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Genome-wide analysis of mRNA expression alterations of mucosa associated lymphoid tissue lymphoma translocation gene 1 (Malt1) -/- or Wild Type (WT) Naïve T cells induced to differentiate into (T helper) Th1 or Th17 cells

ABSTRACT: Microarrays were used to examine gene expression changes at two time points following the induction of differentiation of Malt1 deficient Naive T cells into Th1 or Th17 cells. The present study aims to find the effect that Malt1 deficiency has on lineage specific T cell differentiation. Malt1 is a NF kappa B regulator and plays a key role in peripheral T cell activation and proliferation, but its role in T cell differentiation is not clear. Aspects of the latter are what the current data set investigates. Total RNA obtained from naïve T cells at two time points following induction to lineage specific T helper cells.

ORGANISM(S): Mus musculus

SUBMITTER: carl virtanen

PROVIDER: E-GEOD-40931 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of mRNA expression alterations of mucosa associated lymphoid tissue lymphoma translocation gene 1 (Malt1) -/- or Wild Type (WT) Naïve T cells induced to differentiate into (T helper) Th1 or Th17 cells

Project description:Microarrays were used to examine gene expression changes at two time points following the induction of differentiation of Malt1 deficient Naive T cells into Th1 or Th17 cells. The present study aims to find the effect that Malt1 deficiency has on lineage specific T cell differentiation. Malt1 is a NF kappa B regulator and plays a key role in peripheral T cell activation and proliferation, but its role in T cell differentiation is not clear. Aspects of the latter are what the current data set investigates.

2013-09-01 | GSE40931 | GEO

Genome-wide analysis of mRNA expression alterations in Stage III-IV high-grade serous ovarian cancer patients exhibiting clinically defined differences in ascites volume (high volume ascites versus low volume ascites)

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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

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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

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