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PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages

ABSTRACT: PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages

PROVIDER: PRJNA819091 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18454930_1.fastq.gz	Fastqsanger.gz
	SRR18454930_2.fastq.gz	Fastqsanger.gz
	SRR18454931_1.fastq.gz	Fastqsanger.gz
	SRR18454931_2.fastq.gz	Fastqsanger.gz
	SRR18454932_1.fastq.gz	Fastqsanger.gz

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PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [scRNA-seq]

Project description:PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [scRNA-seq]

| PRJNA819054 | ENA

PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [RNA-Seq]

Project description:PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [RNA-Seq]

| PRJNA819058 | ENA

PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [RNA-Seq]

Project description:STING-Type I interferon (IFN) signaling in myeloid cells plays a critical role in effective antitumor immune responses, but STING agonist as monotherapy has shown limited efficacy in clinical trials. The mechanisms that downregulate STING signaling are not fully understood. Here, we report that Protein phosphatase 2A (PP2A) with its specific B regulatory subunit STRN4 negatively regulated STING-Type I IFN in macrophages. Mice with macrophages PP2A deficiency exhibited reduced tumor progression. The tumor microenvironment showed decreased immunosuppressive and increased IFN-activated macrophages and CD8+ T cells. Mechanistically, we demonstrated that hippo kinase MST1/2 was required for STING activation. STING agonist induced dissociation of PP2A from MST1/2 in normal macrophages, but not in tumor conditioned macrophages. Furthermore, our data showed that STRN4 mediated PP2A binding to and dephosphorylation of hippo kinase MST1/2, resulting in stabilization of YAP/TAZ to antagonize STING activation. In human GBM patients, YAP/TAZ was highly expressed in tumor-associated macrophages but not in non-tumor macrophages. We also demonstrated that PP2A/STRN4 deficiency in macrophages reduced YAP/TAZ expression and sensitized tumor conditioned macrophages to STING stimulation. In summary, we demonstrated that PP2A/STRN4-YAP/TAZ is a previously unappreciated mechanism that mediate immunosuppression in tumor-associated macrophages and targeting PP2A/STRN4-YAP/TAZ axis can sensitize tumors to immunotherapy.

2023-02-09 | GSE199251 | GEO

PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages [scRNA-seq]

2023-02-09 | GSE199247 | GEO

PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma

Project description:PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma

| PRJNA880418 | ENA

PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma [RNA]

Project description:PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma [RNA]

| PRJNA880423 | ENA

PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma [scRNA]

Project description:PP2Ac Deficiency Enhances Tumor Immunogenicity by Activating STING-Type I Interferon Signaling in Glioblastoma [scRNA]

| PRJNA880422 | ENA

C5aR2 regulates STING-mediated interferon beta production in human macrophages

Project description:C5aR2 regulates STING-mediated interferon beta production in human macrophages

| PRJNA1030908 | ENA

PP2Ac/STRN4 negatively regulates STING-Type I interferon signaling in tumor associated macrophages

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-09 | GSE199271 | GEO

Intrinsic self-DNA triggers inflammatory disease dependent on STING (I)

Project description:Inflammatory diseases such as Aicardi-Goutieres Syndrome (AGS) and severe systemic lupus erythematosus (SLE) are generally lethal disorders that have been traced to defects in the exonuclease Trex1 (DNAseIII). Mice lacking Trex1 similarly die at an early age through comparable symptoms, including inflammatory myocarditis, through chronic activation of the STING (stimulator of interferon genes) pathway. Here we demonstrate that phagocytes rather than myocytes are predominantly responsible for causing inflammation, an outcome that could be alleviated following adoptive transfer of normal bone marrow into Trex1-/- mice. Trex1-/- macrophages did not exhibit significant augmented ability to produce pro-inflammatory cytokines compared to normal macrophages following exposure to STING-dependent activators, but rather appeared chronically stimulated by genomic DNA. These results shed molecular insight into inflammation and provide concepts for the design of new therapies. Total RNA obtained from wild type (WT), Trex1 deficient (TKO), STING deficient (SKO), or Trex1 and STING double deficient (STKO) mouse Heart

2014-07-09 | E-GEOD-59217 | biostudies-arrayexpress

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