Jie Shen

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. pmc Impaired neurotransmitter release in Alzheimer's and Parkinson's diseases
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, USA
    Neurodegener Dis 7:80-3. 2010
  2. pmc Regulation of mitochondrial permeability transition pore by PINK1
    Clement A Gautier
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Mol Neurodegener 7:22. 2012
  3. pmc Brain region specific mitophagy capacity could contribute to selective neuronal vulnerability in Parkinson's disease
    Madeleine Diedrich
    Institute for Medical Genetics and Human Genetics, Charite Universitatsmedizin Berlin, D 13353 Berlin, Germany
    Proteome Sci 9:59. 2011
  4. pmc The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:403-9. 2007
  5. ncbi request reprint Mitochondria and dopamine: new insights into recessive parkinsonism
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Neuron 43:301-4. 2004
  6. pmc Presenilins are required for maintenance of neural stem cells in the developing brain
    Woo Young Kim
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, 02115, USA
    Mol Neurodegener 3:2. 2008
  7. doi request reprint Impaired dopamine release and synaptic plasticity in the striatum of parkin-/- mice
    Tohru Kitada
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurochem 110:613-21. 2009
  8. pmc Inactivation of presenilins causes pre-synaptic impairment prior to post-synaptic dysfunction
    Dawei Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA
    J Neurochem 115:1215-21. 2010
  9. pmc Presenilins are essential for regulating neurotransmitter release
    Chen Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 460:632-6. 2009
  10. pmc Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice
    Tohru Kitada
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusets, USA
    J Neurochem 111:696-702. 2009

Detail Information

Publications59

  1. pmc Impaired neurotransmitter release in Alzheimer's and Parkinson's diseases
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, USA
    Neurodegener Dis 7:80-3. 2010
    ..Together, our genetic studies suggest that presynaptic dysfunction might be a converging early pathogenic event before neurodegeneration in AD and PD...
  2. pmc Regulation of mitochondrial permeability transition pore by PINK1
    Clement A Gautier
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Mol Neurodegener 7:22. 2012
    ..We previously reported that loss of PINK1 impairs mitochondrial respiratory activity in mouse brains...
  3. pmc Brain region specific mitophagy capacity could contribute to selective neuronal vulnerability in Parkinson's disease
    Madeleine Diedrich
    Institute for Medical Genetics and Human Genetics, Charite Universitatsmedizin Berlin, D 13353 Berlin, Germany
    Proteome Sci 9:59. 2011
    ..Taken together, the delicate balance between oxidative protection and mitophagy capacity in different brain regions could contribute to brain region-specific pathological patterns in PD...
  4. pmc The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:403-9. 2007
    ..We also speculate that Abeta42 may act primarily to antagonize PS-dependent functions, possibly by operating as an active site-directed inhibitor of gamma-secretase...
  5. ncbi request reprint Mitochondria and dopamine: new insights into recessive parkinsonism
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Neuron 43:301-4. 2004
    ..This review will summarize recent advances in our understanding of these gene products, with emphasis on the surprising convergence of their functions...
  6. pmc Presenilins are required for maintenance of neural stem cells in the developing brain
    Woo Young Kim
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, 02115, USA
    Mol Neurodegener 3:2. 2008
    ..These findings demonstrate that presenilins are essential for neural progenitor cells to re-enter cell cycle and thus ensure proper expansion of neural progenitor pool during embryonic neural development...
  7. doi request reprint Impaired dopamine release and synaptic plasticity in the striatum of parkin-/- mice
    Tohru Kitada
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurochem 110:613-21. 2009
    ....
  8. pmc Inactivation of presenilins causes pre-synaptic impairment prior to post-synaptic dysfunction
    Dawei Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, USA
    J Neurochem 115:1215-21. 2010
    ..J. Neurochem. (2010) 115, 1215-1221...
  9. pmc Presenilins are essential for regulating neurotransmitter release
    Chen Zhang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nature 460:632-6. 2009
    ....
  10. pmc Absence of nigral degeneration in aged parkin/DJ-1/PINK1 triple knockout mice
    Tohru Kitada
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusets, USA
    J Neurochem 111:696-702. 2009
    ..These findings also support the notion that mammalian Parkin and PINK1 may function in the same genetic pathway as in Drosophila...
  11. pmc Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening
    Emilie Giaime
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 7:e40501. 2012
    ..Although it has been reported that DJ-1 serves as scavenger for reactive oxidative species (ROS) by oxidation on its cysteine residues, how loss of DJ-1 affects mitochondrial function is less clear...
  12. pmc Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress
    Clement A Gautier
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 105:11364-9. 2008
    ....
  13. ncbi request reprint Nigrostriatal dopaminergic deficits and hypokinesia caused by inactivation of the familial Parkinsonism-linked gene DJ-1
    Matthew S Goldberg
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    Neuron 45:489-96. 2005
    ..Furthermore, DJ-1(-/-) mice displayed hypoactivity in the open field. Collectively, our findings suggest an essential role for DJ-1 in dopaminergic physiology and D2 receptor-mediated functions...
  14. pmc R1441C mutation in LRRK2 impairs dopaminergic neurotransmission in mice
    Youren Tong
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 106:14622-7. 2009
    ..Together, our data suggest that the R1441C mutation in LRRK2 impairs stimulated dopamine neurotransmission and D2 receptor function, which may represent pathogenic precursors preceding dopaminergic degeneration in PD brains...
  15. ncbi request reprint Hippocampal spatial memory impairments caused by the familial Alzheimer's disease-linked presenilin 1 M146V mutation
    Xiaoyan Sun
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Neurodegener Dis 2:6-15. 2005
    ....
  16. ncbi request reprint Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice
    Carlos A Saura
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 25:6755-64. 2005
    ..These results reveal that in vivo reduction of Abeta via the inactivation of PS1 effectively prevents amyloid-associated neuropathological changes and can, but only temporarily, improve cognitive impairments in APP transgenic mice...
  17. pmc Impaired dopamine release and synaptic plasticity in the striatum of PINK1-deficient mice
    Tohru Kitada
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 104:11441-6. 2007
    ..These results reveal a critical role for PINK1 in DA release and striatal synaptic plasticity in the nigrostriatal circuit and suggest that altered dopaminergic physiology may be a pathogenic precursor to nigrostriatal degeneration...
  18. pmc Characterization of age-dependent and progressive cortical neuronal degeneration in presenilin conditional mutant mice
    Mary Wines-Samuelson
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts, United States of America
    PLoS ONE 5:e10195. 2010
    ....
  19. ncbi request reprint Notch1 signaling influences v2 interneuron and motor neuron development in the spinal cord
    Xudong Yang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Dev Neurosci 28:102-17. 2006
    ..These results provide support for a role of Notch1 in neuronal subtype specification in the ventral spinal cord...
  20. pmc Loss of leucine-rich repeat kinase 2 causes impairment of protein degradation pathways, accumulation of alpha-synuclein, and apoptotic cell death in aged mice
    Youren Tong
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Proc Natl Acad Sci U S A 107:9879-84. 2010
    ....
  21. ncbi request reprint Reduced beta-amyloid production and increased inflammatory responses in presenilin conditional knock-out mice
    Vassilios Beglopoulos
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 279:46907-14. 2004
    ..These results indicate that the memory impairment and neurodegeneration in PS cDKO mice are not caused by Abeta accumulation and that loss of PS function leads to differential up-regulation of inflammatory markers in the cerebral cortex...
  22. ncbi request reprint Parkin protects against mitochondrial toxins and beta-amyloid accumulation in skeletal muscle cells
    Kenneth M Rosen
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA
    J Biol Chem 281:12809-16. 2006
    ..These data support the hypothesis that in myocytes parkin has dual properties in the maintenance of skeletal muscle mitochondrial homeostasis and in the regulation of A beta levels...
  23. pmc CREB binding protein is required for both short-term and long-term memory formation
    Guiquan Chen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 30:13066-77. 2010
    ..Collectively, these findings suggest a crucial role for CBP in the formation of both short- and long-term memory...
  24. pmc Familial frontotemporal dementia-associated presenilin-1 c.548G>T mutation causes decreased mRNA expression and reduced presenilin function in knock-in mice
    Hirotaka Watanabe
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Neurosci 32:5085-96. 2012
    ..Together, our findings demonstrate that the c.548G>T mutation results in a brain-specific loss of presenilin function due to decreased Psen1 mRNA expression...
  25. pmc alpha-synuclein and LRRK2: partners in crime
    Youren Tong
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA, 02115, USA
    Neuron 64:771-3. 2009
    ..The results reveal an interesting interaction between alpha-synuclein and LRRK2, two gene products linked to dominantly inherited Parkinson's disease...
  26. pmc A presenilin-1 mutation identified in familial Alzheimer disease with cotton wool plaques causes a nearly complete loss of gamma-secretase activity
    Elizabeth A Heilig
    Center for Human Genetic Research and Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA
    J Biol Chem 285:22350-9. 2010
    ..Rather, our findings provide support for the hypothesis that pathogenic mutations cause a general loss of presenilin function...
  27. ncbi request reprint Mitochondrial dysfunction and oxidative damage in parkin-deficient mice
    James J Palacino
    Center for Neurologic Diseases, Brigham and Women s Hospital, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 279:18614-22. 2004
    ....
  28. pmc Conditional deletion of Notch1 and Notch2 genes in excitatory neurons of postnatal forebrain does not cause neurodegeneration or reduction of Notch mRNAs and proteins
    Jin Zheng
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 287:20356-68. 2012
    ....
  29. pmc Loss of leucine-rich repeat kinase 2 causes age-dependent bi-phasic alterations of the autophagy pathway
    Youren Tong
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Mol Neurodegener 7:2. 2012
    ..We previously reported that loss of LRRK2 causes impairment of protein degradation pathways as well as increases of apoptotic cell death and inflammatory responses in the kidney of aged mice...
  30. ncbi request reprint Presenilins in the developing, adult, and aging cerebral cortex
    Mary Wines-Samuelson
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, Massachussetts 02115, USA
    Neuroscientist 11:441-51. 2005
    ..These diverse functions of presenilins in cortical development and function and neuronal survival have important implications for the pathogenesis of neurodegenerative dementia...
  31. pmc Altered Ca2+ homeostasis in the skeletal muscle of DJ-1 null mice
    Alexander Shtifman
    Department of Neurology, Caritas St Elizabeth s Medical Center, Tufts University School of Medicine, 736 Cambridge St, CBR 406, Boston, MA 02135, USA
    Neurobiol Aging 32:125-32. 2011
    ..These results provide evidence of DJ-1's association with Ca(2+) regulatory pathways in mouse skeletal muscle, and suggest the potential benefit of resveratrol to functionally compensate for the loss of DJ-1...
  32. pmc Indirect regulation of presenilins in CREB-mediated transcription
    Hirotaka Watanabe
    Center for Neurologic Diseases, Brigham and Women s Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Biol Chem 284:13705-13. 2009
    ....
  33. ncbi request reprint Regulation of CRE-dependent transcription by presenilins: prospects for therapy of Alzheimer's disease
    Vassilios Beglopoulos
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Trends Pharmacol Sci 27:33-40. 2006
    ..Thus, modulation of CRE-dependent transcription might be beneficial for the treatment of dementia in AD...
  34. ncbi request reprint Role of presenilin-1 in cortical lamination and survival of Cajal-Retzius neurons
    Mary Wines-Samuelson
    Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
    Dev Biol 277:332-46. 2005
    ..These findings show a cell-autonomous role for PS1 in cortical lamination and radial glial development, and a non-cell-autonomous role for PS1 in CR neuron survival...
  35. ncbi request reprint Notch activation induces apoptosis in neural progenitor cells through a p53-dependent pathway
    Xudong Yang
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Dev Biol 269:81-94. 2004
    ..Together, these complementary gain-of-function and loss-of-function studies reveal a previously unappreciated role of Notch signaling in the regulation of apoptotic cell death during early mammalian neural development...
  36. ncbi request reprint Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration
    Carlos A Saura
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Neuron 42:23-36. 2004
    ..These results define essential roles and molecular targets of presenilins in synaptic plasticity, learning and memory, and neuronal survival in the adult cerebral cortex...
  37. pmc Increased DJ-1 expression under oxidative stress and in Alzheimer's disease brains
    Stephanie Baulac
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Harvard University, Boston, MA 02115, USA
    Mol Neurodegener 4:12. 2009
    ..Therefore, our results strongly suggest that DJ-1 expression is not necessary during zebrafish development but can be induced in zebrafish exposed to oxidative stress and is present in human AD brains...
  38. pmc A Cdc20-APC ubiquitin signaling pathway regulates presynaptic differentiation
    Yue Yang
    Department of Pathology, Harvard Medical School, Boston, MA 02115, USA
    Science 326:575-8. 2009
    ..Thus, our findings define a Cdc20-APC ubiquitin signaling pathway that governs presynaptic development, which holds important implications for neuronal connectivity and plasticity in the brain...
  39. pmc Cambogin is preferentially cytotoxic to cells expressing PDGFR
    Ze Tian
    Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China
    PLoS ONE 6:e21370. 2011
    ..These results suggest that cambogin is preferentially cytotoxic to cells expressing PDGFR. Our findings may provide a novel approach by targeting PDGFR signaling against MB...
  40. ncbi request reprint Parkin-deficient mice exhibit nigrostriatal deficits but not loss of dopaminergic neurons
    Matthew S Goldberg
    Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, Massachusetts 02115, USA
    J Biol Chem 278:43628-35. 2003
    ..Together these findings provide the first evidence for a novel role of parkin in dopamine regulation and nigrostriatal function, and a non-essential role of parkin in the survival of nigral neurons in mice...
  41. ncbi request reprint Genetic analysis of Parkinson's disease-linked leucine-rich repeat kinase 2
    Youren Tong
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, U S A
    Biochem Soc Trans 40:1042-6. 2012
    ..We conclude that pathogenic mutations in LRRK2 impair the nigrostriatal dopaminergic pathway, and LRRK2 plays an essential role in the dynamic regulation of autophagy function in vivo...
  42. pmc A nasal proteosome adjuvant activates microglia and prevents amyloid deposition
    Dan Frenkel
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
    Ann Neurol 63:591-601. 2008
    ....
  43. ncbi request reprint Gene-targeting technologies for the study of neurological disorders
    Vassilios Beglopoulos
    Center for Neurologic Diseases, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115, USA
    Neuromolecular Med 6:13-30. 2004
    ..The importance of the results obtained by these models for the understanding of the pathogenic mechanism underlying the disorders is discussed...
  44. ncbi request reprint Dulxanthone A induces cell cycle arrest and apoptosis via up-regulation of p53 through mitochondrial pathway in HepG2 cells
    Ze Tian
    Children s Hospital Informatics Program at Harvard MIT Division of Health Sciences and Technology, Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
    Int J Cancer 122:31-8. 2008
    ..Dulxanthone A is therefore likely a promising preventive and/or therapeutic agent against Hepatoma...
  45. pmc Spectrum of heart disease associated with murine and human GATA4 mutation
    Satish K Rajagopal
    Department of Cardiology, Children s Hospital Boston, 300 Longwood Avenue, Boston, MA 02115, USA
    J Mol Cell Cardiol 43:677-85. 2007
    ..Additional studies will be required to determine the degree to which GATA4 mutation contributes to human CHD characterized by ECD or RV hypoplasia...
  46. pmc Presenilins regulate calcium homeostasis and presynaptic function via ryanodine receptors in hippocampal neurons
    Bei Wu
    Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Program in Neuroscience, Harvard Medical School, Boston, MA 02115
    Proc Natl Acad Sci U S A 110:15091-6. 2013
    ....
  47. ncbi request reprint Protein kinases linked to the pathogenesis of Parkinson's disease
    Jie Shen
    Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
    Neuron 44:575-7. 2004
    ..The LRRK2 gene is predicted to encode a large protein containing leucine-rich repeats and Ras/GTPase, tyrosine kinase-like, and WD40 domains...
  48. pmc Trans-dominant negative effects of pathogenic PSEN1 mutations on γ-secretase activity and Aβ production
    Elizabeth A Heilig
    Center for Human Genetic Research, Massachusetts General Hospital and Harvard Medical School, MGH Simches Research Center, Boston, MA 02114, USA
    J Neurosci 33:11606-17. 2013
    ..Our findings reveal a novel mechanism of action for pathogenic PSEN1 mutations and suggest that dominant-negative inhibition of presenilin activity plays an important role in FAD pathogenesis. ..
  49. doi request reprint Histological analysis of neurodegeneration in the mouse brain
    Hiroo Yamaguchi
    Program in Neuroscience, Center for Neurologic Diseases, Harvard Medical School, Brigham and Women s Hospital, Boston, MA, USA
    Methods Mol Biol 1004:91-113. 2013
    ....
  50. pmc Effect of presenilins in the apoptosis of thymocytes and homeostasis of CD8+ T cells
    Antonio Maraver
    Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, 540 1st Avenue, New York, NY 10016, USA
    Blood 110:3218-25. 2007
    ....
  51. ncbi request reprint A regulatory network involving Foxn4, Mash1 and delta-like 4/Notch1 generates V2a and V2b spinal interneurons from a common progenitor pool
    Marta G del Barrio
    Wolfson Institute for Biomedical Research and Department of Biology, University College London, Gower Street, London WC1E 6BT, UK
    Development 134:3427-36. 2007
    ....
  52. pmc Defective signal transduction in B lymphocytes lacking presenilin proteins
    Tomohito Yagi
    Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 105:979-84. 2008
    ..Our findings also suggest that pharmacologic inhibition of PS for the treatment of conditions such as Alzheimer's disease may have potential consequences for immune system function...
  53. ncbi request reprint Regulation of cholesterol and sphingomyelin metabolism by amyloid-beta and presenilin
    Marcus O W Grimm
    Centre for Molecular Biology Heidelberg, INF 282, D 69120 Heidelberg, Germany
    Nat Cell Biol 7:1118-23. 2005
    ..Our results demonstrate a biological function for APP processing and also a functional basis for the link that has been observed between lipids and Alzheimer's disease (AD)...
  54. ncbi request reprint gamma-secretase functions through Notch signaling to maintain skin appendages but is not required for their patterning or initial morphogenesis
    Yonghua Pan
    Department of Molecular Biology and Pharmacology, Division of Dermatology, Washington University School of Medicine, Box 8103, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Dev Cell 7:731-43. 2004
    ....
  55. ncbi request reprint Presenilin-dependent transcriptional control of the Abeta-degrading enzyme neprilysin by intracellular domains of betaAPP and APLP
    Raphaelle Pardossi-Piquard
    Institut de Pharmacologie Moleculaire et Cellulaire, Centre National de la Recherche Scientifique, UMR6097 CNRS UNSA, Valbonne 06560, France
    Neuron 46:541-54. 2005
    ..The presenilin-dependent regulation of neprilysin, mediated by AICDs, provides a physiological means to modulate Abeta levels with varying levels of gamma-secretase activity...
  56. ncbi request reprint Characterization of the reconstituted gamma-secretase complex from Sf9 cells co-expressing presenilin 1, nicastrin [correction of nacastrin], aph-1a, and pen-2
    Lili Zhang
    Department of Neurobiology, Schering Plough Research Institute, Kenilworth, New Jersey 07033, USA
    Biochemistry 44:4450-7. 2005
    ..These studies may provide important insight into the development of a new generation of selective gamma-secretase inhibitors with an improved side effect profile...
  57. ncbi request reprint [Preliminary study on biological behavior and staging of transplanted hepatoma in rats]
    Wei Gu
    Department of Traditional Chinese Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
    Zhong Xi Yi Jie He Xue Bao 3:136-8. 2005
    ..To establish a staging standard for a transplanted hepatoma model in rats, which may be equivalent to the human primary liver cancer...
  58. ncbi request reprint Resistance to drug by different isolates Trypanosoma evansi in China
    Jinlin Zhou
    Shanghai Institute of Animal Parasitology, Chinese Academy of Agricultural Sciences, 3 Lane 345, Shilong Road, Shanghai 200232, China
    Acta Trop 90:271-5. 2004
    ..No drug cross-resistance was observed between suramin and antrycide...
  59. pmc Neointimal hyperplasia persists at six months after sirolimus-eluting stent implantation in diabetic porcine
    Qi Zhang
    Department of Cardiology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China
    Cardiovasc Diabetol 6:16. 2007
    ..The aim of this study was to examine the changes of neointimal hyperplasia after sirolimus-eluting stent (SES) implantation in a diabetic porcine model, and to evaluate the impact of aortic inflammation on this proliferative process...

Research Grants35

  1. PINK1 and Recessive Parkinsonism
    Jie Shen; Fiscal Year: 2007
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of Parkingson's disease and to characterize the molecular pathways responsible for PD pathogenesis. ..
  2. DJ-1 in Dopaminergic Neuronal Function and Survival
    Jie Shen; Fiscal Year: 2007
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of PD and to characterize the molecular pathways responsible for PD pathogenesis. ..
  3. PINK1 and Recessive Parkinsonism
    Jie Shen; Fiscal Year: 2009
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of Parkingson's disease and to characterize the molecular pathways responsible for PD pathogenesis. ..
  4. DJ-1 in Dopaminergic Neuronal Function and Survival
    Jie Shen; Fiscal Year: 2009
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of PD and to characterize the molecular pathways responsible for PD pathogenesis. ..
  5. Presenilins in Synaptic Plasticity and Neurodegeneration
    Jie Shen; Fiscal Year: 2010
    ..Furthermore, identification of the molecular pathways regulated by PS may provide novel therapeutic targets for combating cognitive dysfunction and neurodegeneration in these disorders. ..
  6. PINK1 and Recessive Parkinsonism
    Jie Shen; Fiscal Year: 2009
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of PD and to characterize the molecular pathways responsible for PD pathogenesis. ..
  7. Presenilins, Gamma-Secretase and Notch in Neuronal Death
    Jie Shen; Fiscal Year: 2010
    ..Better understanding of the molecular pathways by which presenilins regulate cognitive and neuronal integrity will provide important insights into the pathogenesis of these disorders and may provide novel therapeutic targets. ..
  8. Function and Dysfunction of LRRK2
    Jie Shen; Fiscal Year: 2010
    ..Completion of our proposed study will provide insights into PD pathogenesis and may identify novel therapeutic targets for development of more effective drugs. ..
  9. PINK1 and Parkin in dopaminergic and mitochondrial functions
    Jie Shen; Fiscal Year: 2010
    ..Completion of our proposed study will provide insights into PD pathogenesis and may identify novel therapeutic targets for development of more effective drugs. ..
  10. Presenilins in Synaptic Plasticity and Neurodegeneration
    Jie Shen; Fiscal Year: 2007
    ..Furthermore, identification of the molecular pathways regulated by PS may provide novel therapeutic targets for combating cognitive dysfunction and neurodegeneration in these disorders. ..
  11. PS-1 in APP Processing and Synaptic Function
    Jie Shen; Fiscal Year: 2004
    ..The significance of the proposed study is that it will elucidate the normal physiological role of PS1 in the adult brain and test the feasibility and suitability of targeting PS1 for anti-amyloidogenic therapy in Alzheimer's disease. ..
  12. Studies of Parkin KO Cells and Mice as PD Models
    Jie Shen; Fiscal Year: 2004
    ..Both the animal and the cellular systems could provide valuable means for identifying and testing molecules and genes with therapeutic potential. ..
  13. PS1 & PS2 in Cortical Development and Notch Signaling
    Jie Shen; Fiscal Year: 2006
    ....
  14. PINK1 and Recessive Parkinsonism
    Jie Shen; Fiscal Year: 2010
    ..Our long-term goal is to develop a genetic mouse model that recapitulates all central features of Parkingson's disease and to characterize the molecular pathways responsible for PD pathogenesis. ..