S D Yan

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. ncbi An intracellular protein that binds amyloid-beta peptide and mediates neurotoxicity in Alzheimer's disease
    S D Yan
    Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
    Nature 389:689-95. 1997
  2. ncbi RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease
    Shirley ShiDu Yan
    Department of Surgery, Physicians and Surgeons College of Columbia University, New York, NY 10032, USA
    Front Biosci (Schol Ed) 4:240-50. 2012
  3. ncbi Amyloid beta -peptide-binding alcohol dehydrogenase is a component of the cellular response to nutritional stress
    S Du Yan
    Departments of Pathology, Surgery, Physiology and Cellular Biophysics, Neurosurgery and Medicine, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 275:27100-9. 2000
  4. ncbi Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis
    S D Yan
    Departments of Pathology, Physiology, and Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    Nat Med 6:643-51. 2000
  5. ncbi Mitochondrial dysfunction and Alzheimer's disease: role of amyloid-beta peptide alcohol dehydrogenase (ABAD)
    Shi Du Yan
    Departments of Pathology, Surgery, Taub Institute for Research on Alzheimer s Disease and the Ageing Brain, College of Physicians and Surgeons of Columbia University, 650 West 168th Street, Black Building Rm 17 01, New York, NY 10032, USA
    Int J Exp Pathol 86:161-71. 2005
  6. ncbi Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system
    Shirley ShiDu Yan
    Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York, USA
    Nat Med 9:287-93. 2003
  7. ncbi Role of ERAB/L-3-hydroxyacyl-coenzyme A dehydrogenase type II activity in Abeta-induced cytotoxicity
    S D Yan
    Departments of Pathology, Physiology and Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 274:2145-56. 1999
  8. ncbi RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease
    S D Yan
    Department of Pathology, Columbia University, College of Physicians and Surgeons, New York 10032, USA
    Nature 382:685-91. 1996
  9. ncbi RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease
    L G Bucciarelli
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Cell Mol Life Sci 59:1117-28. 2002
  10. ncbi Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues
    J Brett
    Department of Physiology and Cellular Biophysics and Surgery, Columbia University, College of Physicians and Surgeons, New York, New York 10032
    Am J Pathol 143:1699-712. 1993

Research Grants

  1. Structural and Functional Properties of cyclophilin D and Abeta interaction.
    Shi Du Yan; Fiscal Year: 2010
  2. Role of LRG-47 (Irgm1) in EAE
    Shi Du Yan; Fiscal Year: 2010
  3. The Role of RAGE and EAE
    Shi Du Yan; Fiscal Year: 2005
  4. ERAB, A BETA, NEUROTOXICITY AND ALZHEIMERS DISEASE
    Shi Du Yan; Fiscal Year: 2003

Collaborators

Detail Information

Publications19

  1. ncbi An intracellular protein that binds amyloid-beta peptide and mediates neurotoxicity in Alzheimer's disease
    S D Yan
    Department of Pathology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, USA
    Nature 389:689-95. 1997
    ..By interacting with intracellular amyloid-beta, ERAB may therefore contribute to the neuronal dysfunction associated with Alzheimer's disease...
  2. ncbi RAGE is a key cellular target for Abeta-induced perturbation in Alzheimer's disease
    Shirley ShiDu Yan
    Department of Surgery, Physicians and Surgeons College of Columbia University, New York, NY 10032, USA
    Front Biosci (Schol Ed) 4:240-50. 2012
    ..Blockade of RAGE significantly attenuates neuronal and synaptic injury. In this review, we summarize the role of RAGE in the pathogenesis of AD, specifically in Abeta-induced cellular perturbation...
  3. ncbi Amyloid beta -peptide-binding alcohol dehydrogenase is a component of the cellular response to nutritional stress
    S Du Yan
    Departments of Pathology, Surgery, Physiology and Cellular Biophysics, Neurosurgery and Medicine, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 275:27100-9. 2000
    ..These data suggest that ABAD contributes to the protective response to metabolic stress, especially in the setting of ischemia...
  4. ncbi Receptor-dependent cell stress and amyloid accumulation in systemic amyloidosis
    S D Yan
    Departments of Pathology, Physiology, and Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    Nat Med 6:643-51. 2000
    ..Antagonizing RAGE suppressed cell stress and amyloid deposition in mouse spleens. These data indicate that RAGE is a potential target for inhibiting accumulation of amyloid A and for limiting cellular dysfunction induced by amyloid A...
  5. ncbi Mitochondrial dysfunction and Alzheimer's disease: role of amyloid-beta peptide alcohol dehydrogenase (ABAD)
    Shi Du Yan
    Departments of Pathology, Surgery, Taub Institute for Research on Alzheimer s Disease and the Ageing Brain, College of Physicians and Surgeons of Columbia University, 650 West 168th Street, Black Building Rm 17 01, New York, NY 10032, USA
    Int J Exp Pathol 86:161-71. 2005
    ..These data suggest that mitochondria ABAD, ordinarily a contributor to metabolic homeostasis, has the capacity to become a pathogenic factor in an Abeta-rich environment...
  6. ncbi Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system
    Shirley ShiDu Yan
    Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York, USA
    Nat Med 9:287-93. 2003
    ..These data reinforce the importance of RAGE-ligand interactions in modulating properties of CD4+ T cells that infiltrate the CNS...
  7. ncbi Role of ERAB/L-3-hydroxyacyl-coenzyme A dehydrogenase type II activity in Abeta-induced cytotoxicity
    S D Yan
    Departments of Pathology, Physiology and Surgery, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 274:2145-56. 1999
    ..We conclude that the generalized alcohol dehydrogenase activity of ERAB/HADH II is central to the cytotoxicity observed in an Abeta-rich environment...
  8. ncbi RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease
    S D Yan
    Department of Pathology, Columbia University, College of Physicians and Surgeons, New York 10032, USA
    Nature 382:685-91. 1996
    ..Increased expressing of RAGE in Alzheimer's disease brain indicates that it is relevant to the pathogenesis of neuronal dysfunction and death...
  9. ncbi RAGE is a multiligand receptor of the immunoglobulin superfamily: implications for homeostasis and chronic disease
    L G Bucciarelli
    College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
    Cell Mol Life Sci 59:1117-28. 2002
    ..Implications for the role of these ligands interacting with RAGE in homeostasis and disease will be considered...
  10. ncbi Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues
    J Brett
    Department of Physiology and Cellular Biophysics and Surgery, Columbia University, College of Physicians and Surgeons, New York, New York 10032
    Am J Pathol 143:1699-712. 1993
    ....
  11. ncbi Expression of Egr-1 in late stage emphysema
    W Zhang
    Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, New York, USA
    Am J Pathol 157:1311-20. 2000
    ....
  12. ncbi RAGE-dependent signaling in microglia contributes to neuroinflammation, Abeta accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease
    Fang Fang
    P and S 17 410, Department Surgery, College of Physicians and Surgeons, Columbia University, 630 West 168th St, New York, NY 10032, USA
    FASEB J 24:1043-55. 2010
    ..G., Stern, D. M., Yan, S., Schmidt, A. M., Chen, J. X., Yan, S. S. RAGE-dependent signaling in microglia contributes to neuroinflammation, Abeta accumulation, and impaired learning/memory in a mouse model of Alzheimer's disease...
  13. ncbi Recognition of structurally diverse substrates by type II 3-hydroxyacyl-CoA dehydrogenase (HADH II)/amyloid-beta binding alcohol dehydrogenase (ABAD)
    A J Powell
    Department of Biochemistry, University of Bristol, Bristol, UK
    J Mol Biol 303:311-27. 2000
    ....
  14. ncbi Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro
    L F Lue
    Sun Health Research Institute, Sun City, Arizona 85372, USA
    Glia 35:72-9. 2001
    ..Taken together with previous in situ hybridization findings, these results demonstrate unequivocally that elderly human microglia provide a brain endogenous source for a wide range of inflammatory mediators...
  15. ncbi Effect of endothelial cell polarity on beta-amyloid-induced migration of monocytes across normal and AD endothelium
    Ranjit Giri
    Department of Biochemistry and Molecular Biology, Keck School of Medicine, University of Southern California, Los Angeles 90033, USA
    Am J Physiol Cell Physiol 283:C895-904. 2002
    ..We suggest that Abeta in the AD brain parenchyma or cerebrovasculature initiates cellular signaling that induces PBM to transmigrate across the BBB and accumulate in the brain...
  16. ncbi The receptor for advanced glycation end products (RAGE) is a central mediator of the interaction of AGE-beta2microglobulin with human mononuclear phagocytes via an oxidant-sensitive pathway. Implications for the pathogenesis of dialysis-related amyloidosi
    T Miyata
    Department of Internal Medicine, Branch Hospital, Nagoya University School of Medicine, Japan
    J Clin Invest 98:1088-94. 1996
    ....
  17. ncbi Preventing activation of receptor for advanced glycation endproducts in Alzheimer's disease
    L F Lue
    Laboratory of Neurovascular Inflammation, Sun Health Research Institute, Sun City, AZ 85351, USA
    Curr Drug Targets CNS Neurol Disord 4:249-66. 2005
    ..The potential for targeting RAGE mechanisms as therapeutic strategies for AD will be discussed...
  18. ncbi Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins
    M Neeper
    Department of Cellular and Molecular Biology, Merck Sharp and Dohme Research Laboratories, West Point, Pennsylvania 19486
    J Biol Chem 267:14998-5004. 1992
    ..These results suggest that RAGE functions as a cell surface receptor for AGEs, which could potentially mediate cellular effects of this class of glycosylated proteins...
  19. ncbi Chronic aminoguanidine attenuates renal dysfunction and injury in aging rats
    J F Reckelhoff
    Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA
    Am J Hypertens 12:492-8. 1999
    ..These findings suggest that aminoguanidine attenuates aging renal dysfunction by inhibiting a pathophysiologic function of iNOS that is independent of free radical-mediated lipid peroxidation or significant effects on AGE deposition...

Research Grants11

  1. Structural and Functional Properties of cyclophilin D and Abeta interaction.
    Shi Du Yan; Fiscal Year: 2010
    ..The results of this proposal will have a profound impact on the AD field by establishing a new target for preventive and therapeutic intervention. ..
  2. Role of LRG-47 (Irgm1) in EAE
    Shi Du Yan; Fiscal Year: 2010
    ....
  3. The Role of RAGE and EAE
    Shi Du Yan; Fiscal Year: 2005
    ....
  4. ERAB, A BETA, NEUROTOXICITY AND ALZHEIMERS DISEASE
    Shi Du Yan; Fiscal Year: 2003
    ..abstract_text> ..