QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.
<h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but it...
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2010
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oai:doaj.org-article:5731ee0d823345e5a308daa7c60dc01a2021-11-18T07:03:51ZQKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells.1932-620310.1371/journal.pone.0013079https://doaj.org/article/5731ee0d823345e5a308daa7c60dc01a2010-09-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20927331/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but its function in these cells is not known.<h4>Methods/principal findings</h4>We studied the effect of small interference RNA (siRNA)-mediated QKI depletion on global gene expression in human astrocyte glioma cells. Microarray measurements were confirmed with real-time quantitative polymerase chain reaction (qPCR). The presence of QKI binding sites (QRE) was assessed by a bioinformatic approach. Viability and cell morphology were also studied. The most significant alteration after QKI silencing was the decreased expression of genes involved in interferon (IFN) induction (P = 6.3E-10), including IFIT1, IFIT2, MX1, MX2, G1P2, G1P3, GBP1 and IFIH1. All eight genes were down-regulated after silencing of the splice variant QKI-7, but were not affected by QKI-5 silencing. Interestingly, four of them were up-regulated after treatment with the antipsychotic agent haloperidol that also resulted in increased QKI-7 mRNA levels.<h4>Conclusions/significance</h4>The coordinated expression of QKI-7 splice variant and IFN-related genes supports the idea that this particular splice variant has specific functions in astrocytes. Furthermore, a role of QKI-7 as a regulator of an inflammatory gene pathway in astrocytes is suggested. This hypothesis is well in line with growing experimental evidence on the role of inflammatory components in schizophrenia.Lin JiangPeter SaetreKatarzyna J RadomskaElena JazinEva Lindholm CarlströmPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 9 (2010) |
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Medicine R Science Q Lin Jiang Peter Saetre Katarzyna J Radomska Elena Jazin Eva Lindholm Carlström QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
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<h4>Background</h4>The human QKI gene, called quaking homolog, KH domain RNA binding (mouse), is a candidate gene for schizophrenia encoding an RNA-binding protein. This gene was shown to be essential for myelination in oligodendrocytes. QKI is also highly expressed in astrocytes, but its function in these cells is not known.<h4>Methods/principal findings</h4>We studied the effect of small interference RNA (siRNA)-mediated QKI depletion on global gene expression in human astrocyte glioma cells. Microarray measurements were confirmed with real-time quantitative polymerase chain reaction (qPCR). The presence of QKI binding sites (QRE) was assessed by a bioinformatic approach. Viability and cell morphology were also studied. The most significant alteration after QKI silencing was the decreased expression of genes involved in interferon (IFN) induction (P = 6.3E-10), including IFIT1, IFIT2, MX1, MX2, G1P2, G1P3, GBP1 and IFIH1. All eight genes were down-regulated after silencing of the splice variant QKI-7, but were not affected by QKI-5 silencing. Interestingly, four of them were up-regulated after treatment with the antipsychotic agent haloperidol that also resulted in increased QKI-7 mRNA levels.<h4>Conclusions/significance</h4>The coordinated expression of QKI-7 splice variant and IFN-related genes supports the idea that this particular splice variant has specific functions in astrocytes. Furthermore, a role of QKI-7 as a regulator of an inflammatory gene pathway in astrocytes is suggested. This hypothesis is well in line with growing experimental evidence on the role of inflammatory components in schizophrenia. |
format |
article |
author |
Lin Jiang Peter Saetre Katarzyna J Radomska Elena Jazin Eva Lindholm Carlström |
author_facet |
Lin Jiang Peter Saetre Katarzyna J Radomska Elena Jazin Eva Lindholm Carlström |
author_sort |
Lin Jiang |
title |
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
title_short |
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
title_full |
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
title_fullStr |
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
title_full_unstemmed |
QKI-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
title_sort |
qki-7 regulates expression of interferon-related genes in human astrocyte glioma cells. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2010 |
url |
https://doaj.org/article/5731ee0d823345e5a308daa7c60dc01a |
work_keys_str_mv |
AT linjiang qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells AT petersaetre qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells AT katarzynajradomska qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells AT elenajazin qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells AT evalindholmcarlstrom qki7regulatesexpressionofinterferonrelatedgenesinhumanastrocytegliomacells |
_version_ |
1718423977597075456 |