K Iqbal

Summary

Publications

  1. ncbi Inhibition of neurofibrillary degeneration: a promising approach to Alzheimer's disease and other tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Drug Targets 5:495-502. 2004
  2. ncbi Hyperphosphorylation-induced self assembly of murine tau: a comparison with human tau
    M O Chohan
    Department of Neurochemistry, NYS Institute for Basic Research, Staten Island, NY 10314, USA
    J Neural Transm 112:1035-47. 2005
  3. ncbi Biological markers in Alzheimer's disease
    I Grundke-Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    Bratisl Lek Listy 107:359-65. 2006
  4. ncbi Phosphorylation of tau at both Thr 231 and Ser 262 is required for maximal inhibition of its binding to microtubules
    A Sengupta
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    Arch Biochem Biophys 357:299-309. 1998
  5. ncbi Tau is phosphorylated by GSK-3 at several sites found in Alzheimer disease and its biological activity markedly inhibited only after it is prephosphorylated by A-kinase
    J Z Wang
    Chemical Neuropathology Department, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    FEBS Lett 436:28-34. 1998
  6. ncbi Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Biol Chem 275:5535-44. 2000
  7. ncbi Aberrant glycosylation modulates phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5
    F Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Neuroscience 115:829-37. 2002
  8. ncbi Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    J Neural Transm Suppl 59:213-22. 2000
  9. ncbi Post-translational modifications of tau protein in Alzheimer's disease
    C X Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    J Neural Transm 112:813-38. 2005
  10. pmc Tau in Alzheimer disease and related tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Alzheimer Res 7:656-64. 2010

Collaborators

Detail Information

Publications24

  1. ncbi Inhibition of neurofibrillary degeneration: a promising approach to Alzheimer's disease and other tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Drug Targets 5:495-502. 2004
    ..Thus, the development of drugs that inhibit neurofibrillary degeneration is a very promising and feasible therapeutic approach to AD and related tauopathies...
  2. ncbi Hyperphosphorylation-induced self assembly of murine tau: a comparison with human tau
    M O Chohan
    Department of Neurochemistry, NYS Institute for Basic Research, Staten Island, NY 10314, USA
    J Neural Transm 112:1035-47. 2005
    ..The filaments obtained from self assembly of murine tau closely resembled those formed from identically treated human tau. Moreover, like human tau, 60-70% of murine tau aggregated on hyperphosphorylation...
  3. ncbi Biological markers in Alzheimer's disease
    I Grundke-Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    Bratisl Lek Listy 107:359-65. 2006
    ..Identification of various subgroups of AD will help improvement in diagnoses and development of potent therapeutic drugs (Tab. 2, Fig. 2, Ref. 53)...
  4. ncbi Phosphorylation of tau at both Thr 231 and Ser 262 is required for maximal inhibition of its binding to microtubules
    A Sengupta
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    Arch Biochem Biophys 357:299-309. 1998
    ..Together, our results indicate that the binding of tau to microtubules is controlled by the phosphorylation of several sites, among which are Thr 231, Ser 235, and Ser 262...
  5. ncbi Tau is phosphorylated by GSK-3 at several sites found in Alzheimer disease and its biological activity markedly inhibited only after it is prephosphorylated by A-kinase
    J Z Wang
    Chemical Neuropathology Department, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314 6399, USA
    FEBS Lett 436:28-34. 1998
    ..Thus a combined role of A-kinase and GSK-3 should be considered in Alzheimer neurofibrillary degeneration...
  6. ncbi Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314 6399, USA
    J Biol Chem 275:5535-44. 2000
    ..A down-regulation of protein phosphatase 2A activity can lead to Alzheimer-like abnormal hyperphosphorylation of tau...
  7. ncbi Aberrant glycosylation modulates phosphorylation of tau by protein kinase A and dephosphorylation of tau by protein phosphatase 2A and 5
    F Liu
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Neuroscience 115:829-37. 2002
    ..The combined impact of this modulation may be to make tau more susceptible to becoming abnormally hyperphosphorylated...
  8. ncbi Mechanism of neurofibrillary degeneration and pharmacologic therapeutic approach
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    J Neural Transm Suppl 59:213-22. 2000
    ..e. PHF/SF. Increase in tau phosphatase activity is a promising approach to inhibit neurofibrillary degeneration and thereby the diseases characterized by this lesion...
  9. ncbi Post-translational modifications of tau protein in Alzheimer's disease
    C X Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    J Neural Transm 112:813-38. 2005
    ..Analyses of the current advances in tau modifications suggest that intervention addressing these abnormalities may offer promising therapeutic opportunities to prevent and treat neurofibrillary degeneration of AD and other tauopathies...
  10. pmc Tau in Alzheimer disease and related tauopathies
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314 6399, USA
    Curr Alzheimer Res 7:656-64. 2010
    ..Inhibition of abnormal hyperphosphorylation of tau offers a promising therapeutic target for AD and related tauopathies...
  11. pmc Hyperphosphorylation induces self-assembly of tau into tangles of paired helical filaments/straight filaments
    A Alonso
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA
    Proc Natl Acad Sci U S A 98:6923-8. 2001
    ....
  12. ncbi Interaction of tau isoforms with Alzheimer's disease abnormally hyperphosphorylated tau and in vitro phosphorylation into the disease-like protein
    A D Alonso
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York 10314, USA
    J Biol Chem 276:37967-73. 2001
    ..Thus, lack of amino-terminal inserts and extra microtubule binding domain repeat in fetal human brain might be protective from Alzheimer's neurofibrillary degeneration...
  13. pmc Hyperphosphorylation of microtubule-associated protein tau: a promising therapeutic target for Alzheimer disease
    C X Gong
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    Curr Med Chem 15:2321-8. 2008
    ..Development of drugs on the basis of these strategies is likely to lead to disease-modifying therapies for AD...
  14. ncbi Metabolically active rat brain slices as a model to study the regulation of protein phosphorylation in mammalian brain
    C X Gong
    New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, NY 10314, USA
    Brain Res Brain Res Protoc 6:134-40. 2001
    ..Furthermore, unlike cultured cells, the neurons in the brain slices reside in the physiological environment of the brain consisting of natural extracellular matrix, neuronal connectivity, and neuronal-glial interactions...
  15. ncbi Multiple forms of phosphatase from human brain: isolation and partial characterization of affi-gel blue nonbinding phosphatase activities
    L Y Cheng
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA
    Neurochem Res 26:425-38. 2001
    ..The resulting dephosphorylated tau regained its activity in promoting the microtubule assembly, suggesting that P7-P11 might regulate the phosphorylation of tau protein in the brain...
  16. ncbi PP2B isolated from human brain preferentially dephosphorylates Ser-262 and Ser-396 of the Alzheimer disease abnormally hyperphosphorylated tau
    A Rahman
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA
    J Neural Transm 113:219-30. 2006
    ..The preferential dephosphorylation of Ser262 and Ser396 by PP2B suggests a possible involvement of this phosphatase in Alzheimer neurofibrillary degeneration...
  17. ncbi From tangles to tau protein
    K Iqbal
    New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA
    Bratisl Lek Listy 107:341-2. 2006
    ..Finally, after one hundred years the exact nature of the neurofibrillary tangles and their role in neurodegeneration is beginning to be unraveled...
  18. pmc Developing pharmacological therapies for Alzheimer disease
    K Iqbal
    Department of Neurochemistry, New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, Staten Island, New York 10314, USA
    Cell Mol Life Sci 64:2234-44. 2007
    ..Restoration of the phosphatase activity which is downregulated in AD brain or inhibition of GSK-3beta and cdk5, which are required for AD-type abnormal hyperphosphorylation of tau, are among the most promising therapeutic strategies...
  19. ncbi Microtubule associated protein tau binds to double-stranded but not single-stranded DNA
    Q Hua
    Laboratory of Visual Information Processing, Center for Brain and Cognitive Sciences, Institute of Biophysics, The Chinese Academy of Sciences, 15 Da Tun Rd, Chaoyang District, Beijing 100101, China
    Cell Mol Life Sci 60:413-21. 2003
    ..Thus, tau appears to bind to DNA reversibly in the presence of histones...
  20. ncbi Consensus paper of the WFSBP Task Force on Biological Markers of Dementia: the role of CSF and blood analysis in the early and differential diagnosis of dementia
    J Wiltfang
    Molecular Neurobiology Lab, Department of Psychiatry and Psychotherapy, University of Erlangen Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany
    World J Biol Psychiatry 6:69-84. 2005
    ..Novel perspectives offered by recently introduced technologies, e.g, fluorescence correlation spectroscopy (FCS) and surface enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF MS) are briefly discussed...
  21. ncbi A pool of beta-tubulin is hyperphosphorylated at serine residues in Alzheimer disease brain
    S Vijayan
    Center for Developmental Neuroscience, The Graduate School and University Center of The City University of New York, NY 10016 4309, USA
    FEBS Lett 509:375-81. 2001
    ..The purified protein was hyperphosphorylated at serine residues in AD...
  22. pmc Alzheimer neurofibrillary degeneration: significance, etiopathogenesis, therapeutics and prevention
    K Iqbal
    Department of Neurochemistry New York State Institute for Basic Research in Developmental Disabilities, Forest Hill Road, Staten Island, New York, NY 10314, USA
    J Cell Mol Med 12:38-55. 2008
    ..The AD subgroup identification of patients can help increase the success of clinical trials and the development of specific and potent disease modifying drugs...
  23. ncbi Post-translational modifications of tau protein
    M Pevalova
    Institute of Neuroimmunology, Slovak Academy of Sciences, Bratislava, Slovakia
    Bratisl Lek Listy 107:346-53. 2006
    ..1, ref. 86)...
  24. ncbi Analysis of N-glycans of pathological tau: possible occurrence of aberrant processing of tau in Alzheimer's disease
    Y Sato
    Department of Glycobiology, Tokyo Metropolitan Institute of Gerontology, Japan
    FEBS Lett 496:152-60. 2001
    ..More truncated glycans were richer in PHF-tau than AD P-tau. This enrichment of more truncated glycans in PHF might be involved in promoting the assembly and or stabilizing the pathological fibrils in AD...