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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

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

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

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

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

Project description:The MALT1 paracaspase plays an essential role in Activated B-cell like Diffuse Large B-cell Lymphoma (ABC DLBCL) downstream of B-cell and Toll-like receptor pathway genes mutated in these tumors. Although MALT1 is considered to be a compelling therapeutic target, development of tractable and specific MALT1 protease inhibitors has thus far been elusive. Herein, we developed a target engagement assay that provides a quantitative readout for specific MALT1 inhibitory effects in living cells. This enabled a structure-guided medicinal chemistry effort culminating in a novel class of substrate-mimetic compounds that bind MALT1 active site and, constitute the first pharmacologically tractable irreversible MALT1 inhibitor. We confirmed MALT1 targeting is effective at suppressing ABC DLBCL cells in vitro and in vivo. We show that reduction in serum IL10 levels exquisitely correlates with drug PK and degree of MALT1 inhibition in vitro and in vivo and constitutes a useful pharmacodynamic biomarker to evaluate these compounds in clinical trials. Our new inhibitor revealed insights into the biology of MALT1 in ABC DLBCL, such as driving JAK-STAT signaling and suppressing type I interferon (IFN) response and MHC class II expression, suggesting that MALT1 inhibition could prime lymphomas for immune recognition by cytotoxic immune cells.

2018-11-14 | GSE108293 | GEO

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

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

Real-time quantitative PCR analysis of microRNA in keratinocytes and reconstituted epidermis

Project description:Analysis of microRNA expression in keratinocytes by relative quantification (RQ) using the comparative Ct method. Real-time quantitative PCR analysis of microRNA in keratinocytes or reconstituted epidermis exposed to IL-22, LPS or UV radiation or a small molecule drug. Keratinocytes or reconstituted human epidermis were exposed to indicated treatments. A qPCR analysis of 365 microRNAs in keratinocytes. RNA (20 ng per reaction) reverse transcribed using 8 x Multiplex RT pools. Each resulting cDNA pool was mixed with TaqMan Universal PCR Master Mix and loaded in corresponding port on the TaqMan Array.

2013-05-23 | E-GEOD-41838 | biostudies-arrayexpress

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