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Tick-borne flavivirus NS5 antagonize interferon signaling by inhibiting TYK2 kinase activity

NIAID Data Ecosystem2026-05-01 收录

病毒免疫逃逸机制

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数据链接：

https://www.omicsdi.org/dataset/bioimages/S-BSST1179 数据链接链接失效反馈

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Confocal images depository for mansucript Tick-borne flavivirus NS5 antagonize interferon signaling by inhibiting TYK2 kinase activity

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创建时间：

2023-09-05

病毒免疫逃逸机制

干扰抑制

Gammaherpesviruses such as KSHV and EBV establish lifelong persistent infections through latency in lymphocytes. These viruses have evolved several strategies to counteract the various components of t

NIAID Data Ecosystem80

Structure of VACV poxin 2'3' cGAMP-specific nuclease

病毒免疫逃逸机制

蛋白质结构解析

Structure of VACV poxin 2'3' cGAMP-specific nuclease Descriptor: Protein B2 Authors: Eaglesham, J.B, Kranzusch, P.J. Deposit date: 2018-08-02 Release date: 2019-02-06 Last modified: 2024-10-23 Method:

Protein Data Bank Japan2024-10-23 更新70

Modulation of T cell responses by type I interferons

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Type I interferons (IFNs) play a key role in linking the innate and adaptive immune responses. IFNs can have both positive and negative effects on the development of memory CD8+ T cells, but their con

NIAID Data Ecosystem50

RNA-SEQ BASED TRANSCRIPTOME ANALYSIS OF THE INTERFERON HOST RESPONSE UPON VACCINIA VIRUS INFECTION.. RNA-SEQ BASED TRANSCRIPTOME ANALYSIS OF THE INTERFERON HOST RESPONSE UPON VACCINIA VIRUS INFECTION.

病毒免疫逃逸机制

转录组调控

Evasion of interferon (IFN)-mediated antiviral immunity is critical for a successful virus infection. So poxviruses have evolved diverse molecular strategies to counteract IFN host response activity a

NIAID Data Ecosystem80

CD95/Fas increases stemness in cancer cells by inducing a STAT1 dependent Type I interferon response [ChIP-seq]

癌细胞调控

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CD95 was found to be important for both the formation of CSCs and their maintenance. Using a stable isotope labeling by amino acids in cell culture (SILAC) analysis we have now identified STAT1 as a

NIAID Data Ecosystem50

Tick-borne flavivirus NS5 antagonize interferon signaling by inhibiting TYK2 kinase activity

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