STING-ΔN, a novel splice isoform of STING, modulates innate immunity and autophagy in response to DNA virus infection
Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to under...
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| Published in | Cell communication and signaling Vol. 23; no. 1; pp. 299 - 21 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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England
BioMed Central
21.06.2025
BMC |
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| Abstract | Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity.
We identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2'3'-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2'3'-cGAMP pull-down assay.
STING-∆N shares an identical C-terminal sequence (aa 121-379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2'3'-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2'3'-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2'3'-cGAMP-STING and STING-TBK1 complexes.
STING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer. |
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| AbstractList | Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity.BACKGROUNDStimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity.We identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2'3'-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2'3'-cGAMP pull-down assay.METHODSWe identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2'3'-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2'3'-cGAMP pull-down assay.STING-∆N shares an identical C-terminal sequence (aa 121-379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2'3'-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2'3'-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2'3'-cGAMP-STING and STING-TBK1 complexes.RESULTSSTING-∆N shares an identical C-terminal sequence (aa 121-379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2'3'-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2'3'-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2'3'-cGAMP-STING and STING-TBK1 complexes.STING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer.CONCLUSIONSSTING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer. BackgroundStimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity.MethodsWe identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2′3′-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2′3′-cGAMP pull-down assay.ResultsSTING-∆N shares an identical C-terminal sequence (aa 121–379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2′3′-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2′3′-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2′3′-cGAMP-STING and STING-TBK1 complexes.ConclusionsSTING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer. Abstract Background Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity. Methods We identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2′3′-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2′3′-cGAMP pull-down assay. Results STING-∆N shares an identical C-terminal sequence (aa 121–379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2′3′-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2′3′-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2′3′-cGAMP-STING and STING-TBK1 complexes. Conclusions STING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer. Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I interferons (IFNs) in response to cytosolic DNA detection, a crucial mechanism in antiviral defense. However, further investigation is needed to understand how post-transcriptional regulation, particularly alternative splicing, modulates STING activity. We identified a novel alternatively spliced isoform of STING, termed STING-∆N, resulting from exon 3 skipping. We examined STING-∆N expression in various human tissues and cell lines and assessed its role in cGAS-STING signaling using RT-qPCR, luciferase reporter assays, SDD-AGE, immunofluorescence, and immunoblot analysis. We evaluated the influence of STING-∆N on HSV-1 proliferation and STING-induced autophagy by viral plaque assay and immunoblotting. To unravel the mechanistic role of STING-∆N, we further investigated its interaction with STING, TBK1, and 2'3'-cGAMP and its effect on the STING-TBK1 complex using co-immunoprecipitation and 2'3'-cGAMP pull-down assay. STING-∆N shares an identical C-terminal sequence (aa 121-379) with STING but lacks a 120-amino acid N-terminal region encoding three conserved transmembrane (TM) domains. STING-∆N is expressed in various human tissues and cell lines. STING-∆N significantly suppressed IFN activation induced by cGAS, 2'3'-cGAMP, and STING. STING-∆N also reduced type I and III IFN induction in response to double-stranded DNA, HPV, and HSV-1. Additionally, STING-∆N promoted HSV-1 replication and inhibited STING-induced autophagy. Mechanistically, STING-∆N interacts with 2'3'-cGAMP, STING, and TBK1, sequestering their binding and disrupting the formation of the 2'3'-cGAMP-STING and STING-TBK1 complexes. STING-∆N acts as a potent negative regulator of the cGAS-STING pathway, revealing a previously unrecognized regulatory mechanism by which alternative splicing modulates immune responses to DNA viruses. These findings suggest that STING-∆N could be a promising therapeutic target for modulating immune responses in viral infections, autoimmune diseases, and cancer. |
| ArticleNumber | 299 |
| Author | Zhang, Jing Deng, Jian Li, Tao Wang, Pei-Hui Zheng, Sheng-Nan Li, Cheng-Hao |
| Author_xml | – sequence: 1 givenname: Jian surname: Deng fullname: Deng, Jian – sequence: 2 givenname: Sheng-Nan surname: Zheng fullname: Zheng, Sheng-Nan – sequence: 3 givenname: Jing surname: Zhang fullname: Zhang, Jing – sequence: 4 givenname: Cheng-Hao surname: Li fullname: Li, Cheng-Hao – sequence: 5 givenname: Tao surname: Li fullname: Li, Tao – sequence: 6 givenname: Pei-Hui surname: Wang fullname: Wang, Pei-Hui |
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| Keywords | Alternative splicing cGAS STING STING-∆N Autophagy Antiviral immunity HPV |
| Language | English |
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| Snippet | Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I... BackgroundStimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production of type I... Abstract Background Stimulator of interferon (IFN) genes (STING) is a central adaptor protein in the cGAS-STING signaling pathway, orchestrating the production... |
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| Title | STING-ΔN, a novel splice isoform of STING, modulates innate immunity and autophagy in response to DNA virus infection |
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