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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [4]

ABSTRACT: ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [4]

PROVIDER: PRJNA1144903 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30150100_1.fastq.gz	Fastqsanger.gz
	SRR30150100_2.fastq.gz	Fastqsanger.gz
	SRR30150101_1.fastq.gz	Fastqsanger.gz
	SRR30150101_2.fastq.gz	Fastqsanger.gz
	SRR30150102_1.fastq.gz	Fastqsanger.gz

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post- transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

2025-05-30 | PXD055858 | Pride

ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [4]

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post-transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post-transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [3]

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post-transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post-transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

2024-08-22 | GSE274071 | GEO

ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [2]

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post-transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post-transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [1]

Project description:Type II interferon (IFNγ) signaling is essential for innate immunity and critical for effective immunological checkpoint blockade in cancer immunotherapy. Genetic screen identification of post-transcriptional regulators of this pathway has been challenging since such factors are often essential for cell viability. Here, we utilize our inducible CRISPR/Cas9 approach to screen for key post-transcriptional regulators of IFNγ signaling, and in this way identify ERH and the ERH-associated splicing and RNA export factors MAGOH, SRSF1, and ALYREF. Loss of these factors impairs post-transcriptional mRNA maturation of JAK2, a crucial kinase for IFNγ signaling, resulting in abrogated JAK2 protein levels and diminished IFNγ signaling. Further analysis highlights a critical role for ERH in preventing intron retention in AU-rich regions in specific transcripts, such as JAK2. This regulation is markedly different from previously described retention of GC-rich introns. Overall, these findings reveal that post-transcriptional JAK2 processing is a critical rate-limiting step for the IFNγ-driven innate immune response.

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [1]

Project description:ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [1]

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ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [2]

Project description:ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [2]

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Project description:ERH regulates type II interferon immune signaling through post-transcriptional regulation of JAK2 mRNA [3]

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MYC induces immunotherapy and interferon-γ resistance through downregulation of JAK2

Project description:Immunotherapy revolutionized the treatment of advanced melanoma. As the pathways mediating resistance to immunotherapy are largely unknown, we conducted transcriptome profiling of pre-immunotherapy tumor biopsies from melanoma patients that received PD-1 blockade (n=36) or adoptive cell therapy with tumor infiltrating lymphocytes (n=37). We identified two melanoma-intrinsic mutually exclusive gene programs, which are controlled by interferon-γ and MYC, and determine immunotherapy outcome. MYC-overexpressing melanoma cells exhibited lower interferon-γ responsiveness, which was linked with JAK2 downregulation. Luciferase activity assays under the control of JAK2 promoter demonstrated reduced activity in MYC-overexpressing cells, which was reversible upon mutagenesis of MYC E-box binding sites in the JAK2 promoter. Moreover, silencing of MYC or its co-factor MAX with siRNA increased JAK2 expression and interferon-γ responsiveness of melanomas, while concomitantly enhancing the effector functions of T-cells co-incubated with MYC-overexpressing cells. Thus, we propose that MYC plays a pivotal role in immunotherapy resistance through downregulation of JAK2.

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