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Quantitative Assessment of transcriptomic changes induced by aberrant BCL10/MALT1 signaling in primary keratinocytes [CDL]

ABSTRACT: Quantitative Assessment of transcriptomic changes induced by aberrant BCL10/MALT1 signaling in primary keratinocytes [CDL]

PROVIDER: PRJNA771675 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16355800.fastq.gz	Fastqsanger.gz
	SRR16355801.fastq.gz	Fastqsanger.gz
	SRR16355802.fastq.gz	Fastqsanger.gz
	SRR16355803.fastq.gz	Fastqsanger.gz
	SRR16355804.fastq.gz	Fastqsanger.gz

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Similar Datasets

Quantitative Assessment of transcriptomic changes induced by aberrant BCL10/MALT1 signaling in primary keratinocytes [CDL]

Project description:Purpose: The goal of this study is to assess the transcriptomic changes induced by aberrant BCL10/MALT1 signaling downstream of a constitutively active Card11 construct (Rosa26Card11dLinker-lox-STOP-lox x K14Cre) in keratinocytes. Methods: Keratinocytes were isolated from newborn mice, cultured for 5 days and harvested for RNA isolation. mRNA profiles were generated by RNA sequencing using Illumina NextSeq 550. Results: Differential expression analysis identified 293 genes (plus the transgene Card11) to be significantly upregulated (log2 fold change > 1.5, FDR < 0.05) in Card11dLinker expressing keratinocytes compared to those isolated from only KRT14Cre-expressing littermate controls.

2022-01-08 | GSE185999 | GEO

Quantitative Assessment of transcriptomic changes induced by the loss of BCL10/MALT1 signaling in primary keratinocytes and its effects on IL-17A stimulation [Bcl10ko]

Project description:Purpose: The goal of this study is to assess the transcriptomic changes induced by the loss BCL10/MALT1 signaling in keratinocytes and ist effect on IL-17A stimulation Methods: Keratinocytes were isolated from newborn Bcl10+/− and Bcl10−/− mice, cultured for 5 days, stimulated with IL-17A for 5 hours and harvested for RNA isolation. mRNA profiles were generated by deep sequencing, using Illumina NextSeq 550. Results: as shown by Gene Set Enrichment Analysis, IL-17A stimulation induced significant enrichment of an IL17 signature defined by Chiricozzi et al (JID 2011) in both Bcl10+/− and Bcl10−/− murine keratinocytes. However, direct comparison of Bcl10+/− and Bcl10−/− keratinocytes demonstrated a stronger enrichment of this signature in Bcl10 competent keratinocytes than in Bcl10 deficient cells.

2022-01-08 | GSE185998 | GEO

Isolinderalactone Suppresses the Progression of Cholangiocarcinoma by Modulating the CARMA1-BCL10-MALT1 Signalosome

Project description:Cholangiocarcinoma (CCA) is a highly aggressive malignancy with poor prognosis and limited therapeutic options. While Isolinderalactone (ILL) has shown anticancer potential, its effects and underlying mechanisms in CCA remain unclear. This study investigated the anti-CCA activity of ILL and elucidated its molecular mechanisms. ILL significantly inhibited CCA cell viability, proliferation, migration, and invasion, while also inducing G0/G1 cell cycle arrest and promoting apoptosis. Transcriptomic and biochemical analyses revealed that ILL suppressed the NF-κB signaling pathway by inhibiting IκB phosphorylation and p65 activation. Mechanistically, ILL was found to directly bind to BCL10, a key adaptor protein. This interaction disrupted the formation of the CARMA1-BCL10-MALT1 (CBM) signalosome and consequently reduced BCL10 ubiquitination. Functional experiments confirmed this mechanism: BCL10 knockdown mimicked ILL's inhibitory effects, while a BCL10 mutation abolished them. Furthermore, activation of NF-κB with Diprovocim partially reversed ILL's suppressive effects. In a xenograft nude mouse model, ILL effectively reduced tumor growth without significant toxicity and suppressed NF-κB activation in tumor tissues. These findings demonstrate that Isolinderalactone suppresses CCA progression by modulating the CBM signalosome and BCL10 ubiquitination to regulate the NF-κB pathway, supporting its potential as a promising therapeutic candidate for CCA.

2026-06-24 | GSE318264 | GEO

Quantitative Assessment of transcriptomic changes induced by the loss of BCL10/MALT1 signaling in primary keratinocytes and its effects on IL-17A stimulation [Bcl10ko]

Project description:Quantitative Assessment of transcriptomic changes induced by the loss of BCL10/MALT1 signaling in primary keratinocytes and its effects on IL-17A stimulation [Bcl10ko]

| PRJNA771671 | ENA

MALT1 protease activity controls the expression of inflammatory genes in keratinocytes upon Zymosan stimulation

Project description:The protease activity of the paracaspase MALT1 plays an important role in antigen receptor-mediated lymphocyte activation by controlling the activity of the transcription factor NF-kB and is thus essential for the expression of inflammatory target genes. MALT1 is not only present in cells of the hematopoietic lineage, but is ubiquitously expressed. Here we report that Zymosan or S. aureus stimulation induced MALT1 protease activity in human primary keratinocytes. Human primary keratinocytes were treated for 8 h with solvent control (DMSO), PMA/Ionomycin (P/I) or P/I with MALT1-inhibitor LVSR-fmk. Three biological replicates of each stimualtion were analyzed for gene expression profiles.

2015-10-24 | E-GEOD-74297 | biostudies-arrayexpress

MALT1 protease activity controls the expression of inflammatory genes in keratinocytes upon Zymosan stimulation

2015-10-24 | GSE74297 | GEO

Isolinderalactone Suppresses the Progression of Cholangiocarcinoma by Modulating the CARMA1-BCL10-MALT1 Signalosome

Project description:Isolinderalactone Suppresses the Progression of Cholangiocarcinoma by Modulating the CARMA1-BCL10-MALT1 Signalosome

| PRJNA1417003 | ENA

A role for the protease MALT1 in EBV-mediated B-cell transformation by Latent Membrane Proteins 1 and 2

Project description:Epstein-Barr virus (EBV) is a human herpesvirus that can cause a variety of hematological malignancies, in particular B-, T- and NK-cell lymphomas. Latency proteins of the virus contribute to lymphomagenesis by activating the transcription factor NF-kB, but the molecular mechanism underlying EBV-driven NF-kB activation remains incompletely understood. Here we show that EBV latent membrane proteins LMP1 and LMP2A or LMP2B synergize to activate the protease MALT1, a key driver of NF-kB-mediated lymphocyte proliferation. EBV-positive B-cell lines co-expressing LMP1 and LMP2 proteins exhibited constitutive activity of the protease MALT1, and treatment with a MALT1 inhibitor or silencing of latent membrane protein-1 (LMP1) or LMP2 impaired MALT1-dependent substrate cleavage and proliferation in these cell lines. Further molecular studies revealed that LMP1 physically interacted with the MALT1-binding partner BCL10, while LMP2A and LMP2B interacted with MALT1. LMP1 also colocalized with LMP2 in dotted structures, suggesting that LMP1 and LMP2 synergize via the coordinated formation of LMP-BCL10-MALT1 (LBM) oligomers. Finally, MALT1 protease inhibition led to reduced expression of a set of NF-kB-driven genes, and reduced tumor growth in an EBV-positive lymphoma xenograft model. These findings establish a key role for the protease MALT1 in LMP1/2-mediated, NF-kB-driven cellular transformation and provide a rationale for inhibiting MALT1 to treat EBV-positive B-cell lymphomas that co-express LMP1 and LMP2.

2026-08-17 | GSE335838 | GEO

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

A mouse model of deregulation of the malt1 oncogene recapitulates the pathogenesis of human malt lymphoma [MALT 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 NF-kappaB 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: lymphoma profiling, MALT lymphoma

2012-07-10 | GSE25638 | GEO

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