JOHN ENYEART

Summary

Affiliation: The Ohio State University
Country: USA

Publications

  1. ncbi request reprint Biochemical and Ionic signaling mechanisms for ACTH-stimulated cortisol production
    John J Enyeart
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210, USA
    Vitam Horm 70:265-79. 2005
  2. pmc Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca2+ channels that regulate cortisol secretion
    John J Enyeart
    Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, Ohio
    Am J Physiol Cell Physiol 308:C899-918. 2015
  3. pmc Dual patch voltage clamp study of low membrane resistance astrocytes in situ
    Baofeng Ma
    Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
    Mol Brain 7:18. 2014
  4. pmc Metabolites of an Epac-selective cAMP analog induce cortisol synthesis by adrenocortical cells through a cAMP-independent pathway
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA
    PLoS ONE 4:e6088. 2009
  5. pmc ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways
    Haiyan Liu
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210, USA
    J Gen Physiol 132:279-94. 2008
  6. pmc Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: properties and modulation by ACTH and AngII
    John J Enyeart
    Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
    J Gen Physiol 142:137-55. 2013
  7. doi request reprint Evidence for cAMP-independent bTREK-1 inhibition by ACTH and NPS-ACTH in adrenocortical cells
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH 43210 1239, USA
    Mol Cell Endocrinol 348:305-12. 2012
  8. pmc Calcium-dependent inhibition of adrenal TREK-1 channels by angiotensin II and ionomycin
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, 43210 1239, USA
    Am J Physiol Cell Physiol 301:C619-29. 2011
  9. pmc cAMP analogs and their metabolites enhance TREK-1 mRNA and K+ current expression in adrenocortical cells
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, 5196 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210 1239, USA
    Mol Pharmacol 77:469-82. 2010
  10. pmc Curcumin inhibits bTREK-1 K+ channels and stimulates cortisol secretion from adrenocortical cells
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, 5196 Graves Hall, 333 W 10th Avenue, Columbus, OH 43210 1239, USA
    Biochem Biophys Res Commun 370:623-8. 2008

Research Grants

Collaborators

  • Haiyan Liu
  • Baofeng Ma
  • Sanjay J Danthi
  • Sanjay Danthi
  • Wei Wang
  • Guangjin Xu
  • Min Zhou

Detail Information

Publications25

  1. ncbi request reprint Biochemical and Ionic signaling mechanisms for ACTH-stimulated cortisol production
    John J Enyeart
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210, USA
    Vitam Horm 70:265-79. 2005
    ....
  2. pmc Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca2+ channels that regulate cortisol secretion
    John J Enyeart
    Department of Neuroscience, Wexner Medical Center, The Ohio State University, Columbus, Ohio
    Am J Physiol Cell Physiol 308:C899-918. 2015
    ..Regardless, the well-correlated selective inhibition of T- and L-type currents and ACTH- and ANG II-stimulated cortisol secretion by TTA-P2 and nifedipine establish the critical importance of these channels in AZF cell physiology...
  3. pmc Dual patch voltage clamp study of low membrane resistance astrocytes in situ
    Baofeng Ma
    Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
    Mol Brain 7:18. 2014
    ..This protocol can be performed routinely in the study of astrocytes. This method will be valuable for identifying and characterizing the individual ion channels that orchestrate the electrical activity of low membrane resistance cells. ..
  4. pmc Metabolites of an Epac-selective cAMP analog induce cortisol synthesis by adrenocortical cells through a cAMP-independent pathway
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH, USA
    PLoS ONE 4:e6088. 2009
    ..The remarkable increases in cortisol synthesis observed in this study appear to be mediated by a novel cAMP-, Epac- and PKA-independent signaling pathway...
  5. pmc ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways
    Haiyan Liu
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, OH 43210, USA
    J Gen Physiol 132:279-94. 2008
    ..The convergent inhibition of bTREK-1 through parallel PKA- and Epac-dependent mechanisms may provide for failsafe membrane depolarization by ACTH...
  6. pmc Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: properties and modulation by ACTH and AngII
    John J Enyeart
    Department of Neuroscience, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA
    J Gen Physiol 142:137-55. 2013
    ..These findings also suggest a model for cortisol secretion in human AZF cells wherein ACTH and AngII receptor activation is coupled to membrane depolarization and the activation of Cav3.2 channels through inhibition of hTREK-1. ..
  7. doi request reprint Evidence for cAMP-independent bTREK-1 inhibition by ACTH and NPS-ACTH in adrenocortical cells
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH 43210 1239, USA
    Mol Cell Endocrinol 348:305-12. 2012
    ..These results indicate that ACTH and NPS-ACTH can inhibit native bTREK-1 K(+) channels in AZF cells by a mechanism that does not involve activation of AC...
  8. pmc Calcium-dependent inhibition of adrenal TREK-1 channels by angiotensin II and ionomycin
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, 43210 1239, USA
    Am J Physiol Cell Physiol 301:C619-29. 2011
    ..bTREK-1 is the first two-pore K(+) channel shown to be inhibited by Ca(2+) through activation of a G protein-coupled receptor...
  9. pmc cAMP analogs and their metabolites enhance TREK-1 mRNA and K+ current expression in adrenocortical cells
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, 5196 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210 1239, USA
    Mol Pharmacol 77:469-82. 2010
    ..These findings raise significant questions regarding the specificity of 8-(4-chlorophenylthio)-cAMP analogs as cAMP mimetics...
  10. pmc Curcumin inhibits bTREK-1 K+ channels and stimulates cortisol secretion from adrenocortical cells
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, 5196 Graves Hall, 333 W 10th Avenue, Columbus, OH 43210 1239, USA
    Biochem Biophys Res Commun 370:623-8. 2008
    ..Since TREK-1 is widely expressed in a variety of cells, it is likely that some of the biological actions of curcumin, including its therapeutic effects, may be mediated through inhibition of these K(+) channels...
  11. pmc Adenosine triphosphate activates a noninactivating K+ current in adrenal cortical cells through nonhydrolytic binding
    J J Enyeart
    Department of Pharmacology, The Ohio State University, College of Medicine, Columbus, Ohio 43210 1239, USA
    J Gen Physiol 110:679-92. 1997
    ....
  12. ncbi request reprint An ACTH- and ATP-regulated background K+ channel in adrenocortical cells is TREK-1
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine, 5190 Graves Hall, 333 W 10th Avenue, Columbus, OH 43210 1239, USA
    J Biol Chem 277:49186-99. 2002
    ..The activation of I(AC) by ATP indicates that native bTREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein...
  13. ncbi request reprint Corticotropin induces the expression of TREK-1 mRNA and K+ current in adrenocortical cells
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine, Columbus, OH, USA
    Mol Pharmacol 64:132-42. 2003
    ....
  14. ncbi request reprint TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells
    Judith A Enyeart
    Dept of Neuroscience, College of Medicine and Public Health, The Ohio State University, 5196 Graves Hall, 333 W 10th Ave, Columbus, OH 43210 1239, USA
    Am J Physiol Endocrinol Metab 287:E1154-65. 2004
    ..Overall, these results identify bTREK-1 K(+) channels as a pivotal control point where ANG II receptor activation is transduced to depolarization-dependent Ca(2+) entry and aldosterone secretion...
  15. ncbi request reprint Angiotensin II inhibits bTREK-1 K+ channels in adrenocortical cells by separate Ca2+- and ATP hydrolysis-dependent mechanisms
    John J Enyeart
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210 1239, USA
    J Biol Chem 280:30814-28. 2005
    ..The novel Ca2+-dependent pathway is distinctive in its lack of ATP dependence, and is clearly different from the calmodulin kinase-dependent mechanism by which AngII modulates T-type Ca2+ channels in these cells...
  16. pmc 8-Phenylthio-adenines stimulate the expression of steroid hydroxylases, Cav3.2 Ca²⁺ channels, and cortisol synthesis by a cAMP-independent mechanism
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210 1269, USA
    Am J Physiol Endocrinol Metab 301:E941-54. 2011
    ..2 Ca(2+) channels. These phenylthio-adenine compounds and ACTH may stimulate cortisol synthesis through the same cAMP-independent mechanism...
  17. ncbi request reprint Angiotensin II inhibits native bTREK-1 K+ channels through a PLC-, kinase C-, and PIP2-independent pathway requiring ATP hydrolysis
    Haiyan Liu
    Dept of Neuroscience, The Ohio State University, College of Medicine and Public Health, 5196 Graves Hall, Columbus, OH 43210 1239, USA
    Am J Physiol Cell Physiol 293:C682-95. 2007
    ..They also indicate that, under physiological conditions, ANG II inhibits bTREK-1 and depolarizes AZF cells by two, novel, independent pathways that diverge proximal to the activation of PLC...
  18. ncbi request reprint Dual actions of lanthanides on ACTH-inhibited leak K(+) channels
    John J Enyeart
    Department of Neuroscience, The Ohio State University, College of Medicine, Columbus, Ohio 43210
    Am J Physiol Endocrinol Metab 282:E1255-66. 2002
    ..Allosteric actions of trivalent and divalent metal cations on hormone binding, mediated through Ca(2+)-specific sites, may be common to a variety of peptide hormone receptors...
  19. ncbi request reprint Caffeic acid esters activate TREK-1 potassium channels and inhibit depolarization-dependent secretion
    Sanjay Danthi
    Department of Neuroscience, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43210 1239, USA
    Mol Pharmacol 65:599-610. 2004
    ..Because of their ability to stabilize the resting membrane potential and oppose electrical activity and depolarization-dependent Ca2+ entry, these compounds may have therapeutic potential as neuroprotective or cardioprotective agents...
  20. ncbi request reprint Modulation of native T-type calcium channels by omega-3 fatty acids
    Sanjay J Danthi
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH 43210 1239, USA
    Biochem Biophys Res Commun 327:485-93. 2005
    ..Inhibition of T-type Ca(2+) channels in neurons and cardiac myocytes could contribute significantly to their protective actions...
  21. pmc N6-substituted cAMP analogs inhibit bTREK-1 K+ channels and stimulate cortisol secretion by a protein kinase A-independent mechanism
    Haiyan Liu
    Department of Neuroscience, OSU College of Medicine and Public Health, Columbus, OH, USA
    Mol Pharmacol 76:1290-301. 2009
    ..Finally, although 6-modified cAMP analogs exhibit high selectivity in activating PKA over Epac, they also may interact with other unidentified proteins expressed by eukaryotic cells...
  22. pmc ACTH induces Cav3.2 current and mRNA by cAMP-dependent and cAMP-independent mechanisms
    Haiyan Liu
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, Ohio 43210 1239, USA
    J Biol Chem 285:20040-50. 2010
    ..Surprisingly, chlorophenylthio-cAMP analogs stimulate the expression of Ca(v)3.2 current indirectly through metabolites. ACTH and the metabolites may induce Ca(v)3.2 expression by the same, unidentified mechanism...
  23. pmc Curcumin inhibits ACTH- and angiotensin II-stimulated cortisol secretion and Ca(v)3.2 current
    Judith A Enyeart
    Department of Neuroscience, The Ohio State University College of Medicine and Public Health, Columbus, Ohio 43210 1239, USA
    J Nat Prod 72:1533-7. 2009
    ..2 current. These results identify curcumin as an effective inhibitor of ACTH- and AngII-stimulated cortisol secretion. The inhibition of Ca(v)3.2 current by curcumin may contribute to its suppression of secretion...
  24. pmc Potent inhibition of native TREK-1 K+ channels by selected dihydropyridine Ca2+ channel antagonists
    Haiyan Liu
    Department of Neuroscience, 5196 Graves Hall, College of Medicine and Public Health, The Ohio State University, 333 W 10th Ave, Columbus, OH 43210 1239, USA
    J Pharmacol Exp Ther 323:39-48. 2007
    ....
  25. pmc Curcumin potently blocks Kv1.4 potassium channels
    Haiyan Liu
    Department of Neuroscience, The Ohio State University, College of Medicine and Public Health, Columbus, OH 43210 1239, USA
    Biochem Biophys Res Commun 344:1161-5. 2006
    ..It remains to be seen whether any of the therapeutic actions of curcumin might originate with its ability to inhibit Kv1.4 or other voltage-gated K+ channel...

Research Grants1

  1. Properties of Ion Channels that Control Secretion
    JOHN ENYEART; Fiscal Year: 2008
    ..abstract_text> ..