H Schulman

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. ncbi request reprint Interaction with the NMDA receptor locks CaMKII in an active conformation
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, California 94305 5125, USA
    Nature 411:801-5. 2001
  2. ncbi request reprint Nitric oxide: a spatial second messenger
    H Schulman
    Department of Neurobiology, Stanford University School of Medicine, CA 94305 5401, USA
    Mol Psychiatry 2:296-9. 1997
  3. ncbi request reprint A mechanism for Ca2+/calmodulin-dependent protein kinase II clustering at synaptic and nonsynaptic sites based on self-association
    Andy Hudmon
    Department of Neurobiology, Stanford University, Stanford, California 94305, USA
    J Neurosci 25:6971-83. 2005
  4. ncbi request reprint Developmental expression of the CaM kinase II isoforms: ubiquitous gamma- and delta-CaM kinase II are the early isoforms and most abundant in the developing nervous system
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305 5125, USA
    Brain Res Mol Brain Res 70:147-54. 1999
  5. pmc CaMKII tethers to L-type Ca2+ channels, establishing a local and dedicated integrator of Ca2+ signals for facilitation
    Andy Hudmon
    Department of Neurobiology, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 171:537-47. 2005
  6. pmc An ultrasensitive Ca2+/calmodulin-dependent protein kinase II-protein phosphatase 1 switch facilitates specificity in postsynaptic calcium signaling
    J Michael Bradshaw
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 100:10512-7. 2003
  7. pmc Alternative splicing modulates the frequency-dependent response of CaMKII to Ca(2+) oscillations
    K Ulrich Bayer
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305 5125, USA
    EMBO J 21:3590-7. 2002
  8. ncbi request reprint Neuronal CA2+/calmodulin-dependent protein kinase II: the role of structure and autoregulation in cellular function
    Andy Hudmon
    Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Stanford, California 94305, USA
    Annu Rev Biochem 71:473-510. 2002
  9. pmc Structure-function of the multifunctional Ca2+/calmodulin-dependent protein kinase II
    Andy Hudmon
    Department of Neurobiology, Fairchild Bldg, D217 299 Campus Drive, Stanford University Medical School, Stanford, CA 94305 5125, USA
    Biochem J 364:593-611. 2002
  10. ncbi request reprint Molecular characterization of calmodulin trapping by calcium/calmodulin-dependent protein kinase II
    S I Singla
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305-5125, USA
    J Biol Chem 276:29353-60. 2001

Collaborators

Detail Information

Publications27

  1. ncbi request reprint Interaction with the NMDA receptor locks CaMKII in an active conformation
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, California 94305 5125, USA
    Nature 411:801-5. 2001
    ..Furthermore, the interaction leads to trapping of CaM that may reduce down-regulation of NMDA receptor activity. CaMKII-NR2B interaction may be prototypical for direct activation of a kinase by its targeting protein...
  2. ncbi request reprint Nitric oxide: a spatial second messenger
    H Schulman
    Department of Neurobiology, Stanford University School of Medicine, CA 94305 5401, USA
    Mol Psychiatry 2:296-9. 1997
    ..Dopamine in turn can alter the strength of glutamatergic synapses and affect synaptic plasticity...
  3. ncbi request reprint A mechanism for Ca2+/calmodulin-dependent protein kinase II clustering at synaptic and nonsynaptic sites based on self-association
    Andy Hudmon
    Department of Neurobiology, Stanford University, Stanford, California 94305, USA
    J Neurosci 25:6971-83. 2005
    ..We discuss the potential function of CaMKII self-association as a tag of synaptic activity...
  4. ncbi request reprint Developmental expression of the CaM kinase II isoforms: ubiquitous gamma- and delta-CaM kinase II are the early isoforms and most abundant in the developing nervous system
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305 5125, USA
    Brain Res Mol Brain Res 70:147-54. 1999
    ..Additionally, we describe the murine betaM-CaM kinase II, a variant of the 'brain-specific' beta-CaM kinase II, which is highly expressed in skeletal muscle...
  5. pmc CaMKII tethers to L-type Ca2+ channels, establishing a local and dedicated integrator of Ca2+ signals for facilitation
    Andy Hudmon
    Department of Neurobiology, Stanford University, Stanford, CA 94305, USA
    J Cell Biol 171:537-47. 2005
    ..These findings clarify the molecular basis of CDF and demonstrate a novel enzymatic mechanism by which ion channel gating can be modulated by activity...
  6. pmc An ultrasensitive Ca2+/calmodulin-dependent protein kinase II-protein phosphatase 1 switch facilitates specificity in postsynaptic calcium signaling
    J Michael Bradshaw
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 100:10512-7. 2003
    ....
  7. pmc Alternative splicing modulates the frequency-dependent response of CaMKII to Ca(2+) oscillations
    K Ulrich Bayer
    Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305 5125, USA
    EMBO J 21:3590-7. 2002
    ..Taken together, our results suggest that alternative splicing provides cells with a mechanism to modulate their sensitivity to Ca(2+) oscillations...
  8. ncbi request reprint Neuronal CA2+/calmodulin-dependent protein kinase II: the role of structure and autoregulation in cellular function
    Andy Hudmon
    Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Stanford, California 94305, USA
    Annu Rev Biochem 71:473-510. 2002
    ....
  9. pmc Structure-function of the multifunctional Ca2+/calmodulin-dependent protein kinase II
    Andy Hudmon
    Department of Neurobiology, Fairchild Bldg, D217 299 Campus Drive, Stanford University Medical School, Stanford, CA 94305 5125, USA
    Biochem J 364:593-611. 2002
    ..The molecular determinants and mechanisms producing these processes are discussed as they relate to the structure-function of this multifunctional protein kinase...
  10. ncbi request reprint Molecular characterization of calmodulin trapping by calcium/calmodulin-dependent protein kinase II
    S I Singla
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305-5125, USA
    J Biol Chem 276:29353-60. 2001
    ....
  11. ncbi request reprint Regulation of signal transduction by protein targeting: the case for CaMKII
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305-5125, USA
    Biochem Biophys Res Commun 289:917-23. 2001
    ..The interaction of CaMKII with the NMDA receptor, for instance, shows that a targeting protein can not only specify the subcellular localization of a signaling effector, but can also directly influence its regulation...
  12. ncbi request reprint Kinetic and pharmacological properties of GABA(A) receptors in single thalamic neurons and GABA(A) subunit expression
    S H Browne
    Department of Neurobiology, Stanford University School of Medicine, Stanford, California 94305-5122, USA
    J Neurophysiol 86:2312-22. 2001
    ..As the gamma2 and delta subunits previously implicated in Zn(2+) sensitivity are both expressed in each cell type, the observed differential Zn(2+) actions at VB versus nRt GABA(A) receptors may involve other subunit differences...
  13. ncbi request reprint The role of Ca2+/calmodulin-dependent protein kinases within the nucleus
    E K Heist
    Department of Neurobiology, Stanford University School of Medicine, CA 94305 5125, USA
    Cell Calcium 23:103-14. 1998
    ..CaM kinases may thus serve to decode Ca2+ signals to the nucleus in order to produce a multitude of cellular responses including control of cell cycle, apoptosis and synaptic efficacy...
  14. ncbi request reprint Calcium regulation of exocytosis in PC12 cells
    Y A Chen
    Howard Hughes Medical Institute, Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, California 94305-5345, USA
    J Biol Chem 276:26680-7. 2001
    ..Finally, we showed that the previously demonstrated stimulation of exocytosis in this system by calmodulin required calcium binding, since calmodulin mutants defective in Ca(2+)-binding were not able to enhance release...
  15. ncbi request reprint Calcium/calmodulin-dependent protein kinase II (CaMKII) localization acts in concert with substrate targeting to create spatial restriction for phosphorylation
    Jennifer Tsui
    Neurosciences Program, Stanford University School of Medicine, Stanford, California 94304, USA
    J Biol Chem 280:9210-6. 2005
    ..Thus, dynamic regulation of both substrate and kinase localization provides a powerful and nuanced way to regulate CaMKII signal specificity...
  16. pmc alphaKAP is an anchoring protein for a novel CaM kinase II isoform in skeletal muscle
    K U Bayer
    Department of Neurobiology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305 5125, USA
    EMBO J 17:5598-605. 1998
    ..A new variant of beta-CaM kinase II, termed betaM-CaM kinase II, is one of the predominant CaM kinase II isoforms associated with alphaKAP in skeletal muscle SR...
  17. ncbi request reprint Chemical quenched flow kinetic studies indicate an intraholoenzyme autophosphorylation mechanism for Ca2+/calmodulin-dependent protein kinase II
    J Michael Bradshaw
    Department of Neurobiology, Stanford University, Stanford, California 94305, USA
    J Biol Chem 277:20991-8. 2002
    ..The ability of CaM kinase II to autophosphorylate through an intraholoenzyme, intersubunit mechanism is likely central to its functions of decoding Ca(2+) spike frequency and providing a sustained response to Ca(2+) signals...
  18. ncbi request reprint CaMKII structure--an elegant design
    Tony Hunter
    Molecular and Cell Biology Laboratory, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA
    Cell 123:765-7. 2005
    ..This study provides new mechanistic insights into the workings of this finely tuned molecular machine...
  19. ncbi request reprint Regulation of calcium/calmodulin-dependent protein kinase II docking to N-methyl-D-aspartate receptors by calcium/calmodulin and alpha-actinin
    A Soren Leonard
    Department of Pharmacology, University of Wisconsin, Madison 53706 1532, USA
    J Biol Chem 277:48441-8. 2002
    ..We conclude that the NR1 C0 region is a key site for recruiting CaMKII to the postsynaptic site, where it may act in concert with calmodulin to modulate the stimulatory role of alpha-actinin interaction with the NMDA receptor...
  20. pmc Transition from reversible to persistent binding of CaMKII to postsynaptic sites and NR2B
    K Ulrich Bayer
    Department of Pharmacology, Program in Neuroscience, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Neurosci 26:1164-74. 2006
    ..This activity-dependent incorporation of CaMKII into postsynaptic sites may play a role in maturation and plasticity of synapses...
  21. ncbi request reprint Activity-dependent regulation of calcium/calmodulin-dependent protein kinase II localization
    Howard Schulman
    SurroMed Inc, Menlo Park, California 94025 1432, USA
    J Neurosci 24:8399-403. 2004
  22. ncbi request reprint Inhibition of CaMKII-mediated c-FLIP expression sensitizes malignant melanoma cells to TRAIL-induced apoptosis
    Chang Xiao
    Department of Laboratory Medicine and Pathology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2
    Exp Cell Res 304:244-55. 2005
    ..These results indicate that the CaMKII-mediated pathway for c-FLIP upregulation protects melanoma cells from TRAIL-induced apoptosis and targeting this pathway may provide novel therapeutic strategies in treatment of melanomas...
  23. ncbi request reprint Neuroprotective effect of activity-dependent neurotrophic factor against toxicity from familial amyotrophic lateral sclerosis-linked mutant SOD1 in vitro and in vivo
    Tomohiro Chiba
    Department of Pharmacology, Keio University School of Medicine, Tokyo, Japan
    J Neurosci Res 78:542-52. 2004
    ..Thus, the neuroprotective activity of ADNF provides a novel insight into the development of curative drugs for ALS...
  24. ncbi request reprint Ca2+/calmodulin-dependent protein kinase II is required for microcystin-induced apoptosis
    Kari E Fladmark
    Department of Anatomy and Cell Biology, University of Bergen, Arstadveien 19, N 5009 Bergen, Norway
    J Biol Chem 277:2804-11. 2002
    ..It is concluded that the apoptogenic toxins, presumably through their known ability to inhibit serine/threonine protein phosphatases, can cause CaMKII-dependent phosphorylation events leading to cell death...
  25. ncbi request reprint Selective regulation of neurite extension and synapse formation by the beta but not the alpha isoform of CaMKII
    Charles C Fink
    Department of Molecular Pharmacology, Stanford University Medical School, Stanford, CA 94305, USA
    Neuron 39:283-97. 2003
    ..These results show that the two main neuronal CaMKII isoforms have markedly different roles in neuronal plasticity, with CaMKIIalpha regulating synaptic strength and CaMKIIbeta controlling the dendritic morphology and number of synapses...
  26. ncbi request reprint The cardiac-specific nuclear delta(B) isoform of Ca2+/calmodulin-dependent protein kinase II induces hypertrophy and dilated cardiomyopathy associated with increased protein phosphatase 2A activity
    Tong Zhang
    Department of Pharmacology and Medicine, University of California, San Diego, La Jolla, California 92093, USA
    J Biol Chem 277:1261-7. 2002
    ..Our findings are the first to demonstrate that CaMKII can induce hypertrophy and dilation in vivo and indicate that compensatory increases in phosphatase activity contribute to the resultant phenotype...
  27. ncbi request reprint Disease mechanisms and emerging therapies: protein kinases and their inhibitors in myocardial disease
    Mark E Anderson
    Cardiovascular Research Center at the University of Iowa, Iowa City 52242 1081, USA
    Nat Clin Pract Cardiovasc Med 3:437-45. 2006
    ....