
DOI . ORG {
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Title[redir]:
QUAKING KH Domain Proteins as Regulators of Glial Cell Fate and Myelination: RNA Biology: Vol 2, No 2
Description:
The quaking viable (qkv) mice have always attracted attention because of their characteristic tremor caused by their dysmyelination. In the central nervous system, qkv mice fail to develop mature m...
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Keywords {๐}
proteins, taylor, francis, group, page, rna, journals, cell, fate, open, qkv, mice, qki, search, quaking, regulators, access, myelination, register, biology, volume, issue, domain, journal, article, citations, date, glial, reprints, pdf, myelin, expression, khtype, binding, separate, research, information, solutions, skip, main, content, publish, login, add, cart, home, bioscience, list, issues, advanced,
Topics {โ๏ธ}
qki kh-type proteins modified post-translationally makes twitter page taylor open francis group receive personalised research separate qki isoforms journals books characteristic tremor caused central nervous system signal transduction activiators qki proteins date altmetric point glial cell fate display uncompacted myelin oligodendrocyte cell fate qkv mice fail qkv mice prevents qkv mice provide article https quaking viable cell fate proteins journal 4161/rna rna separate roles date register register add cart home search published online attracted attention genetic defect proper expression function approach ectopic expression recent advances contact newsroom email sign taylor england & wales sw1p 1wg myelin regulators myelination qkv mice regulators skip //doi
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issueNumber:2
datePublished:2005-04-01
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name:RNA Biology
issn:
1547-6286
1555-8584
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name:RNA Biology
issn:
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articleSection:Point-of-View
name:QUAKING KH Domain Proteins as Regulators of Glial Cell Fate and Myelination
headline:QUAKING KH Domain Proteins as Regulators of Glial Cell Fate and Myelination
abstract:The quaking viable (qkv) mice have always attracted attention because of their characteristic tremor caused by their dysmyelination. In the central nervous system, qkv mice fail to develop mature myelinating oligodendrocytes and display uncompacted myelin. The genetic defect in the qkv mice prevents the proper expression of alternatively spliced KH-type QKI RNA binding proteins. Thus qkv mice provide a unique animal model linking RNA binding proteins to defects in oligodendrocyte cell fate and myelination. The fact that QKI proteins are modified post-translationally makes them Signal Transduction Activiators of RNA (STAR) proteins. We have used a gain-of-function approach with the ectopic expression of the separate QKI isoforms using adenoviruses and retroviruses to determine their separate roles in cell fate and myelination. Herein, we discuss the recent advances in characterizing the QKI KH-type proteins as glial cell fate and myelin regulators.
description:The quaking viable (qkv) mice have always attracted attention because of their characteristic tremor caused by their dysmyelination. In the central nervous system, qkv mice fail to develop mature myelinating oligodendrocytes and display uncompacted myelin. The genetic defect in the qkv mice prevents the proper expression of alternatively spliced KH-type QKI RNA binding proteins. Thus qkv mice provide a unique animal model linking RNA binding proteins to defects in oligodendrocyte cell fate and myelination. The fact that QKI proteins are modified post-translationally makes them Signal Transduction Activiators of RNA (STAR) proteins. We have used a gain-of-function approach with the ectopic expression of the separate QKI isoforms using adenoviruses and retroviruses to determine their separate roles in cell fate and myelination. Herein, we discuss the recent advances in characterizing the QKI KH-type proteins as glial cell fate and myelin regulators.
author:
type:Person
name:Daniel Larocque
type:Person
name:Stรยฉphane Richard
pageStart:37
pageEnd:40
datePublished:2005-02-09
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name:Taylor & Francis
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