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Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

ChEBI2013-10-10 更新2026-07-21 收录

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STING蛋白磷酸化

数据链接：

https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-GEOD-51199 数据链接链接失效反馈

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Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

应用场景：

创建时间：

2013-10-10

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选择性自噬

Original data for MOLECULAR-CELL-D-17-00563_R1, title "Tetherin Suppresses Type I Interferon Signaling by Targeting MAVS for NDP52-Mediated Selective Autophagic Degradation in Human Cells" by Shouheng

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Pathogen virulence factors interfere with various cellular activities, a disruption that can trigger innate immune responses. Interferon-gamma (IFNγ)-inducible antimicrobial factors, such as the guany

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Figure 3B

蛋白质相互作用

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A. MRC-5 cells expressing either vector or UL88 were treated with DMSO, MG132 (10 mM) or Chloroquine (50 mM). Lysates were analysed by western blotting. Blots were probed for UL88, MyD88 and p115 (loa

Figshare2025-06-13 更新10

Threonine Phosphorylation of STAT1 Restricts Interferon Signaling and Promotes Innate Inflammatory Responses

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Since its discovery over three decades ago, signal transducer and activator of transcription 1 (STAT1) has been extensively studied as a central mediator for interferons (IFNs) signaling and antiviral

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Integration of Innate 1 Immune Signaling by Caspase-8-Mediated Cleavage of N4BP1 (NGS2979 RNA-seq). Integration of Innate 1 Immune Signaling by Caspase-8-Mediated Cleavage of N4BP1 (NGS2979 RNA-seq)

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Human mutations in the death receptor Fas or its ligand FasL cause autoimmune lymphoproliferative syndrome (ALPS), whereas mutations in caspase-8 or its adaptor FADD â which mediate cell death downstr

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Cyclic-Di-Nucleotides Trigger ULK1 (ATG1) Phosphorylation of STING to Prevent Sustained Innate Immune Signaling

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