Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Igor Kobsar"'
Publikováno v:
Molecular and Cellular Neuroscience. 35:153-160
Mice homozygously deficient for the myelin component P0 show loss of axons in peripheral nerves. In order to investigate the morphological characteristics of degenerating axons, we crossbred the myelin mutants with a transgenic mouse line expressing
Publikováno v:
Experimental Neurology. 203:55-62
Mouse mutants heterozygously deficient for the myelin protein P0 (P0+/-) resemble certain forms of human hereditary neuropathies. Endoneurial macrophages of intrinsic origin are intimately involved in the pathogenesis of the demyelinating neuropathy
Publikováno v:
Molecular and Cellular Neuroscience. 31:685-691
Mouse mutants heterozygously deficient for the myelin component P0 mimic some forms of inherited neuropathies in humans. We have previously shown that both T lymphocytes and macrophages contribute to the demyelinating neuropathy. Both cell types appe
Autor:
Carsten Wessig, Peggy Putthoff, Gabriele Loers, Rudolf Martini, Torsten Fink, Annette E. Rünker, Thomas Tilling, Melitta Schachner, Igor Kobsar
Publikováno v:
The Journal of Cell Biology
Mutations in the gene of the peripheral myelin protein zero (P0) give rise to the peripheral neuropathies Charcot-Marie-Tooth type 1B disease (CMT1B), Déjérine-Sottas syndrome, and congenital hypomyelinating neuropathy. To investigate the pathome
Autor:
Stefano Carenini, Rudolf Martini, Christoph D. Schmid, Mathias Mäurer, Martin Berghoff, Igor Kobsar
Publikováno v:
Journal of Anatomy. 200:405-414
Mice heterozygously deficient in the peripheral myelin adhesion molecule P0 (P0+/- mice) are models for some forms of Charcot-Marie-Tooth (CMT) neuropathies. In addition to the characteristic hallmarks of demyelination, elevated numbers of CD8-positi
Publikováno v:
Neuroscience Letters. 320:17-20
Mice deficient in the gap junction protein connexin 32 (Cx32) develop a slowly progressing demyelinating neuropathy, with enlarged periaxonal collars, abnormal non-compacted myelin domains and axonal sprouts. These mice serve as a model for the X-lin
Autor:
Rudolf Martini, Igor Kobsar, Christoph Kleinschnitz, Chi Wang Ip, Stefan Fischer, Marcus Müller, Barrett J. Rollins
Publikováno v:
Molecular and cellular neurosciences. 37(2)
Macrophages are critically involved in the pathogenesis of genetically caused demyelination, as it occurs in models for inherited demyelinating neuropathies. It is presently unknown which factors link the Schwann cell-based myelin mutation to the act
Autor:
S. Rock Levinson, Jochen C. Ulzheimer, Rudolf Martini, Igor Kobsar, Nurcan Üçeyler, Lydia Biko, Claudia Sommer
Publikováno v:
Journal of neuroscience research. 84(1)
Patients with hereditary neuropathies are more susceptible to vincristine (VIN)-induced neuropathy than patients without this comorbidity. The heterozygous P0(+/-) mouse is an animal model of a distinct form of inherited neuropathies. These mice prod
Autor:
Stefan Fischer, Chi Wang Ip, Igor Kobsar, Rudolf Martini, Antje Kroner, Martin Berghoff, Mathias Mäurer
Publikováno v:
Neuromolecular medicine. 8(1-2)
Mice expressing half of the normal dose of protein zero (P0+/- mice) or completely deficient gap-junction protein connexin 32 -/- mice mimic demyelinating forms of inherited neuropathies, such as Charcot-Marie-Tooth (CMT) neuropathies type 1B and CMT
Publikováno v:
Journal of neuroscience research. 81(6)
Charcot-Marie-Tooth neuropathy type 1A (CMT 1 A) is the most common inherited neuropathy in humans and is mostly caused by a 1.5-Mb tandem duplication of chromosome 17 comprising the gene for the peripheral myelin protein 22-kDa (PMP 22). Although th