ArticleNeurochemical research2007
Expression of a myelin proteolipid protein (Plp)-lacZ transgene is reduced in both the CNS and PNS of Plp(jp) mice.
Article in Neurochemical research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Myelin repair and functional recovery mediated by neural cell transplantation in a mouse model of multiple sclerosis.Neuroscience bulletin · 2013Article
- The expression of TAG-1 in glial cells is sufficient for the formation of the juxtaparanodal complex and the phenotypic rescue of tag-1 homozygous mutants in the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Article
- Identification of direct regulatory targets of the transcription factor Sox10 based on function and conservation.BMC genomics · 2008Article
- Constitutively active Akt induces enhanced myelination in the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Proteomic analysis of nuclear factors binding to an intronic enhancer in the myelin proteolipid protein gene.Journal of neurochemistry · 2008Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Jimpy (Plp(jp)) is an X-linked recessive mutation in mice that causes CNS dysmyelination and early death in affected males. It results from a point mutation in the acceptor splice site of myelin proteolipid protein (Plp) exon 5, producing transcripts that are missing exon 5, with a concomitant shift in the downstream reading frame. Expression of the mutant PLP product in Plp(jp) males leads to hypomyelination and oligodendrocyte death. Expression of our Plp-lacZ fusion gene, PLP(+)Z, in transgenic mice is an excellent readout for endogenous Plp transcriptional activity. The current studies assess expression of the PLP(+)Z transgene in the Plp(jp) background. These studies demonstrate that expression of the transgene is decreased in both the central and peripheral nervous systems of affected Plp(jp) males. Thus, expression of mutated PLP protein downregulates Plp gene activity both in oligodendrocytes, which eventually die, and in Schwann cells, which are apparently unaffected in Plp(jp) mice.
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Registered trials
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