Mark Estacion

Summary

Affiliation: Yale University
Country: USA

Publications

  1. doi request reprint A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Neurol 224:362-8. 2010
  2. doi request reprint A sodium channel gene SCN9A polymorphism that increases nociceptor excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven CT
    Ann Neurol 66:862-6. 2009
  3. pmc Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel
    Yang Yang
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nat Commun 3:1186. 2012
  4. pmc Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable
    Sulayman D Dib-Hajj
    Deptartment of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 4:37. 2008
  5. pmc Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 7:92. 2011
  6. doi request reprint A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia
    Tanya Z Fischer
    Department of Neurology, Yale University School of Medicine, New Haven, CT 16510, USA
    Ann Neurol 65:733-41. 2009
  7. doi request reprint A new Nav1.7 mutation in an erythromelalgia patient
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Biochem Biophys Res Commun 432:99-104. 2013
  8. pmc Molecular architecture of a sodium channel S6 helix: radial tuning of the voltage-gated sodium channel 1.7 activation gate
    Yang Yang
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 288:13741-7. 2013
  9. doi request reprint Differential effect of D623N variant and wild-type Nav1.7 sodium channels on resting potential and interspike membrane potential of dorsal root ganglion neurons
    Hye Sook Ahn
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510 8018, United States Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, United States Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516, United States
    Brain Res 1529:165-77. 2013
  10. pmc Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 6:35. 2010

Collaborators

Detail Information

Publications12

  1. doi request reprint A sodium channel mutation linked to epilepsy increases ramp and persistent current of Nav1.3 and induces hyperexcitability in hippocampal neurons
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Exp Neurol 224:362-8. 2010
    ..Our data provide a pathophysiological basis for the pathogenicity of the first epilepsy-linked mutation within Na(V)1.3 channels and hippocampal neurons...
  2. doi request reprint A sodium channel gene SCN9A polymorphism that increases nociceptor excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven CT
    Ann Neurol 66:862-6. 2009
    ..Our results suggest that polymorphisms in the Na(V)1.7 channel may influence susceptibility to pain...
  3. pmc Structural modelling and mutant cycle analysis predict pharmacoresponsiveness of a Na(V)1.7 mutant channel
    Yang Yang
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Nat Commun 3:1186. 2012
    ..We suggest that this approach might identify variants that confer enhanced pharmacoresponsiveness on a variety of channels...
  4. pmc Paroxysmal extreme pain disorder M1627K mutation in human Nav1.7 renders DRG neurons hyperexcitable
    Sulayman D Dib-Hajj
    Deptartment of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 4:37. 2008
    ..Carbamazepine has been effective in relieving symptoms, while other drugs including other anti-epileptics are less effective...
  5. pmc Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 7:92. 2011
    ..In this paper we describe three patients who house the NaV1.7/I228M variant...
  6. doi request reprint A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia
    Tanya Z Fischer
    Department of Neurology, Yale University School of Medicine, New Haven, CT 16510, USA
    Ann Neurol 65:733-41. 2009
    ..Inherited erythromelalgia (IEM) has been linked to gain-of-function mutations of Na(v)1.7. We now report a novel mutation (V400M) in a three-generation Canadian family in which pain is relieved by carbamazepine (CBZ)...
  7. doi request reprint A new Nav1.7 mutation in an erythromelalgia patient
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Biochem Biophys Res Commun 432:99-104. 2013
    ..9 mV), which is predicted to attenuate the effect of this mutation on DRG neuron firing. These changes are consistent with previously characterized Erytheromelalgia associated mutations of Nav1.7...
  8. pmc Molecular architecture of a sodium channel S6 helix: radial tuning of the voltage-gated sodium channel 1.7 activation gate
    Yang Yang
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06510, USA
    J Biol Chem 288:13741-7. 2013
    ..In-frame deletion mutation (Del-L955) in NaV1.7 sodium channel from a kindred with erythromelalgia hyperpolarizes activation...
  9. doi request reprint Differential effect of D623N variant and wild-type Nav1.7 sodium channels on resting potential and interspike membrane potential of dorsal root ganglion neurons
    Hye Sook Ahn
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510 8018, United States Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, United States Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare System, West Haven, CT 06516, United States
    Brain Res 1529:165-77. 2013
    ..7 associated with painful neuropathy depolarizes resting membrane potential and produces an enhanced inward current during interspike intervals, thereby contributing to DRG neuron hyperexcitability. ..
  10. pmc Effects of ranolazine on wild-type and mutant hNav1.7 channels and on DRG neuron excitability
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, USA
    Mol Pain 6:35. 2010
    ..7 and on DRG neuron excitability have not been investigated. We used voltage- and current-clamp recordings to evaluate the hypothesis that ranolazine may be effective in regulating Nav1.7-induced DRG neuron hyperexcitability...
  11. doi request reprint The response of Na(V)1.3 sodium channels to ramp stimuli: multiple components and mechanisms
    Mark Estacion
    Department of Neurology, Yale University School of Medicine, New Haven, Connecticut, USA
    J Neurophysiol 109:306-14. 2013
    ....
  12. pmc Nav1.9, G-proteins, and nociceptors
    Stephen G Waxman
    Department of Neurology and Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, CT 06510, USA
    J Physiol 586:917-8. 2008