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Regulation of KIR3DL3 Expression via miRNA.

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Title: Regulation of KIR3DL3 Expression via miRNA.
Authors: Nutalai, Rungtiwa1,2,3 (AUTHOR), Gaudieri, Silvana4,5,6 (AUTHOR), Jumnainsong, Amonrat2,3 (AUTHOR), Leelayuwat, Chanvit2,3 (AUTHOR) chanvit@kku.ac.th
Source: Genes. Aug2019, Vol. 10 Issue 8, p603-603. 1p.
Subject Terms: *RNA, *MICRORNA, *GENETIC regulation, *KILLER cells, *SMALL interfering RNA, *DECIDUA
Abstract: Killer-cell immunoglobulin-like receptor (KIR) 3DL3 is a framework gene present in all human KIR haplotypes. Although the structure of KIR3DL3 is suggestive of an inhibitory receptor, the function of KIR3DL3 has not been demonstrated and cognate ligands have not been identified. KIR3DL3 has been shown to be constitutively expressed at a low RNA level in peripheral blood mononuclear cell (PBMC) and decidual natural kill (NK) cells, but cell surface expression of KIR3DL3 cannot be detected. Accordingly, post-transcriptional regulation of KIR3DL3 should exist. Using bioinformatics analysis, we identified three candidate micro ribonucleic acids (miRNAs; miR-26a-5p, -26b-5p and -185-5p) that potentially regulate KIR3DL3 expression. Luciferase reporter assays utilizing constructs with mutated miRNA-binding sites of miR-26a-5p, -26b-5p and -185-5p in the 3'-untranslated region (3' UTR) of KIR3DL3 resulted in up-regulation of luciferase activity demonstrating a potential mechanism of gene regulation. Furthermore, knockdown of the same endogenous miRNAs using silencing ribonucleic acid (siRNA) led to induced surface expression of KIR3DL3. In conclusion, we provide a novel mechanism of functional regulation of KIR3DL3 via miRNAs. These findings are relevant in understanding the generation of KIR repertoire and NK cell clonality. [ABSTRACT FROM AUTHOR]
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  Data: Regulation of KIR3DL3 Expression via miRNA.
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  Data: <searchLink fieldCode="AR" term="%22Nutalai%2C+Rungtiwa%22">Nutalai, Rungtiwa</searchLink><relatesTo>1,2,3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Gaudieri%2C+Silvana%22">Gaudieri, Silvana</searchLink><relatesTo>4,5,6</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Jumnainsong%2C+Amonrat%22">Jumnainsong, Amonrat</searchLink><relatesTo>2,3</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Leelayuwat%2C+Chanvit%22">Leelayuwat, Chanvit</searchLink><relatesTo>2,3</relatesTo> (AUTHOR)<i> chanvit@kku.ac.th</i>
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  Data: <searchLink fieldCode="JN" term="%22Genes%22">Genes</searchLink>. Aug2019, Vol. 10 Issue 8, p603-603. 1p.
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  Data: *<searchLink fieldCode="DE" term="%22RNA%22">RNA</searchLink><br />*<searchLink fieldCode="DE" term="%22MICRORNA%22">MICRORNA</searchLink><br />*<searchLink fieldCode="DE" term="%22GENETIC+regulation%22">GENETIC regulation</searchLink><br />*<searchLink fieldCode="DE" term="%22KILLER+cells%22">KILLER cells</searchLink><br />*<searchLink fieldCode="DE" term="%22SMALL+interfering+RNA%22">SMALL interfering RNA</searchLink><br />*<searchLink fieldCode="DE" term="%22DECIDUA%22">DECIDUA</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Killer-cell immunoglobulin-like receptor (KIR) 3DL3 is a framework gene present in all human KIR haplotypes. Although the structure of KIR3DL3 is suggestive of an inhibitory receptor, the function of KIR3DL3 has not been demonstrated and cognate ligands have not been identified. KIR3DL3 has been shown to be constitutively expressed at a low RNA level in peripheral blood mononuclear cell (PBMC) and decidual natural kill (NK) cells, but cell surface expression of KIR3DL3 cannot be detected. Accordingly, post-transcriptional regulation of KIR3DL3 should exist. Using bioinformatics analysis, we identified three candidate micro ribonucleic acids (miRNAs; miR-26a-5p, -26b-5p and -185-5p) that potentially regulate KIR3DL3 expression. Luciferase reporter assays utilizing constructs with mutated miRNA-binding sites of miR-26a-5p, -26b-5p and -185-5p in the 3'-untranslated region (3' UTR) of KIR3DL3 resulted in up-regulation of luciferase activity demonstrating a potential mechanism of gene regulation. Furthermore, knockdown of the same endogenous miRNAs using silencing ribonucleic acid (siRNA) led to induced surface expression of KIR3DL3. In conclusion, we provide a novel mechanism of functional regulation of KIR3DL3 via miRNAs. These findings are relevant in understanding the generation of KIR repertoire and NK cell clonality. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
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  Data: <i>Copyright of Genes is the property of MDPI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.3390/genes10080603
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        Text: English
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      – SubjectFull: GENETIC regulation
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      – SubjectFull: KILLER cells
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      – SubjectFull: SMALL interfering RNA
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      – TitleFull: Regulation of KIR3DL3 Expression via miRNA.
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            NameFull: Nutalai, Rungtiwa
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            NameFull: Gaudieri, Silvana
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              Text: Aug2019
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              Y: 2019
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