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RNA-seq of E0771-Vector control and E0771-Malt1-WT at basal condition

ABSTRACT: To reveal the downstream signal change induced by Malt1, we collected mRNA samples from Vector control- and WT-Malt1-expressing E0771 cancer cells, and performed RNA-seq analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE265893 | GEO | 2024/04/26

REPOSITORIES: GEO

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RNA-seq of E0771-Vector control, E0771-Malt1-WT and E0771 Malt1-PD (Without T cell coculture)

Project description:To reveal the downstream paracrine signals from WT-Matl1 or PD-Malt1 tumor cells which responsible for the above observed macrophage phenotypes, we collected mRNA samples from Vector control-, WT-Malt1-, PD-Malt1-, V87R-Malt1-, or L88D-Malt1-expressing E0771 cancer cells, and performed RNA-seq analysis.

2024-04-18 | GSE242878 | GEO

Gene expression profile at single cell level of CD45+ immune cells from E0771-Vector control tumor tissue, E0771 wildtype Malt1 overexpression tumor tissue and E0771 paracaspase-deficient Malt1 overexpression tumor tissue.

Project description:To invesitigate the additional paracaspase-independent tumor-promoting effect exist for Malt1. We thus collected E0771-Vector control tumor tissue, E0771 wildtype Malt1 (Malt1-WT) overexpression tumor tissue and E0771 paracaspase-deficient Malt1 (Malt1-PD) overexpression tumor tissue, and sorted out immune cells for 10× Genomics single cell RNA-sequencing (scRNA-seq).

2024-04-18 | GSE242554 | GEO

RNA-seq of E0771-Vector control, E0771-Malt1-WT and E0771 Malt1-PD after T cell killing

Project description:To understand potential downstream signaling molecules that are responsible for wild type-Malt1 induced resistance of tumor cell to CD8 T cell killing , we first use E0771 cells expressing either -Vector control, wild type-Malt1 (M-WT), or Malt1 PD mutant (M-PD) to coculture with activated CD8 T cell at a effctor: target ratio(E:T ration) of 3 for 12 hours. Then wash the cells with PBS, digest the cells by 0.25% trypsin solution, harvest the cells in 15 ml tubes by centrifugation (1000 rpm 5min) and seed cells into the original plate with DMEM+10%FBS+1%P/S medium. 6 hours after sseding, wash cells with PBS, lyse cells with TRIZOL for RNA extraction, perform reverse transcription and cDNA library for RNA-Seq analysis.

2024-04-18 | GSE242764 | GEO

Expression data for MALT1-responsive genes

Project description:In lymphocyte lineages, mucosa-associated lymphoid tissue 1 (MALT1) mediates the nuclear factor-M-NM-:B activation signal that stimulates progression of malignant tumors. However, its expression is inactivated in oral carcinoma patients with worse prognosis. Unveiling genes under the control of MALT1 will provide valuable information for understanding of the mechanism of carcinoma progression. We profiled gene datasets altered in response to MALT1 in oral carcinoma cells by the microarray analysis. Totally, 2,933 genes with a fold change M-bM-^IM-% M-BM-12.0 and P < 0.05 were identified. HSC2 oral carcinoma cells were used for RNA extraction and hybridization on Affimetrix microarrays. We sought to obtain homogenous populations of MALT1-resonsive genes in order to increase the resolution of expression profiles. To this end, we used HSC2 cells stably expressing MALT1 (n=3) and vector alone (n=3) for the analysis.

2013-06-18 | E-GEOD-42335 | biostudies-arrayexpress

Expression data for MALT1-responsive genes

Project description:In lymphocyte lineages, mucosa-associated lymphoid tissue 1 (MALT1) mediates the nuclear factor-κB activation signal that stimulates progression of malignant tumors. However, its expression is inactivated in oral carcinoma patients with worse prognosis. Unveiling genes under the control of MALT1 will provide valuable information for understanding of the mechanism of carcinoma progression. We profiled gene datasets altered in response to MALT1 in oral carcinoma cells by the microarray analysis. Totally, 2,933 genes with a fold change ≥ ±2.0 and P < 0.05 were identified.

2013-06-18 | GSE42335 | GEO

Transcriptome analysis of Jurkat T cells expressing MALT1 or its mutants MALT1-R149A and MALT1-C464A or the MALT1-R149A-C464A double mutant.

Project description:Purpose: study the role of MALT1 auto-proteolysis in T cell receptor mediated activation of NF-kB. Methods: Jurkat cells were generated that express wild type MALT1, the auto-cleavage deficient MALT1-R149A mutant, the catalytic inactive MALT1-C464A mutant or the R149A-C464A double mutant (RACA). Expression of endogenous MALT1 was inactivated using TALEN technology for the Jurkat cells expressing MALT1-R149A (JDM-RA) and MALT1-C464A (JDM-CA). Illumina HISeq 2000 deep sequencing was performed to determine the mRNA profiles for MALT1, JDM-RA, JDM-CA and RACA cells in unstimulated conditions or after treatment with 75ng/ml PMA and 150 ng/ml ionomycin for 3 or 18 hrs. Results: PMA ionomycin stimulation of the MALT1 auto-cleavage defective JDM-RA cells fails to activate NF-kB-dependent transcription like for the MALT1 catalytic inactive JDM-CA cells and the double RACA mutant cells. Conclusion: MALT1 autoproteolysis is essential for transcription of NF-kB target genes

2014-11-28 | GSE52934 | GEO

E0771 WXS

Project description:E0771 whole exom sequencing

| PRJEB30681 | ENA

Uncoupling Malt1 threshold function from paracaspase activity results in destructive autoimmune inflammation

Project description:The paracaspase Malt1 is a central regulator of antigen receptor signaling that is frequently mutated in human lymphoma. As a scaffold, it assembles protein complexes for NF-kB activation, and its proteolytic domain cleaves negative NF-kB regulators for signal enforcement. Still, the physiological functions of Malt1-protease are unknown. We demonstrate that targeted Malt1-paracaspase inactivation induces a lethal inflammatory syndrome with lymphocyte-dependent neurodegeneration in vivo. Paracaspase activity is essential for regulatory T-cell and innate-like B-cell development, but it is largely dispensable for overcoming Malt1-dependent thresholds for lymphocyte activation. In addition to NF-kB inhibitors, Malt1 cleaves an entire set of mRNA stability regulators, including Roquin-1, Roquin-2 and Regnase-1, and paracaspase inactivation results in excessive IFNγ production by effector lymphocytes that drives pathology. Together, our results reveal distinct threshold and modulatory functions of Malt1 that differentially control lymphocyte differentiation and activation pathways and demonstrate that selective paracaspase blockage skews systemic immunity towards destructive autoinflammation.

2014-10-27 | GSE55360 | GEO

TMT10-TAILS for monitoring MALT1 substrate cleavage

Project description:We used TMT-TAILS to monitor MALT1 substrate cleavage in normal EBV B lymphocytes stimulated with PMA/ionomycin to evaluate kinetic profiles of MALT1 inhibitors

2018-10-02 | PXD008421 | Pride

Uncoupling Malt1 threshold function from paracaspase activity results in destructive autoimmune inflammation

Project description:The paracaspase Malt1 is a central regulator of antigen receptor signaling that is frequently mutated in human lymphoma. As a scaffold, it assembles protein complexes for NF-kB activation, and its proteolytic domain cleaves negative NF-kB regulators for signal enforcement. Still, the physiological functions of Malt1-protease are unknown. We demonstrate that targeted Malt1-paracaspase inactivation induces a lethal inflammatory syndrome with lymphocyte-dependent neurodegeneration in vivo. Paracaspase activity is essential for regulatory T-cell and innate-like B-cell development, but it is largely dispensable for overcoming Malt1-dependent thresholds for lymphocyte activation. In addition to NF-kB inhibitors, Malt1 cleaves an entire set of mRNA stability regulators, including Roquin-1, Roquin-2 and Regnase-1, and paracaspase inactivation results in excessive IFNÎ³ production by effector lymphocytes that drives pathology. Together, our results reveal distinct threshold and modulatory functions of Malt1 that differentially control lymphocyte differentiation and activation pathways and demonstrate that selective paracaspase blockage skews systemic immunity towards destructive autoinflammation. Total RNA obtained from T cells with (1h and 4 h) and without stimulation, 3 biological replicates, 3 genotypes (Malt+/-, Malt-/-, MaltPM/-)

2014-10-27 | E-GEOD-55360 | biostudies-arrayexpress

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