STEVEN SIMON SCHERER

Summary

Affiliation: University of Pennsylvania
Country: USA

Publications

  1. ncbi request reprint Ezrin, radixin, and moesin are components of Schwann cell microvilli
    S S Scherer
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci Res 65:150-64. 2001
  2. ncbi request reprint Kv3.1b is a novel component of CNS nodes
    Jerome Devaux
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 23:4509-18. 2003
  3. ncbi request reprint Genetic and physiological evidence that oligodendrocyte gap junctions contribute to spatial buffering of potassium released during neuronal activity
    Daniela M Menichella
    Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 26:10984-91. 2006
  4. pmc X-linked Charcot-Marie-Tooth disease
    Steven S Scherer
    Department of Neurology, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Peripher Nerv Syst 17:9-13. 2012
  5. ncbi request reprint Finding the causes of inherited neuropathies
    Steven S Scherer
    University of Pennsylvania Medical School, Philadelphia 19104 6077, USA
    Arch Neurol 63:812-6. 2006
  6. ncbi request reprint Recent progress on the molecular organization of myelinated axons
    Steven S Scherer
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia 19104, USA
    J Peripher Nerv Syst 7:1-12. 2002
  7. pmc Myelination: some receptors required
    Steven S Scherer
    The University of Pennsylvania Medical Center, Philadelphia, PA 19104 6077, USA
    J Cell Biol 156:13-5. 2002
  8. pmc The debut of a rational treatment for an inherited neuropathy?
    Steven S Scherer
    Department of Neurology, The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104 6077, USA
    J Clin Invest 121:4624-7. 2011
  9. ncbi request reprint Transgenic expression of human connexin32 in myelinating Schwann cells prevents demyelination in connexin32-null mice
    Steven S Scherer
    Department of Neurology and Cell and Molecular Biology Graduate Group, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 25:1550-9. 2005
  10. ncbi request reprint Genetic dysmyelination alters the molecular architecture of the nodal region
    Edgardo J Arroyo
    Department of Neurology, The University of Pennsylvania Medical Center, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 22:1726-37. 2002

Research Grants

  1. The Role of Connexin32 in the Pathogenesis of CMTX
    Steven Scherer; Fiscal Year: 2006
  2. Axonal alterations in demyelinating diseases
    STEVEN SIMON SCHERER; Fiscal Year: 2011

Collaborators

Detail Information

Publications52

  1. ncbi request reprint Ezrin, radixin, and moesin are components of Schwann cell microvilli
    S S Scherer
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci Res 65:150-64. 2001
    ..In contrast, ERM proteins did not surround nodes in the CNS. The colocalization of ERM proteins with actin indicates that they have functions different from those of merlin in myelinating Schwann cells...
  2. ncbi request reprint Kv3.1b is a novel component of CNS nodes
    Jerome Devaux
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 23:4509-18. 2003
    ..These effects were also observed in Kv3.1-deficient mice. In conclusion, Kv3.1b is the first K+ channel subunit to be identified in CNS nodes; but Kv3.1b does not account for the effects of 4-aminopyridine on central myelinated tracts...
  3. ncbi request reprint Genetic and physiological evidence that oligodendrocyte gap junctions contribute to spatial buffering of potassium released during neuronal activity
    Daniela M Menichella
    Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 26:10984-91. 2006
    ..1 function in a common pathway. Together, these results implicate oligodendrocytes and their connexins as having critical roles in the buffering of K+ released during neuronal activity...
  4. pmc X-linked Charcot-Marie-Tooth disease
    Steven S Scherer
    Department of Neurology, The Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Peripher Nerv Syst 17:9-13. 2012
    ..Animal models of CMT1X demonstrate that loss of Cx32 in myelinating Schwann cells causes a demyelinating neuropathy. An effective therapy remains to be developed...
  5. ncbi request reprint Finding the causes of inherited neuropathies
    Steven S Scherer
    University of Pennsylvania Medical School, Philadelphia 19104 6077, USA
    Arch Neurol 63:812-6. 2006
  6. ncbi request reprint Recent progress on the molecular organization of myelinated axons
    Steven S Scherer
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia 19104, USA
    J Peripher Nerv Syst 7:1-12. 2002
    ..Understanding how axon-Schwann interactions create the molecular architecture of myelinated axons is fundamental and almost certainly involved in the pathogenesis of peripheral neuropathies...
  7. pmc Myelination: some receptors required
    Steven S Scherer
    The University of Pennsylvania Medical Center, Philadelphia, PA 19104 6077, USA
    J Cell Biol 156:13-5. 2002
    ..Their results reveal that signaling by an extracellular matrix receptor plays a key role in the differentiation of myelinating Schwann cells...
  8. pmc The debut of a rational treatment for an inherited neuropathy?
    Steven S Scherer
    Department of Neurology, The Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania 19104 6077, USA
    J Clin Invest 121:4624-7. 2011
    ..As oral L-serine reduces the severity of neuropathy in the mouse model of HSAN1, these data suggest a rational candidate therapy for this devastating condition...
  9. ncbi request reprint Transgenic expression of human connexin32 in myelinating Schwann cells prevents demyelination in connexin32-null mice
    Steven S Scherer
    Department of Neurology and Cell and Molecular Biology Graduate Group, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 25:1550-9. 2005
    ..These results indicate that the loss of Schwann-cell-autonomous expression of Cx32 is sufficient to account for demyelination in CMT1X...
  10. ncbi request reprint Genetic dysmyelination alters the molecular architecture of the nodal region
    Edgardo J Arroyo
    Department of Neurology, The University of Pennsylvania Medical Center, Children s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 22:1726-37. 2002
    ..1 and Kv1.2...
  11. ncbi request reprint Unique distributions of the gap junction proteins connexin29, connexin32, and connexin47 in oligodendrocytes
    Kleopas A Kleopa
    Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, USA
    Glia 47:346-57. 2004
    ..This diversity of connexins in oligodendrocytes (in different populations of cells and in different subcellular compartments) likely reflects functional differences between these connexins and perhaps the oligodendrocytes themselves...
  12. ncbi request reprint Pannexin1 is expressed by neurons and glia but does not form functional gap junctions
    Yan Huang
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    Glia 55:46-56. 2007
    ..Thus, at least in these mammalian cells lines, Panx1 does not form morphological or functional gap junctions, and it remains to be demonstrated that Panx1 forms gap junction-forming protein in the CNS...
  13. ncbi request reprint Diverse trafficking abnormalities of connexin32 mutants causing CMTX
    Sabrina W Yum
    Division of Neurology, St Christopher s Hospital For Children, MCP Hahnemann University, Philadelphia, Pennsylvania 19134, USA
    Neurobiol Dis 11:43-52. 2002
    ..Thus, many CMTX mutants have trafficking abnormalities, whereas the carboxy-terminus mutants reach the cell membrane and probably cause disease through other mechanisms...
  14. ncbi request reprint Severe neuropathy with leaky connexin32 hemichannels
    Grace S Lin Liang
    Department of Neurology, Parkinson s Disease and Movement Disorders Center, University of Pennsylvania Medical Center, Philadelphia, PA 19107, USA
    Ann Neurol 57:749-54. 2005
    ..Abnormal leakiness of connexin hemichannels is likely a mechanism of cellular toxicity in this and perhaps other diseases caused by connexin mutations...
  15. pmc Cx29 and Cx32, two connexins expressed by myelinating glia, do not interact and are functionally distinct
    Meejin Ahn
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci Res 86:992-1006. 2008
    ..Substituting the intracellular loop and/or tail of Cx32 with those of Cx29 appears to prevent Cx32 from forming functional gap junctions...
  16. ncbi request reprint The effects of a dominant connexin32 mutant in myelinating Schwann cells
    Linda Jo Bone Jeng
    Cell and Molecular Biology Graduate Group, The University of Pennsylvania Medical Center, Philadelphia, PA 19104 6077, USA
    Mol Cell Neurosci 32:283-98. 2006
    ..Thus, the R142W mutant protein has dominant effects that are distinct from overexpression...
  17. ncbi request reprint A common ankyrin-G-based mechanism retains KCNQ and NaV channels at electrically active domains of the axon
    Zongming Pan
    Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 26:2599-613. 2006
    ..This includes the historical period when myelin also evolved...
  18. pmc A novel recessive Nefl mutation causes a severe, early-onset axonal neuropathy
    Sabrina W Yum
    Section of Neurology, St Christopher s Hospital For Children, Drexel University College of Medicine, Philadelphia, PA 19134, USA
    Ann Neurol 66:759-70. 2009
    ..To report the first cases of a homozygous recessive mutation in NEFL, the gene that encodes the light subunit of neurofilaments...
  19. ncbi request reprint Schwann cell caveolin-1 expression increases during myelination and decreases after axotomy
    Daniel D Mikol
    Department of Neurology, University of Michigan, Ann Arbor 48109, USA
    Glia 38:191-9. 2002
    ..We speculate that caveolin-1 plays a role in the biology of myelinating Schwann cells...
  20. pmc Loss-of-function GJA12/Connexin47 mutations cause Pelizaeus-Merzbacher-like disease
    Jennifer L Orthmann-Murphy
    Department of Neurology, University of Pennsylvania School of Medicine, Room 464 Stemmler Hall, 3450 Hamilton Walk, Philadelphia, PA 19104 6077, USA
    Mol Cell Neurosci 34:629-41. 2007
    ..Thus, the Cx47 mutants associated with PMLD likely disrupt the gap junction coupling between astrocytes and oligodendrocytes...
  21. ncbi request reprint Altered ion channels in an animal model of Charcot-Marie-Tooth disease type IA
    Jérôme J Devaux
    Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 25:1470-80. 2005
    ..Thus, the profound reorganization of axonal ion channels and the aberrant expression of novel ion channels likely contribute to the altered conduction in Trembler-J nerves...
  22. ncbi request reprint Acute demyelination disrupts the molecular organization of peripheral nervous system nodes
    Edgardo J Arroyo
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Comp Neurol 479:424-34. 2004
    ..Thus, acute demyelination has distinct effects on the molecular organization of the nodal, paranodal, and juxtaparanodal region, reflecting altered axon-Schwann cell interactions...
  23. ncbi request reprint Prenylation-defective human connexin32 mutants are normally localized and function equivalently to wild-type connexin32 in myelinating Schwann cells
    Yan Huang
    Department of Neurology, The University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104, USA
    J Neurosci 25:7111-20. 2005
    ..These results indicate that Cx32 is prenylated, but that prenylation is not required for proper trafficking of Cx32 and perhaps not even for certain aspects of its function, in myelinating Schwann cells...
  24. ncbi request reprint KCNQ2 is a nodal K+ channel
    Jérôme J Devaux
    Department of Neurology, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 24:1236-44. 2004
    ..The diminished activity of mutant KCNQ2 channels accounts for neonatal epilepsy and myokymia; the cellular locus of these effects may be axonal initial segments and nodes...
  25. ncbi request reprint Cellular mechanisms of connexin32 mutations associated with CNS manifestations
    Kleopas A Kleopa
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA
    J Neurosci Res 68:522-34. 2002
    ..These results indicate that Cx32 mutants that are associated with a CNS phenotype do not interact with Cx45, but may instead have other toxic effects in oligodendrocytes...
  26. pmc A patient with neurofibromatosis type 1 and Charcot-Marie-Tooth disease type 1B
    Eric Lancaster
    Department of Neurology, University of Pennsylvania Medical Center, 3400 Spruce Street, 3W Gates Neurology, Philadelphia, Pennsylvania 19104, USA
    Muscle Nerve 41:555-8. 2010
    ..Although one might expect an overwhelming tumor burden due to the combination of these two disorders, the two mutations did not appear to interact...
  27. pmc Hereditary spastic paraplegia is a novel phenotype for GJA12/GJC2 mutations
    Jennifer L Orthmann-Murphy
    Department of Neurology, University of Pennsylvania School of Medicine, Room 464 Stemmler Hall, Philadelphia, PA 19104 6077, USA
    Brain 132:426-38. 2009
    ..Thus, GJA12/GJC2 mutations can result in a milder phenotype than previously appreciated, but whether I33M retains a function of Cx47 not directly related to forming functional gap junction channels is not known...
  28. ncbi request reprint Inherited neuropathies
    Kleopas A Kleopa
    University of Pennsylvania Medical Center, 3400 Spruce Street, 3 West Gates, Philadelphia, PA 19104, USA
    Neurol Clin 20:679-709. 2002
    ..Increasing knowledge of the molecular-genetic causes of inherited neuropathies facilitates faster, more accurate diagnosis, and sets the stage for development of specific therapeutic interventions...
  29. pmc Gap junctions couple astrocytes and oligodendrocytes
    Jennifer L Orthmann-Murphy
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, USA
    J Mol Neurosci 35:101-16. 2008
    ..Mutations of these connexin genes demonstrate that the proper functioning of myelin and oligodendrocytes requires the expression of these connexins. The physiological function of O/A and A/A junctions, however, remains to be illuminated...
  30. ncbi request reprint Two distinct heterotypic channels mediate gap junction coupling between astrocyte and oligodendrocyte connexins
    Jennifer L Orthmann-Murphy
    Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 6077, USA
    J Neurosci 27:13949-57. 2007
    ..Finally, Cx47 mutants that cause Pelizaeus-Merzbacher-like disease do not efficiently form functional channels with Cx43, indicating that disrupted Cx47/Cx43 channels cause this disease...
  31. ncbi request reprint The CNS phenotype of X-linked Charcot-Marie-Tooth disease: more than a peripheral problem
    Robert A Taylor
    Department of Neurology, Hospital of the University of Pennsylvania, Philadelphia, USA
    Neurology 61:1475-8. 2003
  32. ncbi request reprint TGFbeta1 modulates the phenotype of Schwann cells at the transcriptional level
    Rajeshwar Awatramani
    Department of Neurology, Wayne State University, Elliman Building 3206, 421 East Canfield, Detroit, Michigan 48201, USA
    Mol Cell Neurosci 19:307-19. 2002
    ..Thus, TGFbeta1 suppresses the expression of genes that characterize the different phenotypes of SCs, and these changes occur at least in part at a transcriptional level...
  33. ncbi request reprint Inherited neuropathies: new genes don't fit old models
    Steven S Scherer
    Department of Neurology, 464 Stemmler Hall, University of Pennsylvania School of Medicine, Philadelphia, 19104, USA
    Neuron 51:672-4. 2006
    ..In this issue of Neuron, Seburn et al. have identified and characterized a mutant mouse with a dominantly inherited axonal neuropathy caused by a Gars mutation that is inferred to have a gain of function...
  34. ncbi request reprint Human connexin26 and connexin30 form functional heteromeric and heterotypic channels
    Sabrina W Yum
    Section of Neurology, St Christopher s Hospital For Children, Erie Ave at Front St, Philadelphia, PA 19134, USA
    Am J Physiol Cell Physiol 293:C1032-48. 2007
    ..These results indicate that Cx26 and Cx30 form functional heteromeric and heterotypic channels, whose biophysical properties and permeabilities are different from their homotypic counterparts...
  35. pmc Dominant connexin26 mutants associated with human hearing loss have trans-dominant effects on connexin30
    Sabrina W Yum
    Division of Neurology, The Children s Hospital of Philadelphia, Department of Neurology, University of Pennsylvania, Philadelphia, PA 19104, USA
    Neurobiol Dis 38:226-36. 2010
    ..Furthermore, 8/9 Cx26 mutants inhibited the transfer of neurobiotin or calcein, indicating that these Cx26 mutants have trans-dominant effects on Cx30, an effect that may contribute to the pathogenesis of hearing loss...
  36. ncbi request reprint Identification of genes that are downregulated in the absence of the POU domain transcription factor pou3f1 (Oct-6, Tst-1, SCIP) in sciatic nerve
    John R Bermingham
    McLaughlin Research Institute, Great Falls, Montana 59405, USA
    J Neurosci 22:10217-31. 2002
    ..Our results suggest that pou3f1 functions to activate gene expression in the differentiation of myelinating Schwann cells...
  37. pmc Both laminin and Schwann cell dystroglycan are necessary for proper clustering of sodium channels at nodes of Ranvier
    Simona Occhi
    DIBIT, San Raffaele Scientific Institute, 20132 Milan, Italy
    J Neurosci 25:9418-27. 2005
    ..Finally, abnormal sodium channel clusters are present in a patient with MDC1A, providing a molecular basis for the reduced nerve conduction velocity in this disorder...
  38. pmc Distinct claudins and associated PDZ proteins form different autotypic tight junctions in myelinating Schwann cells
    Sebastian Poliak
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    J Cell Biol 159:361-72. 2002
    ..The presence of these different tight junction proteins in regions of noncompact myelin may be required to maintain the intricate cytoarchitecture of myelinating Schwann cells...
  39. ncbi request reprint Molecular genetics of X-linked Charcot-Marie-Tooth disease
    Kleopas A Kleopa
    Department of Clinical Neurosciences, The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus
    Neuromolecular Med 8:107-22. 2006
    ..No definite phenotype-genotype correlation has yet been established for CMT1X and effective molecular based therapeutics for this disease, remain to be developed...
  40. pmc Notch1 control of oligodendrocyte differentiation in the spinal cord
    Stephane Genoud
    Department of Biology, Institute of Cell Biology, Swiss Federal Institute of Technology, ETH Honggerberg, CH 8093 Zurich, Switzerland
    J Cell Biol 158:709-18. 2002
    ..These findings establish a widespread function of Notch1 in the late steps of mammalian OPC development in vivo...
  41. ncbi request reprint Connexin29 is uniquely distributed within myelinating glial cells of the central and peripheral nervous systems
    Bruce M Altevogt
    Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 22:6458-70. 2002
    ..Together, these data show that Cx29 and Cx32 are expressed by myelinating glial cells with distinct distributions...
  42. ncbi request reprint Proliferation of Schwann cells and regulation of cyclin D1 expression in an animal model of Charcot-Marie-Tooth disease type 1A
    Suzana Atanasoski
    Institute of Cell Biology, Department of Biology, Swiss Federal Institute of Technology, ETH Honggerberg, CH 8093 Zurich, Switzerland
    J Neurosci Res 67:443-9. 2002
    ..Thus, cyclin D1 expression and its subcellular localization correlate directly with distinct physiological states of Schwann cells in this animal model of CMT1A...
  43. ncbi request reprint Connexins are critical for normal myelination in the CNS
    Daniela M Menichella
    Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA
    J Neurosci 23:5963-73. 2003
    ..These data provide the first evidence that gap-junction communication is crucial for normal central myelination...
  44. pmc Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease
    Laia Pedrola
    Department of Genomics and Proteomics, Instituto de Biomedicina, CSIC, Valencia, Spain
    J Cell Mol Med 12:679-89. 2008
    ....
  45. ncbi request reprint Disease mechanisms in inherited neuropathies
    Ueli Suter
    Institute of Cell Biology, Swiss Federal Institute of Technology Zurich, ETH Honggerberg, CH 8093 Zurich, Switzerland
    Nat Rev Neurosci 4:714-26. 2003
  46. pmc Nectin-like proteins mediate axon Schwann cell interactions along the internode and are essential for myelination
    Patrice Maurel
    Department of Cell Biology and Neurology, Smilow Neuroscience Program, New York University School of Medicine, New York, NY 10016, USA
    J Cell Biol 178:861-74. 2007
    ..These results demonstrate a key role for Necl-4 in initiating peripheral nervous system myelination and implicate the Necl proteins as mediators of axo-glial interactions along the internode...
  47. ncbi request reprint Expression analysis of the N-Myc downstream-regulated gene 1 indicates that myelinating Schwann cells are the primary disease target in hereditary motor and sensory neuropathy-Lom
    Philipp Berger
    Department of Biology, Institute of Cell Biology, Swiss Federal Institute of Technology, ETH Honggerberg, CH 8093 Zurich, Switzerland
    Neurobiol Dis 17:290-9. 2004
    ..Our data predict that the loss of NDRG1 leads to a Schwann cell autonomous phenotype resulting in demyelination, with secondary axonal loss...
  48. pmc A central role for Necl4 (SynCAM4) in Schwann cell-axon interaction and myelination
    Ivo Spiegel
    Department of Molecular Cell Biology, The Weizmann Institute of Science, POB 26, Rehovot 76100, Israel
    Nat Neurosci 10:861-9. 2007
    ..These results suggest that Necl proteins are important for mediating axon-glia contact during myelination in peripheral nerves...
  49. ncbi request reprint T118M PMP22 mutation causes partial loss of function and HNPP-like neuropathy
    Michael E Shy
    Department of Neurology and Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48201, USA
    Ann Neurol 59:358-64. 2006
    ..To determine the clinical consequences of the PMP22 point mutation, T118M, which has been previously considered to either cause an autosomal recessive form of Charcot-Marie-Tooth (CMT) disease or be a benign polymorphism...
  50. ncbi request reprint ErbB2 signaling in Schwann cells is mostly dispensable for maintenance of myelinated peripheral nerves and proliferation of adult Schwann cells after injury
    Suzana Atanasoski
    Institute of Cell Biology, Department of Biology, ETH Zurich, CH 8093 Zurich, Switzerland
    J Neurosci 26:2124-31. 2006
    ..We conclude that adult Schwann cells do not require major neuregulin signaling through erbB2 for proliferation and survival after nerve injury, in contrast to development and in cell culture...
  51. ncbi request reprint Neuromyotonia and limbic encephalitis sera target mature Shaker-type K+ channels: subunit specificity correlates with clinical manifestations
    Kleopas A Kleopa
    Department of Clinical Neurosciences, Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus, PA, USA
    Brain 129:1570-84. 2006
    ..Although more than one type of antibody is often detectable in individual sera, higher affinity for certain subunits or subunit combinations may determine the range of clinical manifestations...
  52. pmc Human oligodendrocytes express Cx31.3: function and interactions with Cx32 mutants
    Irene Sargiannidou
    Clinical Neurosciences Section, Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus
    Neurobiol Dis 30:221-33. 2008
    ..3. Thus, Cx31.3 shares many characteristics with its ortholog Cx29. Cx32 mutants with CNS phenotypes do not affect the trafficking or function of Cx31.3, and may have other toxic effects in oligodendrocytes...

Research Grants2

  1. The Role of Connexin32 in the Pathogenesis of CMTX
    Steven Scherer; Fiscal Year: 2006
    ....
  2. Axonal alterations in demyelinating diseases
    STEVEN SIMON SCHERER; Fiscal Year: 2011
    ..Aim #3: What Na,K-ATPase isoforms are expressed by myelinated axons and demyelinated axons? we will localize alpha1-3 by immunoelectron microscopy in CMSand PNS myelinated axons, along with their beta subunits. ..