Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA771671 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16355776.fastq.gz	Fastqsanger.gz
	SRR16355777.fastq.gz	Fastqsanger.gz
	SRR16355778.fastq.gz	Fastqsanger.gz
	SRR16355779.fastq.gz	Fastqsanger.gz
	SRR16355780.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

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 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

IL-36 and IL-17A Cooperatively Induce a Psoriasis-like Gene Expression Response in Human Keratinocytes

Project description:In this study we tested interactions between IL-36 and IL-17A in human keratinocytes. 24 hours of IL-36 stimulation in keratinocytes promoted IL-36, IL-17C, and characteristic psoriasis-related molecule expressions in normal human epidermal keratinocytes in dose-dependent manners as measured by mRNA and protein quantification.

2021-12-31 | GSE160904 | GEO

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

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

| PRJNA771675 | 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

Interleukin-17A based dysregulation of Human Primary Keratinocyte proteome

Project description:To delineate mechanisms for psoriasis pathogenesis driven by the interleukin-17A, proteomic dysregulations were studied in a Human Primary Keratinocyte model system. Label-free quantification was performed and fold-changes were obtained for abundances of proteins in IL-17A treated keratinocytes versus those from IL-17A treated keratinocytes. Briefly, Human Primary Keratinocytes were isolated and treated with the cytokine IL-17A (50ng/ml) in incomplete media devoid of any growth factors. Tryptic digested and desalted peptide samples were injected in Thermoscientific Q-Exactive Plus instruments through EasyNLC HPLC autosampler. The instruments were set to MS1 resolution of 70000 and MS2 resolution of 17500. The acquisition experiments were optimized to run on 120 min gradients. The MS spectra were analyzed using the Thermoscientific mass informatics platform Proteome discoverer version 2.2. The common workflows for discovery proteomics were used with Mascot and SequestHT as search engines. This dataset helped to simulate the IL-17A-driven inflammation in keratinocytes and uncovered many putative druggable targets in the context of psoriasis.

2022-08-11 | MSV000090116 | MassIVE

IL-17A plays a central role in the expression of psoriasis signature genes through induction of IkappaB-zeta in keratinocytes

Project description:In psoriasis lesions, a diverse mixture of cytokines is upregulated which influence each other generating a complex inflammatory situation. Although this is the case, the inhibition of Interleukin-17A (IL-17A) alone showed unprecedented clinical results in patients, indicating that IL-17A is a critical inducer of psoriasis pathogenesis. To elucidate IL-17A-driven keratinocyte-intrinsic signaling pathways, we treated monolayers of normal human epidermal keratinocytes in vitro with a mixture of 6 cytokines (IL-17A, TNF-a, IL-17C, IL-22, IL-36g and IFN-g) involved in psoriasis, to mimic the inflammatory milieu in psoriasis lesions. Microarray and gene set enrichment analysis revealed that this cytokine mixture induced similar gene expression changes with the previous transcriptome studies using psoriasis lesions. Importantly, we identified a set of IL-17A-regulated genes in keratinocytes, which recapitulate typical psoriasis genes exemplified by DEFB4A, S100A7, IL19 and CSF3, based on differences in the expression profiles of cells stimulated with 6 cytokines versus cells stimulated with only 5 cytokines lacking IL-17A. Furthermore a specific IL-17A-induced gene, NFKBIZ, which encodes IkappaB-zeta, a transcriptional regulator for NF-kappaB, was demonstrated to have a significant role for IL-17A-induced gene expression. Thus, we present novel in vitro data from normal human keratinocytes that would help elucidating the IL-17A-driven keratinocyte activation in psoriasis. Cytokine mixture-induced gene expression in primary normal human epidermal keratinocytes (NHEKs) was measured at 24 hours after exposure. NHEKs were exposed to the combination of selected six cytokines (IL-17A: 100 ng/ml, TNF-a: 10 ng/ml, IFN-g: 10 ng/ml, IL-17C: 100 ng/ml, IL-22: 100 ng/ml, IL-36g: 500 ng/ml) , or to the different combinations of five of the six cytokines (in total, 7 different treatments and one untreated control). No replicate experiments were conducted.

2016-03-08 | E-GEOD-77719 | biostudies-arrayexpress

IL-17A plays a central role in the expression of psoriasis signature genes through induction of IkappaB-zeta in keratinocytes

2016-03-08 | GSE77719 | GEO