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  1. 教員研究業績
  2. 感染制御学研究室
  3. 原著論文

Involvement of herpes simplex virus type 1 UL13 protein kinase in the induction of SOCS genes, the negative regulator of cytokine signaling

https://gifu-pu.repo.nii.ac.jp/records/13272
https://gifu-pu.repo.nii.ac.jp/records/13272
f68be063-6c9d-44fb-8916-90399d041b8d
Item type 研究室原著論文(1)
公開日 2018-06-21
タイトル
タイトル Involvement of herpes simplex virus type 1 UL13 protein kinase in the induction of SOCS genes, the negative regulator of cytokine signaling
言語 en
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
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アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
抄録
値 The suppressor of cytokine signaling (SOCS) family has eight members and suppresses various cytokine signaling pathways, including IFN signaling. Therefore, some viruses have evolved molecular mechanisms for inducing SOCS proteins and thus escaping host immunity. Herpes simplex virus type 1 (HSV-1) has a mechanism for escaping from type I IFN by induction of both SOCS1 and SOCS3. In this study, expression of the eight members of the SOCS family stimulated by HSV-1 infection was comparatively analyzed by qRT-PCR. It was found that SOCS1 and SOCS3 are induced by HSV-1-infection at 4 hr post infection. However, such induction was not observed in UL13 deficient virus-infected cells, suggesting that UL13 protein kinase participates in induction of both genes. The transcription factor Sp1-binding sites of SOCS3 promoter/enhancer region were identified as the regulatory elements for induction of SOCS3 in HSV-1 infected cells. Accumulation of activated Sp1 was detectable in the nuclei of HSV-1-infected cells before induction of SOCS3. Taken together, these results suggest that HSV-1 has a potent mechanism for escaping from the IFN system.
書誌情報 en : Microbiology and Immunology

巻 61, 号 5, p. 159-167, 発行日 2017-05
DOI
値 10.1111/1348-0421.12483
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