Elizabeth Ann Jonas

Summary

Affiliation: Yale University
Country: USA

Publications

  1. pmc Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticity
    Elizabeth A Jonas
    Dept of Internal Medicine, P O Box 208001, Yale University School of Medicine, New Haven, CT 06520, USA Dept of Neurobiology, P O Box 208020, Yale University School of Medicine, New Haven, CT 06520, USA Electronic address
    Biochim Biophys Acta 1842:1168-78. 2014
  2. pmc A Bcl-xL-Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis
    Hongmei Li
    Department of Internal Medicine, Yale University, New Haven, Connecticut 06520, USA
    Nat Cell Biol 15:773-85. 2013
  3. pmc N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death
    Dimitry Ofengeim
    Dominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, USA
    Nat Neurosci 15:574-80. 2012
  4. pmc Molecular participants in mitochondrial cell death channel formation during neuronal ischemia
    Elizabeth Ann Jonas
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Exp Neurol 218:203-12. 2009
  5. ncbi request reprint BCL-xL regulates synaptic plasticity
    Elizabeth Jonas
    Yale University School of Medicine, Section of Endocrinology, Department of Internal Medicine, 333 Cedar Street, PO Box 208020, New Haven, CT 06520 8020, USA
    Mol Interv 6:208-22. 2006
  6. ncbi request reprint Actions of BAX on mitochondrial channel activity and on synaptic transmission
    Elizabeth A Jonas
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Antioxid Redox Signal 7:1092-100. 2005
  7. ncbi request reprint Exposure to hypoxia rapidly induces mitochondrial channel activity within a living synapse
    Elizabeth A Jonas
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 280:4491-7. 2005
  8. ncbi request reprint Regulation of synaptic transmission by mitochondrial ion channels
    Elizabeth Jonas
    Department of Internal Medicine Endocrinology, Yale University School of Medicine, 333 Cedar St, PO Box 208020, New Haven, Connecticut 06520, USA
    J Bioenerg Biomembr 36:357-61. 2004
  9. pmc Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel
    Laurent M Dejean
    Department of Basic Sciences, College of Dentistry, New York University, New York, NY 10010, USA
    Mol Biol Cell 16:2424-32. 2005
  10. pmc Modulation of mitochondrial function by endogenous Zn2+ pools
    Stefano L Sensi
    Department of Neurology, University of California, Irvine 92697 4292, USA
    Proc Natl Acad Sci U S A 100:6157-62. 2003

Research Grants

  1. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2004
  2. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
  3. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
  4. Role of BCL-xL in synaptic plasticity in the hippocampus
    Elizabeth Jonas; Fiscal Year: 2009
  5. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Ann Jonas; Fiscal Year: 2010
  6. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
  7. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2007
  8. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2006
  9. Role of BCL-xL in synaptic plasticity in the hippocampus
    Elizabeth Ann Jonas; Fiscal Year: 2010
  10. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2005

Collaborators

Detail Information

Publications21

  1. pmc Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticity
    Elizabeth A Jonas
    Dept of Internal Medicine, P O Box 208001, Yale University School of Medicine, New Haven, CT 06520, USA Dept of Neurobiology, P O Box 208020, Yale University School of Medicine, New Haven, CT 06520, USA Electronic address
    Biochim Biophys Acta 1842:1168-78. 2014
    ..Bcl-xL is crucial to the normal health of neurons and synapses and its malfunction may contribute to neurodegenerative disease...
  2. pmc A Bcl-xL-Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis
    Hongmei Li
    Department of Internal Medicine, Yale University, New Haven, Connecticut 06520, USA
    Nat Cell Biol 15:773-85. 2013
    ..Mutagenesis studies suggest that formation of the Bcl-xL-Drp1 complex is necessary for the enhanced rate of vesicle endocytosis produced by Bcl-xL, thus providing a mechanism for presynaptic plasticity. ..
  3. pmc N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death
    Dimitry Ofengeim
    Dominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, USA
    Nat Neurosci 15:574-80. 2012
    ..These findings suggest that truncated Bcl-x(L) could be a potentially important therapeutic target in ischemic brain injury...
  4. pmc Molecular participants in mitochondrial cell death channel formation during neuronal ischemia
    Elizabeth Ann Jonas
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Exp Neurol 218:203-12. 2009
    ..The variety of possible molecular participants within the ion channel complex may be matched only by the variety of different types of programmed cell death...
  5. ncbi request reprint BCL-xL regulates synaptic plasticity
    Elizabeth Jonas
    Yale University School of Medicine, Section of Endocrinology, Department of Internal Medicine, 333 Cedar Street, PO Box 208020, New Haven, CT 06520 8020, USA
    Mol Interv 6:208-22. 2006
    ..BCL-xL, therefore, not only affects the life and death of the cell soma, but its actions in the synapse may underlie the regulation of basic synaptic processes that subtend learning, memory and synaptic development...
  6. ncbi request reprint Actions of BAX on mitochondrial channel activity and on synaptic transmission
    Elizabeth A Jonas
    Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
    Antioxid Redox Signal 7:1092-100. 2005
    ..Furthermore, the occasional large openings may reflect the function of "activated" BAX either to facilitate cell death or to play a physiological role in decreasing synaptic activity...
  7. ncbi request reprint Exposure to hypoxia rapidly induces mitochondrial channel activity within a living synapse
    Elizabeth A Jonas
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
    J Biol Chem 280:4491-7. 2005
    ....
  8. ncbi request reprint Regulation of synaptic transmission by mitochondrial ion channels
    Elizabeth Jonas
    Department of Internal Medicine Endocrinology, Yale University School of Medicine, 333 Cedar St, PO Box 208020, New Haven, Connecticut 06520, USA
    J Bioenerg Biomembr 36:357-61. 2004
    ..The opposing activities of BCL-xL and its proteolytic fragment may regulate the release of ATP from mitochondria during synaptic transmission...
  9. pmc Oligomeric Bax is a component of the putative cytochrome c release channel MAC, mitochondrial apoptosis-induced channel
    Laurent M Dejean
    Department of Basic Sciences, College of Dentistry, New York University, New York, NY 10010, USA
    Mol Biol Cell 16:2424-32. 2005
    ..These findings indicate Bax is a component of MAC in staurosporine-treated HeLa cells and suggest Bax and Bak are functionally redundant as components of MAC...
  10. pmc Modulation of mitochondrial function by endogenous Zn2+ pools
    Stefano L Sensi
    Department of Neurology, University of California, Irvine 92697 4292, USA
    Proc Natl Acad Sci U S A 100:6157-62. 2003
    ..Finally, strong mobilization of protein-bound Zn(2+) appeared to induce partial loss of Deltapsi(m), suggesting that movement of Zn(2+) between cytosolic and mitochondrial pools might be of functional significance in intact neurons...
  11. ncbi request reprint Modulation of synaptic transmission by the BCL-2 family protein BCL-xL
    Elizabeth A Jonas
    Department of Pharmacology, Yale University School of Medicine, New Haven, Connecticut 06250, USA
    J Neurosci 23:8423-31. 2003
    ....
  12. pmc Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals
    Elizabeth A Jonas
    Department of Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 101:13590-5. 2004
    ....
  13. pmc Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neurons
    Takahiro Miyawaki
    Dominick P Purpura Department of Neuroscience, Rose F Kennedy Center, Albert Einstein College of Medicine, Bronx, NY 10461, USA
    Proc Natl Acad Sci U S A 105:4892-7. 2008
    ..These findings implicate PI3K/Akt signaling in maintenance of the integrity of the mitochondrial outer membrane...
  14. pmc Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons
    Hongmei Li
    Department of Internal Medicine, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520, USA
    Proc Natl Acad Sci U S A 105:2169-74. 2008
    ..These findings suggest that Bcl-xL positively regulates Drp1 to alter mitochondrial function in a manner that stimulates synapse formation...
  15. pmc Bcl-xL inhibitor ABT-737 reveals a dual role for Bcl-xL in synaptic transmission
    John A Hickman
    Institut de Recherches Servier, Croissy sur Seine, France
    J Neurophysiol 99:1515-22. 2008
    ..These observations support the possibility that endogenous proteolysis or a functionally equivalent modification of BCL-xL is responsible for the deleterious effects of hypoxia on synaptic activity...
  16. ncbi request reprint Expression of the voltage-gated sodium channel NaV1.5 in the macrophage late endosome regulates endosomal acidification
    Michael D Carrithers
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA
    J Immunol 178:7822-32. 2007
    ..These results demonstrate a functionally relevant intracellular voltage-gated sodium channel and reveal a novel mechanism to regulate macrophage endosomal acidification...
  17. ncbi request reprint Hypoxia increases BK channel activity in the inner mitochondrial membrane
    Xiang Q Gu
    Department of Pediatrics Section of Respiratory Medicine, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0735, USA
    Biochem Biophys Res Commun 358:311-6. 2007
    ..We speculate that this increase in K(+) efflux from mitochondria into the cytosol is important during hypoxia in maintaining cytosolic K(+)...
  18. ncbi request reprint Zinc-dependent multi-conductance channel activity in mitochondria isolated from ischemic brain
    Laura Bonanni
    Department of Oncology and Neuroscience and Center for Excellence on Aging, d Annunzio Foundation, Università G d Annunzio Chieti, 66013 Chieti, Italy
    J Neurosci 26:6851-62. 2006
    ....
  19. ncbi request reprint The role of the mitochondrial apoptosis induced channel MAC in cytochrome c release
    Sonia Martinez-Caballero
    Department of Basic Sciences, New York University College of Dentistry, 345 East 24th Street, New York, NY 10010, USA
    J Bioenerg Biomembr 37:155-64. 2005
    ..Finally, the regulation of MAC by the Bcl-2 family proteins and insights concerning its molecular composition are also discussed...
  20. ncbi request reprint BAK alters neuronal excitability and can switch from anti- to pro-death function during postnatal development
    Yihru Fannjiang
    Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
    Dev Cell 4:575-85. 2003
    ..BAK can alter neurotransmitter release in a direction consistent with its protective effects on neurons and mice. These findings suggest that BAK inhibits cell death by modifying neuronal excitability...
  21. pmc PKC-induced intracellular trafficking of Ca(V)2 precedes its rapid recruitment to the plasma membrane
    Yalan Zhang
    Department of Pharmacology, Section of Endocrinology, Yale School of Medicine, New Haven, Connecticut 06520, USA
    J Neurosci 28:2601-12. 2008
    ..Only after activation of PKC do Ca(V)2 channels associate with actin and undergo insertion into the plasma membrane...

Research Grants11

  1. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2004
    ..The studies may also lead to new insights in the field of learning and memory. ..
  2. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
    ..We hypothesize that in the setting of brain ischemia, such channel activity leads to cell death in the brain and that this death can be prevented by a pharmacological inhibitor of BCL-2-induced mitochondrial ion channels. ..
  3. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
    ..We hypothesize that in the setting of brain ischemia, such channel activity leads to cell death in the brain and that this death can be prevented by a pharmacological inhibitor of BCL-2-induced mitochondrial ion channels. ..
  4. Role of BCL-xL in synaptic plasticity in the hippocampus
    Elizabeth Jonas; Fiscal Year: 2009
    ..We hypothesize that these changes are required for long term changes in synaptic strength after high frequency synaptic stimulation, therefore we plan to test whether inhibition of BClxl prevents l TP. ..
  5. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Ann Jonas; Fiscal Year: 2010
    ..We hypothesize that in the setting of brain ischemia, such channel activity leads to cell death in the brain and that this death can be prevented by a pharmacological inhibitor of BCL-2-induced mitochondrial ion channels. ..
  6. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2009
    ..We hypothesize that in the setting of brain ischemia, such channel activity leads to cell death in the brain and that this death can be prevented by a pharmacological inhibitor of BCL-2-induced mitochondrial ion channels. ..
  7. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2007
    ..The studies may also lead to new insights in the field of learning and memory. ..
  8. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2006
    ..The studies may also lead to new insights in the field of learning and memory. ..
  9. Role of BCL-xL in synaptic plasticity in the hippocampus
    Elizabeth Ann Jonas; Fiscal Year: 2010
    ..We hypothesize that these changes are required for long term changes in synaptic strength after high frequency synaptic stimulation, therefore we plan to test whether inhibition of BClxl prevents l TP. ..
  10. Mitochondrial ion channels in hypoxic neurons
    Elizabeth Jonas; Fiscal Year: 2005
    ..The studies may also lead to new insights in the field of learning and memory. ..