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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data for MALT1-responsive genes

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Kazushi Imai

PROVIDER: E-GEOD-42335 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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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.

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

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

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2018-11-14 | GSE108293 | GEO

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

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2024-04-18 | GSE242764 | GEO

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

B-cell receptor driven MALT1 activity regulates MYC signaling in mantle cell lymphoma

Project description:Mantle cell lymphoma (MCL) is a mature B-cell lymphoma characterized by poor clinical outcome. Recent studies revealed the importance of BCR signaling in maintaining MCL survival. However, it remains unclear which role MALT1, an essential component of the CARD11-BCL10-MALT1 (CBM) complex that transfers BCR signaling to the NF-kB pathway, plays in the biology of MCL. Here we show that a subset of MCLs is addicted to MALT1, as its inhibition by either RNA or pharmacologic interference induced cytotoxicity both in vitro and in vivo. Gene expression profiling following MALT1 inhibition demonstrated that MALT1 controls a MYC-driven gene expression network predominantly through increased MYC protein stability. Thus our analyses identify a previously unappreciated regulatory mechanism of MYC expression. Investigating primary mouse splenocytes, we could demonstrate that MALT1 induced MYC regulation is not restricted to MCL, but represents a common mechanism of MYC regulation. MYC itself is pivotal for MCL survival as its downregulation and pharmacologic inhibition induced cytotoxicity in all MCL models. Collectively, these results provide a strong mechanistic rationale to investigate the therapeutic efficacy in targeting the MALT1-MYC axis in MCL patients.

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