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RNA-Seq in control and TET2 Knockout cells with IFNγ treatment

ABSTRACT: RNA-Seq in control and TET2 Knockout cells with IFNγ treatment

PROVIDER: PRJNA547830 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9217650_1.fastq.gz	Fastqsanger.gz
	SRR9217650_2.fastq.gz	Fastqsanger.gz
	SRR9217660_1.fastq.gz	Fastqsanger.gz
	SRR9217660_2.fastq.gz	Fastqsanger.gz
	SRR9217651_1.fastq.gz	Fastqsanger.gz

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RNA-Seq in control and TET2 Knockout cells with IFNγ treatment

Project description:Detect overall RNA level change under TET2 knockout in response to IFNγ. Loss of TET2 alters IFNγ transcriptome, TET2 mediates the IFNγ signaling pathway.

2020-01-01 | GSE132408 | GEO

hMeDIP-Seq of Tet2 knockout hippocampal neurons

Project description:Tet2 regulates gene expression by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine. Profiling the genomic locations of 5-hydroxymethylcytosine after Tet2 manipulation can inform us of the targets of Tet2 regulation. We profiled hydroxymethylcytosine in Tet2 knockout neurons to determine the targets of Tet2 in neurons.

2023-03-25 | GSE199597 | GEO

STUB1 dampens IFNγ response in tumors by destabilizing the IFNγ receptor complex

Project description:Despite its success, immune checkpoint blockade (ICB) cannot induce durable responses in most patients. This is partially attributed to reduced sensitivity to interferon gamma (IFNγ). Thus, elevating tumor IFNγ-receptor 1 (IFNγ-R1) expression to enhance IFNγ-mediated cytotoxicity is of clinical interest. Here, we demonstrate higher IFNγ-R1 expression to sensitize tumors to IFNγ-mediated killing. To unveil the largely undefined mechanisms of IFNγ-R1 expression, we performed a genome-wide CRISPR/Cas9 knockout screen for suppressors of IFNγ-R1 tumor cell surface abundance. We uncovered STUB1 as key mediator for proteasomally degrading IFNγ-R1/JAK1 complex. Conversely, STUB1 inactivation in tumor cells amplified IFNγ signaling and sensitized to cytotoxic T cells, but permitted IFNγ-induced PD-L1 expression. Rationally combining STUB1 inactivation with anti-PD-1 treatment effectively eliminated tumors in vivo. Clinically corroborating this is a STUB1 transcriptomic signature that associates with response to anti-PD-1 treatment in two patient cohorts. Thus, uncovering STUB1 as a pivotal regulator of IFNγ signaling and a synergistic target for anti-PD-1 treatment.

2022-02-24 | GSE154040 | GEO

UBIQUITIN LIGASE STUB1 DESTABILIZES IFNγ-RECEPTOR COMPLEX TO SUPPRESS TUMOR IFNγ SIGNALING

Project description:The cytokine IFNγ differentially impacts on tumors upon immune checkpoint blockade (ICB). Despite our understanding of downstream signaling events, less is known about 36 regulation of its receptor (IFNγ-R1). With an unbiased genome-wide CRISPR/Cas9 screen for critical regulators of IFNγ-R1 cell surface abundance, we identified STUB1 as an E3 ubiquitin ligase for IFNγ-R1 in complex with its signal-relaying kinase JAK1. STUB1 mediates ubiquitination-dependent proteasomal degradation of IFNγ-R1/JAK1 complex through IFNγ-R1K285 and JAK1K249. Conversely, STUB1 inactivation amplifies IFNγ signaling, sensitizing tumor cells to cytotoxic T cells in vitro. This was corroborated by an anticorrelation between STUB1 expression and IFNγ response in ICB-treated patients. Consistent with the context-dependent effects of IFNγ in vivo, anti-PD-1 response was increased in heterogenous tumors comprising both wildtype and STUB1-deficient cells but not full STUB1 knockout tumors. These results uncover STUB1 as a critical regulator of IFNγ-R1, and highlight the context-dependency of STUB1-regulated IFNγ signaling for ICB outcome.

2022-03-07 | PXD030580 | Pride

IFNγ-dependent remodelling of the myeloid immune landscape underlies control of IFNγ-insensitive tumors

Project description:IFNγ-dependent remodelling of the myeloid immune landscape underlies control of IFNγ-insensitive tumors

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Gene expression profiles of Tet1 knockout (T1KO), Tet2 knockout (T2KO) and Tet1/Tet2 double knockout (DKO) mouse embryonic stem cells.

Project description:Global gene expression profile of single and double mutant mouse ES cells were compared to wt ES cells. Two male Tet1 KO, one male Tet2 KO, two male double KO, two female double KO, two male WT and two female WT mouse ES cells were compared. Global gene expression profile of single and double knockout mouse embryonic stem cells were compared to that of wild type mouse ES cells. All used ES lines were derived from C57/BL/6 mixed background mice. RNA from feeder free mutant mouse ES cells was competetively hybridized against RNA from WT ES cells. Same sex lines were compared. Two independent ES line of each genotype were used, with the exception of Tet2 KO ES cells where only one male line was used.

2013-02-01 | E-GEOD-42991 | biostudies-arrayexpress

Chromatin accessibility in naive and primed HeLa cells upon IFNγ treatment

Project description:chromatin accessibility (ATAC-seq) experiment. HeLa cells were primed with IFNγ for 24 hours, followed by IFNγ washout. After 48h, naïve and primed cells were induced by IFNγ for 1h and 3h. Cells were harvested at indicated time points and processed for ATAC-seq.

2023-05-06 | E-MTAB-12624 | biostudies-arrayexpress

hMeDIP-Seq of Tet2 knockout hippocampal neurons

Project description:hMeDIP-Seq of Tet2 knockout hippocampal neurons

| PRJNA820784 | ENA

Context Dependent Effects of Ascorbic Acid Treatment in TET2 Mutant Myeloid Neoplasia

Project description:Loss-of-function TET2 mutations (TET2MT) are common in myeloid neoplasia. TET2, a DNA dioxygenase, requires 2-oxoglutarate and Fe(II) to oxidize 5-methylcytosine. TET2MT thus result in hypermethylation and transcriptional repression. Ascorbic acid (AA) increases dioxygenase activity by facilitating Fe(III)/Fe(II) redox reaction and may alleviate some biological consequences of TET2MT by restoring dioxygenase activity. Here, we report the utility of AA in the prevention of TET2MT MN, clarify the mechanistic underpinning of the TET2-AA interactions, and demonstrate that the ability of AA to restore TET2 activity in cells depends on N- and C-terminal lysine acetylation and nature of TET2MT. Consequently, pharmacologic modulation of acetyltransferases and histone deacetylases may regulate TET dioxygenase-dependent AA effects. Thus, our study highlights the contribution of factors that may enhance or attenuate AA effects on TET2 and provides a rationale for novel therapeutic approaches including combinations of AA with class I/II HDAC inhibitor or sirtuin activators in TET2MT leukemia.

2020-09-09 | PXD020550 | Pride

Genomic analysis of Tet2 knockout macrophages

Project description:Ten-Eleven-Translocation-2 (Tet2) is a DNA methylcytosine dioxygenase that functions as a tumor suppressor in hematopoietic malignancies. In this study, we revealed a role for Tet2 in sustaining the immunosuppressive function of tumor-tissue myeloid cells. We found that Tet2 expression is increased in intratumoral myeloid cells both in mouse models of melanoma and in melanoma patients, and that this increased expression is dependent on an IL-1R-MyD88 pathway. Ablation of Tet2 in myeloid cells suppressed melanoma growth in vivo, and shifted the immunosuppressive gene expression program in tumor-associated macrophages to a proinflammatory one, with a concomitant reduction of the immunosuppressive function. This resulted in increased numbers of effector T cells in the tumor, and T cell depletion abolished the reduced tumor growth observed upon myeloid-specific deletion of Tet2. Our findings reveal a non-cell-intrinsic, tumor-promoting function for Tet2, and suggest that Tet2 may present a therapeutic target for the treatment of non-hematologic malignancies.

2017-08-15 | GSE98964 | GEO

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