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  1. ASN NEURO
  2. Year: 2011, Volume: 3
  3. Year: 2011, Volume: 3, Issue: 4
  4. YY1 negatively regulates mouse myelin proteolipid protein (Plp1) gene expression in oligodendroglial cells
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Year: 2016, Volume: 8
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Year: 2011, Volume: 3
Year: 2011, Volume: 3, Issue: 5
Year: 2011, Volume: 3, Issue: 4
Hypothesis: are neoplastic macrophages/microglia present in glioblastoma multiforme?
Targeting VIP and PACAP receptor signalling: new therapeutic strategies in multiple sclerosis
Peripheral neuropathy in the Twitcher mouse involves the activation of axonal caspase 3
YY1 negatively regulates mouse myelin proteolipid protein (Plp1) gene expression in oligodendroglial cells
Early effects of lipopolysaccharide-induced inflammation on foetal brain development in rat
Year: 2011, Volume: 3, Issue: 3
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YY1 negatively regulates mouse myelin proteolipid protein (Plp1) gene expression in oligodendroglial cells

Content Provider PubMed Central
Author Zolova, Olga E. Wight, Patricia A.
Copyright Year 2011
Abstract YY1 (Yin and Yang 1) is a multifunctional, ubiquitously expressed, zinc finger protein that can act as a transcriptional activator, repressor, or initiator element binding protein. Previous studies have shown that YY1 modulates the activity of reporter genes driven by the myelin PLP (proteolipid protein) (PLP1/Plp1) promoter. However, it is known that Plp1 intron 1 DNA contains regulatory elements that are required for the dramatic increase in gene activity, coincident with the active myelination period of CNS (central nervous system) development. The intron in mouse contains multiple prospective YY1 target sites including one within a positive regulatory module called the ASE (anti-silencer/enhancer) element. Results presented here demonstrate that YY1 has a negative effect on the activity of a Plp1-lacZ fusion gene [PLP(+)Z] in an immature oligodendroglial cell line (Oli-neu) that is mediated through sequences present in Plp1 intron 1 DNA. Yet YY1 does not bind to its alleged site in the ASE (even though the protein is capable of recognizing a target site in the promoter), indicating that the down-regulation of PLP(+)Z activity by YY1 in Oli-neu cells does not occur through a direct interaction of YY1 with the ASE sequence. Previous studies with Yy1 conditional knockout mice have demonstrated that YY1 is essential for the differentiation of oligodendrocyte progenitors. Nevertheless, the current study suggests that YY1 functions as a repressor (not an activator) of Plp1 gene expression in immature oligodendrocytes. Perhaps YY1 functions to keep the levels of PLP in check in immature cells before vast quantities of the protein are needed in mature myelinating oligodendrocytes.
Related Links http://dx.doi.org/10.1042/an20110021
Starting Page 67
File Format PDF
ISSN 17590914
e-ISSN 17590914
Journal ASN NEURO
Issue Number 4
Volume Number 3
Language English
Publisher American Society for Neurochemistry
Publisher Date 2011-11-01
Access Restriction Open
Rights Holder American Society for Neurochemistry
Subject Keyword Neuroscience(all) Clinical Neurology Research in Higher Education
Content Type Text
Resource Type Article
Subject Neuroscience Neurology (clinical)
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