalance epigenetic histone modification and, as such, may provide the rationale for the design of human clinical trials in HD patients... - Dose ranging and efficacy study of high-dose coenzyme Q10 formulations in Huntington's disease miceKaren M Smith
Geriatric Research Education and Clinical Center, Bedford VA Medical Center, Bedford 01730, and Neurology Department, Boston University School of Medicine, MA 02180, USA
Biochim Biophys Acta 1762:616-26. 2006.... - Role of cyclooxygenase-2 induction by transcription factor Sp1 and Sp3 in neuronal oxidative and DNA damage responseJunghee Lee
Geriatric Research Education and Clinical Center, Bedford Veteran s Affairs Medical Center, 200 Springs Rd, Bedford, MA 01730, USA
FASEB J 20:2375-7. 2006..These results indicate that in primary neurons Sp1 and Sp3 play an essential role in the modulation of COX-2 transcription, which mediates neuronal homeostasis and survival by preventing DNA damage in response to neuronal stress... - Chemotherapy for the brain: the antitumor antibiotic mithramycin prolongs survival in a mouse model of Huntington's diseaseRobert J Ferrante
Geriatric Research and Education and Clinical Center, Veterans Administration Medical Center, Bedford, MA, USA
J Neurosci 24:10335-42. 2004..Because it is Food and Drug Administration-approved, mithramycin is a promising drug for the treatment of HD... - Activation of Ets-2 by oxidative stress induces Bcl-xL expression and accounts for glial survival in amyotrophic lateral sclerosisJunghee Lee
Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA
FASEB J 23:1739-49. 2009..This survival pathway may contribute to the glial survival and activation seen in the spinal cord of ALS patients... - Sp1 and Sp3 are oxidative stress-inducible, antideath transcription factors in cortical neuronsHoon Ryu
Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
J Neurosci 23:3597-606. 2003..Taken together, these results establish Sp1 and Sp3 as oxidative stress-induced transcription factors in cortical neurons that positively regulate neuronal survival... - Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitisSandra Camelo
Laboratory of Transcriptional and Immune Regulation, Brigham and Women's Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02139, USA
J Neuroimmunol 164:10-21. 2005..A transcriptional imbalance in MS may contribute to immune dysregulation and neurodegeneration, and we identify HDAC inhibition as a transcriptional intervention to ameliorate this imbalance... 
Therapeutic attenuation of mitochondrial dysfunction and oxidative stress in neurotoxin models of Parkinson's diseaseEdward C Stack
Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
Biochim Biophys Acta 1782:151-62. 2008..Together these findings show cystamine's therapeutic benefit to reduce neuronal loss through attenuation of oxidative stress and mitochondrial dysfunction, providing the rationale for human clinical trials in PD patients...- Prosurvival and prodeath effects of hypoxia-inducible factor-1alpha stabilization in a murine hippocampal cell lineLeila R Aminova
Department of Neurology and Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
J Biol Chem 280:3996-4003. 2005..Together, these data demonstrate that HIF-1 can mediate prodeath or prosurvival responses in the same cell type depending on the injury stimulus... - Chronology of behavioral symptoms and neuropathological sequela in R6/2 Huntington's disease transgenic miceEdward C Stack
Geriatric Research Education and Clinical Center, Bedford Veterans Administration Medical Center, Bedford, Massachusetts 01730, USA
J Comp Neurol 490:354-70. 2005.... - Motor neuronal protection by L-arginine prolongs survival of mutant SOD1 (G93A) ALS miceJunghee Lee
Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
Biochem Biophys Res Commun 384:524-9. 2009..Our findings show that L-arginine has potent in vitro and in vivo neuroprotective properties and may be a candidate for therapeutic trials in ALS... - Monoallele deletion of CBP leads to pericentromeric heterochromatin condensation through ESET expression and histone H3 (K9) methylationJunghee Lee
Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
Hum Mol Genet 17:1774-82. 2008..These results establish an alternative pathway that loss of CBP leads to the pericentric heterochromatin condensation through ESET expression and trimethylation of H3 (K9)... - Differential regulation of neuronal and inducible nitric oxide synthase (NOS) in the spinal cord of mutant SOD1 (G93A) ALS miceJunghee Lee
Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
Biochem Biophys Res Commun 387:202-6. 2009..This suggests that therapy focused on iNOS inhibition might be a fruitful direction for future ALS therapeutic trials... - Histone deacetylase inhibitors prevent oxidative neuronal death independent of expanded polyglutamine repeats via an Sp1-dependent pathwayHoon Ryu
Department of Neurology and Program in Neuroscience, Harvard Medical School and Beth Israel Deaconess Medical Center, Harvard Institutes of Medicine, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 100:4281-6. 2003..Together, these results demonstrate that HDAC inhibitors inhibit oxidative death independent of polyglutamine expansions by activating an Sp1-dependent adaptive response... - MKK6 binds and regulates expression of Parkinson's disease-related protein LRRK2Cindy H Hsu
Department of Pharmacology, Boston University School of Medicine, Boston, Massachusetts 02118 2526, USA
J Neurochem 112:1593-604. 2010..These results were confirmed by deletion of sek-1 in C. elegans. These data demonstrate that MKKs and LRRK2 function in similar biological pathways, and support a role for LRRK2 in modulating the cellular stress response... - Increased stem cell proliferation in the spinal cord of adult amyotrophic lateral sclerosis transgenic miceYing jun Guan
Neuroapoptosis Laboratory, Department of Neurosurgery, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
J Neurochem 102:1125-38. 2007..Further studies will determine if this endogenous regenerative process can be enhanced and directed so as to slow or even reverse the natural progression of this devastating disease... - Mitochondrial nuclear receptors and transcription factors: who's minding the cell?Junghee Lee
Department of Neurology, Boston University School of Medicine, Boston, Massachusetts, USA
J Neurosci Res 86:961-71. 2008..Thus, the modulation of signaling pathways via mitochondria-targeting nuclear receptors and transcription factors is rapidly emerging as a novel therapeutic target... - Translational therapeutic strategies in amyotrophic lateral sclerosisHoon Ryu
Experimental Neuropathology Unit and Translational Therapeutics Laboratory, GRECC Unit 182B, Bedford VA Medical Center, 200 Springs Road, Bedford, MA 01730, USA
Mini Rev Med Chem 7:141-50. 2007..As in other neurodegenerative diseases, the most effective neuroprotection may result from combined treatment strategies... - Genetic and pharmacological inactivation of the adenosine A2A receptor attenuates 3-nitropropionic acid-induced striatal damageJ Stephen Fink
Department of Neurology, Boston University School of Medicine, MA 02118, USA
J Neurochem 88:538-44. 2004.... - Translational control of inducible nitric oxide synthase expression by arginine can explain the arginine paradoxJunghee Lee
Deparment of Neurology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 100:4843-8. 2003..These results provide an explanation for the arginine paradox for iNOS and define a distinct mechanism by which a substrate can regulate the activity of its associated enzyme... - The failure of mitochondria leads to neurodegeneration: Do mitochondria need a jump start?Junghee Lee
Department of Neurology, Boston University School of Medicine, MA 02118, USA
Adv Drug Deliv Rev 61:1316-23. 2009..This review focuses on how mitochondria are involved in neurodegeneration and what therapeutics are available to target mitochondrial pathways... - In vitro model of oxidative stress in cortical neuronsRajiv R Ratan
Department of Neurology, Harvard Medical School, Boston, Massachusetts 02115, USA
Methods Enzymol 352:183-90. 2002 - Emerging chemotherapeutic strategies for Huntington's diseaseHoon Ryu
Boston University School of Medicine, Edith Nourse Rogers Veterans Administration Medical Center, Bedford, Massachusetts 01730, USA
Expert Opin Emerg Drugs 10:345-63. 2005..These compounds are discussed herein... - The therapeutic role of creatine in Huntington's diseaseHoon Ryu
Experimental Neuropathology Unit and Translational Therapeutics Laboratory, Geriatric Research Education Clinical Center, Bedford VA Medical Center, MA 01730, USA
Pharmacol Ther 108:193-207. 2005.... - ASC is a Bax adaptor and regulates the p53-Bax mitochondrial apoptosis pathwayTakao Ohtsuka
Cancer Biology Program, Hematology Oncology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02115, USA
Nat Cell Biol 6:121-8. 2004..Our findings demonstrate that ASC has an essential role in the intrinsic mitochondrial pathway of apoptosis through a p53-Bax network... - Neuroprotective effects of phenylbutyrate in the N171-82Q transgenic mouse model of Huntington's diseaseGabriella Gardian
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York-Presbyterian Hospital, New York, New York 10021, USA
J Biol Chem 280:556-63. 2005.... - Molecular basis of vitamin E action: tocotrienol modulates 12-lipoxygenase, a key mediator of glutamate-induced neurodegenerationSavita Khanna
Laboratory of Molecular Medicine, Department of Surgery, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, Ohio 43210, USA
J Biol Chem 278:43508-15. 2003..These findings lend further support to alpha-tocotrienol as a potent neuroprotective form of vitamin E... - Depletion of intracellular glutathione mediates zinc-induced cell death in rat primary astrocytesRyun Ryu
Department of Pharmacology, College of Pharmacy, Seoul National University, San 56-1, Shillim-dong, Kwanak-Gu, Seoul 151-742, Korea
Exp Brain Res 143:257-63. 2002..In summary, ROS generation, GSH depletion and mitochondrial dysfunction may be key factors in Zn2+-induced glial toxicity...
Research Grants
- Estrogenic Regulation of Mitochondrial Transcription in Huntington's DiseaseHoon Ryu; Fiscal Year: 2009..These studies will provide novel mechanisms for preventing mitochondrial transcriptional dysfunction and help in the design of applicable compounds that modulate mitochondrial function. ..
- Estrogenic Regulation of Mitochondrial Transcription in Huntington's DiseaseHoon Ryu; Fiscal Year: 2007..These studies will provide novel mechanisms for preventing mitochondrial transcriptional dysfunction and help in the design of applicable compounds that modulate mitochondrial function. ..