Evidence against altered forms of MAG in the dysmyelinated mouse mutant claw paw

Evidence against altered forms of MAG in the dysmyelinated mouse mutant claw paw Short Communications Incorporating Mouse Genome Mammalian Genome 9, 903–904 (1998). © Springer-Verlag New York Inc. 1998 Evidence against altered forms of MAG in the dysmyelinated mouse mutant claw paw 1 2 1 Stephan Niemann, Richard L. Sidman, Klaus-Armin Nave Zentrum fu ¨ r Molekulare Biologie (ZMBH), University of Heidelberg, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany Harvard Medical School, New England Regional Primate Research Center, Southborough, Massachusetts 01772-9102, USA Received: 19 November 1997 / Accepted: 10 July 1998 In the mammalian nervous system, the formation of myelin by In an attempt to demonstrate the function of MAG in vivo, a glial cells enables a rapid saltatory impulse conduction. Myelina- null allele of the Mag gene has been created by gene targeting tion depends on the coordinated expression of myelin-specific (Montag et al. 1994; Li et al. 1994). Surprisingly, MAG-deficient structural proteins, based on interactions of axons with oligoden- mouse mutants displayed no obvious developmental defects, ex- drocytes in the central nervous system (CNS) and Schwann cells in cept for subtle ultrastructural abnormalities of myelin, in marked the peripheral nervous system (PNS). Mice with defects in myelin contrast to the dysmyelinated phenotype of claw paw, which is assembly comprise a http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Evidence against altered forms of MAG in the dysmyelinated mouse mutant claw paw

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Publisher
Springer-Verlag
Copyright
Copyright © 1998 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003359900892
Publisher site
See Article on Publisher Site

Abstract

Short Communications Incorporating Mouse Genome Mammalian Genome 9, 903–904 (1998). © Springer-Verlag New York Inc. 1998 Evidence against altered forms of MAG in the dysmyelinated mouse mutant claw paw 1 2 1 Stephan Niemann, Richard L. Sidman, Klaus-Armin Nave Zentrum fu ¨ r Molekulare Biologie (ZMBH), University of Heidelberg, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany Harvard Medical School, New England Regional Primate Research Center, Southborough, Massachusetts 01772-9102, USA Received: 19 November 1997 / Accepted: 10 July 1998 In the mammalian nervous system, the formation of myelin by In an attempt to demonstrate the function of MAG in vivo, a glial cells enables a rapid saltatory impulse conduction. Myelina- null allele of the Mag gene has been created by gene targeting tion depends on the coordinated expression of myelin-specific (Montag et al. 1994; Li et al. 1994). Surprisingly, MAG-deficient structural proteins, based on interactions of axons with oligoden- mouse mutants displayed no obvious developmental defects, ex- drocytes in the central nervous system (CNS) and Schwann cells in cept for subtle ultrastructural abnormalities of myelin, in marked the peripheral nervous system (PNS). Mice with defects in myelin contrast to the dysmyelinated phenotype of claw paw, which is assembly comprise a

Journal

Mammalian GenomeSpringer Journals

Published: Nov 1, 1998

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