Targeting Inflammation, PHA-767491 Shows a Broad Spectrum in Protein Aggregation Diseases

[1]  M. Kassiou,et al.  O-GlcNAc Modification Protects against Protein Misfolding and Aggregation in Neurodegenerative Disease. , 2019, ACS chemical neuroscience.

[2]  Yih-Ru Wu,et al.  Shaoyao Gancao Tang (SG-Tang), a formulated Chinese medicine, reduces aggregation and exerts neuroprotection in spinocerebellar ataxia type 17 (SCA17) cell and mouse models , 2019, Aging.

[3]  H. Hsieh-Li,et al.  MGCD0103, a selective histone deacetylase inhibitor, coameliorates oligomeric Aβ25‐35‐induced anxiety and cognitive deficits in a mouse model , 2018, CNS neuroscience & therapeutics.

[4]  H. Hsieh-Li,et al.  Administration of Momordica charantia Enhances the Neuroprotection and Reduces the Side Effects of LiCl in the Treatment of Alzheimer’s Disease , 2018, Nutrients.

[5]  Guan-Chiun Lee,et al.  Chronic low dose of AM404 ameliorates the cognitive impairment and pathological features in hyperglycemic 3xTg-AD mice , 2018, Psychopharmacology.

[6]  M. Scarpa,et al.  Possible strategies to cross the blood–brain barrier , 2018, Italian Journal of Pediatrics.

[7]  D. Stanimirovic,et al.  Emerging Technologies for Delivery of Biotherapeutics and Gene Therapy Across the Blood–Brain Barrier , 2018, BioDrugs.

[8]  Yih-Ru Wu,et al.  The indole compound NC009–1 inhibits aggregation and promotes neurite outgrowth through enhancement of HSPB1 in SCA17 cells and ameliorates the behavioral deficits in SCA17 mice , 2018, Neurotoxicology.

[9]  R. Chang,et al.  Evidence of the impact of systemic inflammation on neuroinflammation from a non-bacterial endotoxin animal model , 2018, Journal of neuroinflammation.

[10]  Xiaowei Dong,et al.  Current Strategies for Brain Drug Delivery , 2018, Theranostics.

[11]  Maode Wang,et al.  CDC7-dependent transcriptional regulation of RAD54L is essential for tumorigenicity and radio-resistance of glioblastoma , 2018, Translational oncology.

[12]  Berislav V. Zlokovic,et al.  Blood–brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders , 2018, Nature Reviews Neurology.

[13]  Alexandra Silva,et al.  Polyglutamine expansion diseases: More than simple repeats. , 2017, Journal of structural biology.

[14]  P. Szabó-Révész,et al.  From the Cover: In Vitro and In Vivo Blood-Brain Barrier Penetration Studies with the Novel Cyanide Antidote Candidate Dimethyl Trisulfide in Mice , 2017, Toxicological sciences : an official journal of the Society of Toxicology.

[15]  T. Takeuchi,et al.  Protein Misfolding and Aggregation as a Therapeutic Target for Polyglutamine Diseases , 2017, Brain sciences.

[16]  Guan-Chiun Lee,et al.  Investigation of the bindings of a class of inhibitors with GSK3β kinase using thermodynamic integration MD simulation and kinase assay , 2017, Chemical biology & drug design.

[17]  Z. Erbayraktar,et al.  Cell division cycle 7-kinase inhibitor PHA-767491 hydrochloride suppresses glioblastoma growth and invasiveness , 2016, Cancer Cell International.

[18]  H. Hsieh-Li,et al.  Targeting the prodromal stage of spinocerebellar ataxia type 17 mice: G-CSF in the prevention of motor deficits via upregulating chaperone and autophagy levels , 2016, Brain Research.

[19]  K. Stoeber,et al.  Cdc7 is a potent anti-cancer target in pancreatic cancer due to abrogation of the DNA origin activation checkpoint , 2016, Oncotarget.

[20]  H. Hsieh-Li,et al.  Administration of NaHS Attenuates Footshock-Induced Pathologies and Emotional and Cognitive Dysfunction in Triple Transgenic Alzheimer’s Mice , 2015, Front. Behav. Neurosci..

[21]  Guan-Chiun Lee,et al.  Trehalose Attenuates the Gait Ataxia and Gliosis of Spinocerebellar Ataxia Type 17 Mice , 2015, Neurochemical Research.

[22]  G. Hou,et al.  Cyclin-dependent kinase 9 may as a novel target in downregulating the atherosclerosis inflammation (Review). , 2014, Biomedical reports.

[23]  Chung-Hsin Wu,et al.  Indole and synthetic derivative activate chaperone expression to reduce polyQ aggregation in SCA17 neuronal cell and slice culture models , 2014, Drug design, development and therapy.

[24]  J. Ávila,et al.  GSK-3β, a pivotal kinase in Alzheimer disease , 2014, Front. Mol. Neurosci..

[25]  Haibin Liu,et al.  AlzPlatform: An Alzheimer’s Disease Domain-Specific Chemogenomics Knowledgebase for Polypharmacology and Target Identification Research , 2014, J. Chem. Inf. Model..

[26]  A. Mietelska-Porowska,et al.  Tau Protein Modifications and Interactions: Their Role in Function and Dysfunction , 2014, International journal of molecular sciences.

[27]  E. Benarroch,et al.  Microglia , 2013, Methods in Molecular Biology.

[28]  T. Bird,et al.  CDC7 inhibition blocks pathological TDP‐43 phosphorylation and neurodegeneration , 2013, Annals of neurology.

[29]  W. Pardridge,et al.  Drug Transport across the Blood–Brain Barrier , 2012, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[30]  Bin Zhao,et al.  Roles of glycogen synthase kinase 3 in Alzheimer's disease. , 2012, Current Alzheimer research.

[31]  J. Morillas-Ruiz,et al.  A Review: Inflammatory Process in Alzheimer's Disease, Role of Cytokines , 2012, TheScientificWorldJournal.

[32]  H. Hsieh-Li,et al.  Neuroprotective effects of granulocyte‐colony stimulating factor in a novel transgenic mouse model of SCA17 , 2011, Journal of neurochemistry.

[33]  S. Zahler,et al.  Flavopiridol Protects Against Inflammation by Attenuating Leukocyte-Endothelial Interaction via Inhibition of Cyclin-Dependent Kinase 9 , 2011, Arteriosclerosis, Thrombosis and Vascular Biology.

[34]  Thomas Möller,et al.  Neuroinflammation in Huntington’s disease , 2010, Journal of Neural Transmission.

[35]  A. Kamer.  SYSTEMIC INFLAMMATION AND DISEASE PROGRESSION IN ALZHEIMER DISEASE , 2010, Neurology.

[36]  Tracy O'Connor,et al.  Protein aggregation diseases: pathogenicity and therapeutic perspectives , 2010, Nature Reviews Drug Discovery.

[37]  V. Perry,et al.  SYSTEMIC INFLAMMATION AND DISEASE PROGRESSION IN ALZHEIMER DISEASE. AUTHORS' REPLY , 2010 .

[38]  A. Reichel.  Addressing Central Nervous System (CNS) Penetration in Drug Discovery: Basics and Implications of the Evolving New Concept , 2009, Chemistry & biodiversity.

[39]  V. Perry,et al.  Systemic inflammation and disease progression in Alzheimer disease , 2009, Neurology.

[40]  A. Isacchi,et al.  A Cdc7 kinase inhibitor restricts initiation of DNA replication and has antitumor activity. , 2008, Nature chemical biology.

[41]  Admadi Soeroso.  C Y T O K I N E S , 2007 .

[42]  S. Warren,et al.  Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration , 2007, Nature Neuroscience.

[43]  Heather T. McFarlane,et al.  Atomic structures of amyloid cross-β spines reveal varied steric zippers , 2007, Nature.

[44]  Yen F. Tai,et al.  Imaging microglial activation in Huntington's disease , 2007, Brain Research Bulletin.

[45]  R. J. Kelleher,et al.  The presenilin hypothesis of Alzheimer's disease: Evidence for a loss-of-function pathogenic mechanism , 2007, Proceedings of the National Academy of Sciences.

[46]  Alexander Gerhard,et al.  Microglial activation in presymptomatic Huntington's disease gene carriers. , 2005, Brain : a journal of neurology.

[47]  U Walter,et al.  Morphological basis for the spectrum of clinical deficits in spinocerebellar ataxia 17 (SCA17). , 2006, Brain : a journal of neurology.

[48]  Q. Tian,et al.  Activation of glycogen synthase kinase-3 induces Alzheimer-like tau hyperphosphorylation in rat hippocampus slices in culture , 2005, Journal of Neural Transmission.

[49]  D. van Rossum,et al.  Microglia , 2004, Metabolic Brain Disease.

[50]  Charles Duyckaerts,et al.  Behavioral disorder, dementia, ataxia, and rigidity in a large family with TATA box-binding protein mutation. , 2004, Archives of neurology.

[51]  Osamu Onodera,et al.  SCA17 homozygote showing Huntington's disease‐like phenotype , 2004, Annals of neurology.

[52]  Tony Wyss-Coray,et al.  Inflammation in Neurodegenerative Disease—A Double-Edged Sword , 2002, Neuron.

[53]  T. Klockgether,et al.  Inflammatory Genes Are Upregulated in Expanded Ataxin-3-Expressing Cell Lines and Spinocerebellar Ataxia Type 3 Brains , 2001, The Journal of Neuroscience.

[54]  I. Kanazawa,et al.  SCA17, a novel autosomal dominant cerebellar ataxia caused by an expanded polyglutamine in TATA-binding protein. , 2001, Human molecular genetics.

[55]  P G Bhide,et al.  Early and Progressive Accumulation of Reactive Microglia in the Huntington Disease Brain , 2001, Journal of neuropathology and experimental neurology.

[56]  小出 玲爾,et al.  A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene : a new polyglutamine disease? , 2000 .

[57]  S Kobayashi,et al.  A neurological disease caused by an expanded CAG trinucleotide repeat in the TATA-binding protein gene: a new polyglutamine disease? , 1999, Human molecular genetics.

[58]  D. Housman,et al.  Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[59]  R. Meyermann,et al.  Reactive microgIia in Creutzfeldt‐Jakob disease , 1995, Neuropathology and applied neurobiology.

[60]  P. Mcgeer,et al.  The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases , 1995, Brain Research Reviews.

[61]  B. Gostout,et al.  "Cryptic" repeating triplets of purines and pyrimidines (cRRY(i)) are frequent and polymorphic: analysis of coding cRRY(i) in the proopiomelanocortin (POMC) and TATA-binding protein (TBP) genes. , 1993, American journal of human genetics.