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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE242764 | GEO | 2024/04/18

REPOSITORIES: GEO

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

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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

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

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

Development of Specific Covalent MALT1 Inhibitors and Biomarkers for B-cell Lymphomas

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2018-11-14 | GSE108293 | GEO

Oncogene-induced MALT1 protease activity drives post-transcriptional gene expression in malignant lymphomas

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A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MouseSca1 dataset]

Project description:Attempts at modeling chromosomal translocations involving MALT1 gene, hallmarks of human mucosa-associated lymphoid tissue (MALT) lymphoma, have failed to reproduce the disease in mice. Here we describe a transgenic model in which MALT1 expression was targeted to mouse hematopoietic stem/progenitor cells. In Sca1-MALT1 mice, MALT1 deregulation activated the NF-kappaB pathway in Sca1+ cells, promoting selective B-cell differentiation and mature lymphocyte accumulation in extranodal tissues, progressively leading to the development of clonal B-cell lymphomas. These tumors recapitulated the histopathological features of human MALT lymphomas, presenting typical lymphoepithelial lesions and plasmacytic differentiation. Transcriptional profiling of Sca1-MALT1 murine lymphomas revealed overlapping molecular signatures with human MALT lymphomas, including MALT1-mediated NFkappaB activation, pro-inflammatory signaling and XBP1-induced plasmacytic differentiation. Moreover, murine Malt1 showed proteolytic activity by cleaving Bcl10 in Sca1-MALT1 lymphomas. Our novel technological approach has allowed modeling human MALT lymphoma in mice, which represent unique tools study MALT lymphoma biology and evaluate anti-MALT1 therapies. Keywords: Genetic modification, wt vs. transgenic, MALT1 expression

2012-07-10 | GSE25636 | GEO

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