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Genome-wide mapping of histone H3 T6 phosphorylation in mouse B lymphocytes [ChIP-seq]

ABSTRACT: The changes in gene expression can be epigenetically regulated by histone modifications. As PKCB is known to phosphorylate H3T6 leading to gene activation, we examined if the changes in gene expression seen in B cell activation were associated with H3T6 phosphorylation. We want to examine how PKCB mutation will affect H3T6 phosphorylation on a genome-wide level and so we performed ChIP-seq with H3T6 phosphorylation in wildtype and C57BL/6 Tilcara (Til) mouse, a PKCβ mutant mice model.

ORGANISM(S): Mus musculus

PROVIDER: GSE137466 | GEO | 2022/09/14

REPOSITORIES: GEO

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Expression data of B lymphocytes isolated from C57BL/6 Tilcara (Til) mouse mutant compared with wild-type C57BL/6 mouse [microarray]

Project description:Recent studies show that PKCs can have a nuclear function as epigenetic enzymes to directly regulate gene expression in the immune system. Using a PKCβ mutant mice model, C57BL/6 Tilcara (Til) mouse mutant, we examined the role of PKCβ as a histone kinase in regulating inducible gene expression in immune cells. We investigated if PKCβ is important for the expression of key inducible genes upon B cell activation.

2022-09-14 | GSE137465 | GEO

Genome-wide mapping of histone H3 T6 phosphorylation in mouse B lymphocytes [ChIP-seq]

Project description:Genome-wide mapping of histone H3 T6 phosphorylation in mouse B lymphocytes [ChIP-seq]

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L-plastin Ser5 phosphorylation via RSKs, downstream effectors of the MAPK/ERK pathway, in (breast) cancer cells (and in vitro)

Project description:Deregulated cell migration and invasion, which are hallmarks of metastatic cancer cells, are correlated to structural and functional alterations of the actin cytoskeleton associated to a large panel of actin-binding proteins. Among these, the actin-bundling protein L-plastin, initially detected in leukocytes, is ectopically expressed in several solid tumours and is often considered as a metastatic marker. Phosphorylation of L-plastin on residue serine 5 (Ser5) has been shown to activate L-plastin and to be crucial for invasion and metastasis formation. Here, we investigate the signalling pathway leading to L-plastin Ser5 phosphorylation in four breast cancer cell lines. Whole genome microarray analysis comparing cell lines with different invasive capacities and corresponding L-plastin Ser5 phosphorylation levels revealed that genes of the MAPK/ERK pathway are differentially expressed. In line, in vitro kinase assays showed that MAPK/ERK pathway downstream kinases RSK1 and RSK2 are able to directly phosphorylate L-plastin on Ser5. In parallel to a knockdown approach, activation and inhibition studies of signalling molecules of the MAPK/ERK pathway, followed by computational modelling analysis, confirmed that RSK is an important activator of L-plastin in all four studied cell lines. Finally and rounding up our study, RSK knockdown significantly impaired migratory and invasive capacities of a selected invasive cell line, thus consolidating RSK as a promising therapeutic target in certain invasive carcinomas. Altogether, our data provide substantial evidence that the MAPK/ERK pathway is involved in L-plastin Ser5 phosphorylation in breast cancer cells with its downstream kinases RSK1 and RSK2 being able to directly phosphorylate L-plastin on Ser5.

2016-03-26 | E-MTAB-3487 | biostudies-arrayexpress

Effect of T350 phosphorylation on gene repression activity of EZH2 in BJ cells

Project description:The Polycomb group (PcG) protein enhancer of zeste homolog 2 (EZH2) plays an essential role in histone methylation-mediated epigenetic gene silencing. We demonstrate that under physiological conditions, cyclin-dependent kinase 1 (CDK1) and 2 (CDK2) bind to and phosphorylate EZH2 at threonine 350 (T350) in an evolutionally conserved motif. T350 phosphorylation is required for EZH2 function in silencing of genes that promote differentiation and inhibit proliferation and migration. Blockage of T350 phosphorylation by generating a T350A mutation largely diminishes the global effect of EZH2 on gene silencing. Four experiments have been designed. BJ cells were transfected with si-Control, si-EZH2, si-EZH2 plus RNAi resistant lentivirus expressed EZH2, or si-EZH2 plus RNAi resistant lentivirus expressed T350A mutant for 60 hours. Each experiment was triplicated.

2010-11-10 | E-GEOD-22427 | biostudies-arrayexpress

CD4 Polarized T cells Reduce the Expansion of Tumor Infiltrating Lymphocytes in Melanoma Patients Treated with Adoptive Cell Therapy [ChIP-seq]

Project description:Background: Adoptive cell therapy (ACT) with tumor infiltrating lymphocytes (TIL) is effective in treating PD-1 refractory melanoma, but requires adequate ex vivo expansion of TIL. Methods: CD4+ and CD8+ TIL from metastatic melanoma patients treated with TIL ACT were analyzed by RNA-seq (n=12) and ChIP-seq of acetylated histone 3 (n=19). Patients were grouped into “TIL high” and “TIL low” based on division at the median number of TIL infused. The number of TIL infused and CD4+ TIL frequency were correlated with overall survival (OS). Results: The number of TIL infused correlated with longer OS (R2=0.57, p=0.00076), and the percent of CD4+ infused was negatively correlated with the total number of TIL infused (R2=0.64, p=0.00047). RNA-seq analysis of CD4+ TIL showed increases in Th2/Th17/Treg transcripts and pathways in the TIL low group. ChIP-seq analysis of CD8+ TIL showed decreased acetylation in the TIL low group in genes upregulated during CD8+ activation. Conclusion: The numbers of TIL infused were associated with increased overall survival, while RNA-seq suggested that polarized CD4+ cells in the transferred TIL were associated with decreased overall expansion. These data suggest that improper CD4+ TIL polarization may reduce expansion and treatment efficacy.

2023-07-17 | GSE218005 | GEO

CD4 Polarized T cells Reduce the Expansion of Tumor Infiltrating Lymphocytes in Melanoma Patients Treated with Adoptive Cell Therapy [RNA-seq]

2023-07-17 | GSE218004 | GEO

ChipSeq of mouse embryonic fibroblasts from conditional knock-in mouse carrying a phosphorylation-deficient S180A (SA) mutation in exon 5 of the endogenous mouse Trp53 gene locus

Project description:The mouse S180A (SA) mutation of the Trp53 is a p53 phosphorylation-deficient mutant protein with native conformation. Here we want to assess the impact of DNA binding site phosphorylation of the p53 target gene spectrum and transcriptional activity under untreated conditions and following p53 stabilization with the Mdm2 inhibitor nutlin-3a.

2020-06-04 | E-MTAB-9170 | biostudies-arrayexpress

RNAseq of mouse embryonic fibroblasts from conditional knock-in mice carrying a phosphorylation-deficient S180A (SA) mutation in exon 5 of the endogenous mouse Trp53 gene locus

2020-08-25 | E-MTAB-9171 | biostudies-arrayexpress

RNA Profiling in Patients' tumor infiltrating lymphocytes

Project description:Identifying tumor antigen-specific T cells from cancer patients has been a goal of tumor immunologists for several decades. Co-expression of CD103 and CD39 on CD8 TIL highly enriches for tumor-reactive T cells. CD39+CD103+ CD8 TIL have a distinct TCR repertoire compared to other CD8 TIL subsets and are clonally expanded within the tumor. They are highly enriched for tumor antigen recognition and efficiently killed autologous tumor cells. Patients with head and neck cancer whose CD8 TIL contained a higher frequency of CD39+CD103+ cells experienced a greater overall survival. This work describes a simple and effective method for detecting tumor-reactive CD8 TIL.

2018-05-26 | GSE114944 | GEO

Histone H3 Ser10 phosphorylation in hpr1-101

Project description:R-loops are transcription by-products that may constitute a threat to genome integrity.We previously show in Saccharomyces cerevisiae that R-loops are tightly and specifically linked with histone H3-Ser10 phosphorylation (H3S10P), a mark of chromatin condensation. Here we analyse the hpr1-101 mutant. A point mutation that impairs transcription and mRNP biogenesis without increasing recombination. Importantly, ChIP-chip analyses reveal a clear H3S10P does not accumulate at the pericentromeric chromatin during the G1-phase of the cell cycle but during S-phase in non-accumulating R-loop hpr1-101. ChIP-chip studies were perfomed with antibodies against Histone H3 and the phosphorylated Histone H3 at Serine10 in the yeast S. cerevisiae.

2017-05-01 | E-GEOD-50110 | biostudies-arrayexpress

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