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PD-L1 ubiquitination by MIB2 enables its translocation to the plasma membrane for tumor immune evasion

ABSTRACT: PD-L1 ubiquitination by MIB2 enables its translocation to the plasma membrane for tumor immune evasion

PROVIDER: PRJNA906110 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22430454.fastq.gz	Fastqsanger.gz
	SRR22430455.fastq.gz	Fastqsanger.gz
	SRR22430456.fastq.gz	Fastqsanger.gz

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Similar Datasets

PD-L1 ubiquitination by MIB2 enables its translocation to the plasma membrane for tumor immune evasion

Project description:Programmed death-ligand 1 (PD-L1), a critical immune checkpoint ligand, is a transmembrane protein synthesized in the endoplasmic reticulum of tumor cells and transported to the plasma membrane to interact with programmed death 1 (PD-1) expressed on T cell surface. This interaction delivers co-inhibitory signals to T cells, thereby suppressing their function and evading antitumor immunity. Most companion or complementary diagnostic devices for PD-L1 expression levels in tumor cells used in the clinic or clinical trials require membranous staining. However, the mechanism driving PD-L1 translocation to the plasma membrane after de novo synthesis is poorly understood. Herein, we showed that mind bomb homolog 2 (MIB2) is required for PD-L1 transportation from the trans-Golgi network (TGN) to the plasma membrane of cancer cells. MIB2 deficiency leaded to fewer PD-L1 proteins on the tumor cell surface and promotes antitumor immunity in mice.We performed a single-cell RNA sequencing (scRNA-seq) of B16-F10 tumors from C57BL/6 syngeneic mice. Knockdown of MIB2 resulted in an increase in the percentage of CD8+ CTLs (approximately 5-fold) and CD4+/CD8+ effector/activated T cells (approximately 2-fold), indicating that MIB2 downregulation enhanced the antitumor immune activity centered on CD8+ CTLs and changed their transcriptional profile. Our findings demonstrate that non-proteolytic ubiquitination of PD-L1 by MIB2 is required for its transportation to the plasma membrane and tumor cells' immune evasion.

2023-12-31 | GSE218906 | GEO

PD-L1 translocation to the plasma membrane enables tumor immune evasion through MIB2 ubiquitination.

Project description:Programmed death-ligand 1 (PD-L1), a critical immune checkpoint ligand, is a transmembrane protein synthesized in the endoplasmic reticulum of tumor cells and transported to the plasma membrane to interact with programmed death 1 (PD-1) expressed on T cell surface. This interaction delivers coinhibitory signals to T cells, thereby suppressing their function and allowing evasion of antitumor immunity. Most companion or complementary diagnostic devices for assessing PD-L1 expression levels in tumor cells used in the clinic or in clinical trials require membranous staining. However, the mechanism driving PD-L1 translocation to the plasma membrane after de novo synthesis is poorly understood. Herein, we showed that mind bomb homolog 2 (MIB2) is required for PD-L1 transportation from the trans-Golgi network (TGN) to the plasma membrane of cancer cells. MIB2 deficiency led to fewer PD-L1 proteins on the tumor cell surface and promoted antitumor immunity in mice. Mechanistically, MIB2 catalyzed nonproteolytic K63-linked ubiquitination of PD-L1, facilitating PD-L1 trafficking through Ras-associated binding 8-mediated (RAB8-mediated) exocytosis from the TGN to the plasma membrane, where it bound PD-1 extrinsically to prevent tumor cell killing by T cells. Our findings demonstrate that nonproteolytic ubiquitination of PD-L1 by MIB2 is required for its transportation to the plasma membrane and tumor cell immune evasion.

| S-EPMC9888393 | biostudies-literature

PHF8 enables immune evasion by silencing endogenous retroelements.

Project description:PHF8 enables immune evasion by silencing endogenous retroelements.

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PHF8 enables immune evasion by silencing endogenous retroelements

Project description:PHF8 enables immune evasion by silencing endogenous retroelements

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PHF8 enables immune evasion by silencing endogenous retroelements [ATAC-seq]

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RNA N-glycosylation enables innate immune evasion and homeostatic efferocytosis

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PHF8 enables immune evasion by silencing endogenous retroelements [ChIP-seq]

Project description:PHF8 enables immune evasion by silencing endogenous retroelements [ChIP-seq]

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PHF8 enables immune evasion by silencing endogenous retroelements [CHIP-seq]

Project description:PHF8 enables immune evasion by silencing endogenous retroelements [CHIP-seq]

| PRJNA870727 | ENA

PHF8 enables immune evasion by silencing endogenous retroelements [RNA-Seq]

Project description:PHF8 enables immune evasion by silencing endogenous retroelements [RNA-Seq]

| PRJNA870462 | ENA

CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity

Project description:CDK5-dependent phosphorylation and nuclear translocation of TRIM59 promotes macroH2A1 ubiquitination and tumorigenicity

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