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Acerihabitans sp. TG2

ABSTRACT: Acerihabitans sp. TG2 Genome sequencing and assembly

PROVIDER: PRJNA1041642 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR26888815.fastq.gz	Fastqsanger.gz
	SRR26888816.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of mouse splenic B cells that are either TG2-sufficient or TG2-deficient

Project description:To compare the transcriptomes of TG2-sufficient and TG2-deficient mouse splenic B cells under resting and stimulated conditions.

2019-11-08 | E-MTAB-7567 | biostudies-arrayexpress

Gene expression profiling of ATRA-differentiated wild-type and TG2 knockout NB4 cells

Project description:Treatment of acute promyelocytic leukemia (APL) with all-trans-retinoic acid (ATRA) results in terminal differentiation of leukemic cells toward neutrophil granulocytes. Administration of ATRA leads to massive changes in gene expression, including down-regulation of cell proliferation-related genes and induction of genes involved in immune function. One of the most induced genes in APL NB4 cells is transglutaminase 2 (TG2). RNAi-mediated stable silencing of TG2 in NB4 cells (TG2-KD NB4) coupled with whole genome microarray analysis revealed that TG2 is involved in the expression of a large number of ATRA-regulated genes. The affected genes participate in granulocyte functions and their silencing lead to reduced adhesive, migratory and phagocytic capacity of neutrophils and less superoxide production. The expression of genes related to cell cycle control also changed, suggesting that TG2 regulates myeloid cell differentiation. CC chemokines CCL2, 3, 22, 24 and cytokines IL1B and IL8 involved in the development of differentiation syndrome (DS) are expressed at significantly lower levels in TG2-KD NB4 cells than in wild-type NB4 cells upon ATRA treatment. Based on our results, we propose that reduced expression of TG2 in differentiating APL cells may suppress effector functions of neutrophil granulocytes and attenuate the ATRA-induced inflammatory phenotype of DS. We used microarrays to detail the global program of gene expression underlying ATRA-induced differentiation of TG2 knockout NB4 cells. TG2 knockout NB4 cells were differentiated for 48 and 72 hours in the presence of ATRA and their gene expression profiles were compared to the wild-type cells at the same time points. Undifferentiated wild-type and TG2 knockout NB4 cells were used as untreated controls. Three biological replicates each.

2010-12-01 | E-GEOD-23702 | biostudies-arrayexpress

Gene expression profiling of ATRA-differentiated wild-type and TG2 knockout NB4 cells

2010-12-01 | GSE23702 | GEO

The transcriptional role of TG2-mediated H3Q5ser in CRC [ChIP-seq]

Project description:We investigated the alteration of H2Bub1, H3K4me3, and H3Q5ser upon RNF40-depleted or TG2-depleted HCT116 cells.

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Project description:WTCCC2 project Schizophrenia (SP) samples

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The transcriptional role of TG2-mediated H3Q5ser in CRC [RNA-seq]

Project description:We investigated the alteration of H3Q5ser upon RNF40-depleted or TG2-depleted HCT116 cells.

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Next Generation Sequencing of Ovarian Cancer Cells upon Exposure to Ascites from Wild Type and TG2-/- Mice

Project description:The goal of this study was to compare signaling pathways in ovarian cancer cells exposed in vitro or in vivo to peritoneal tumor microenvironment of host TG2+/+ vs. TG2-/- mice. For this, we performed NGS-derived transcriptome profiling (RNA-seq) followed by Ingenuity Pathway Analysis (IPA) of ID8 ovarian cancer cells.

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Project description:Background and Aims: Celiac disease (CeD) is an autoimmune disease triggered by dietary gluten in genetically predisposed individuals. Deamidation of gluten peptides by the CeD autoantigen and enzyme transglutaminase 2 (TG2) is central to the pathogenesis of CeD. Inhibition of TG2 with the specific inhibitor ZED1227 effectively prevents gluten-induced histological damage in CeD patients. Here we aimed to explore the blood DNA methylomic changes in ZED1227-treated CeD patients undergoing a gluten challenge. Results: Drug treatment revealed consistent patterns suggesting normalization of the DNA methylome indicating that ZED1227 attenuated the systemic responses to gluten challenge. Conclusions: These findings provide evidence that ZED1227 can significantly prevent the gluten-induced CeD-associated systemic changes. Clinical trial: EudraCT 2017-002241-30

2026-06-18 | GSE319777 | GEO

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