Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase
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Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase. / Magyar, J P; Bartsch, U; Wang, Z Q; Howells, N; Aguzzi, A; Wagner, E F; Schachner, M.
in: J CELL BIOL, Jahrgang 127, Nr. 3, 11.1994, S. 835-45.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Degeneration of neural cells in the central nervous system of mice deficient in the gene for the adhesion molecule on Glia, the beta 2 subunit of murine Na,K-ATPase
AU - Magyar, J P
AU - Bartsch, U
AU - Wang, Z Q
AU - Howells, N
AU - Aguzzi, A
AU - Wagner, E F
AU - Schachner, M
PY - 1994/11
Y1 - 1994/11
N2 - We generated mice, null mutant in the adhesion molecule on glia (AMOG), the beta 2 subunit of the murine Na,K-ATPase gene. These mice exhibit motor incoordination at 15 d of age, subsequently tremor and paralysis of extremities, and die at 17-18 d after birth. At these ages, the mutants have enlarged ventricles, degenerating photoreceptor cells, and swelling and degeneration of astrocytic endfeet, leading to vacuoles adjoining capillaries of brain stem, thalamus, striatum, and spinal cord. In tissue homogenates from entire brains of 16-17-d-old mutants, Na,K-ATPase activity and expression of the beta 1 subunit of the Na,K-ATPase and of the neural adhesion molecules L1, N-CAM, and MAG appear normal. We suggest that the mutant phenotype can be related primarily to reduced pump activity, with neural degeneration as a possible consequence of osmotic imbalance.
AB - We generated mice, null mutant in the adhesion molecule on glia (AMOG), the beta 2 subunit of the murine Na,K-ATPase gene. These mice exhibit motor incoordination at 15 d of age, subsequently tremor and paralysis of extremities, and die at 17-18 d after birth. At these ages, the mutants have enlarged ventricles, degenerating photoreceptor cells, and swelling and degeneration of astrocytic endfeet, leading to vacuoles adjoining capillaries of brain stem, thalamus, striatum, and spinal cord. In tissue homogenates from entire brains of 16-17-d-old mutants, Na,K-ATPase activity and expression of the beta 1 subunit of the Na,K-ATPase and of the neural adhesion molecules L1, N-CAM, and MAG appear normal. We suggest that the mutant phenotype can be related primarily to reduced pump activity, with neural degeneration as a possible consequence of osmotic imbalance.
KW - Adenosine Triphosphatases
KW - Amino Acid Sequence
KW - Animals
KW - Base Sequence
KW - Blotting, Southern
KW - Brain
KW - Capillaries
KW - Cation Transport Proteins
KW - Cell Adhesion Molecules, Neuronal
KW - Cerebellar Cortex
KW - Cerebrovascular Circulation
KW - Cloning, Molecular
KW - Embryo, Mammalian
KW - Extracellular Matrix Proteins
KW - In Situ Hybridization
KW - Macromolecular Substances
KW - Mice
KW - Mice, Neurologic Mutants
KW - Microscopy, Electron
KW - Molecular Sequence Data
KW - Motor Activity
KW - Nerve Degeneration
KW - Neuroglia
KW - Neurons
KW - Oligodeoxyribonucleotides
KW - Polymerase Chain Reaction
KW - Restriction Mapping
KW - Sodium-Potassium-Exchanging ATPase
KW - Spinal Cord
KW - Stem Cells
KW - Vacuoles
KW - Journal Article
KW - Research Support, Non-U.S. Gov't
M3 - SCORING: Journal article
C2 - 7525597
VL - 127
SP - 835
EP - 845
JO - J CELL BIOL
JF - J CELL BIOL
SN - 0021-9525
IS - 3
ER -