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Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [CITE-seq]

ABSTRACT: Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [CITE-seq]

PROVIDER: PRJNA1268494 | ENA |

REPOSITORIES: ENA

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Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [CITE-seq]

Project description:Owing to their immunoprotective properties, natural killer (NK) cells are critical for the innate response to pathogens, as well as a new wave of cancer immunotherapy that harnesses natural cytotoxicity. We sought to understand the genetic and epigenetic drivers behind human specific NK cell receptors, so that we can better understand the underlying cellular function. Here, we present a transcriptomic, proteomic (CITE-seq), and chromatin (single nuclei ATAC-seq and Hi-C) analysis of human peripheral NK cell subsets, uncovering key regulatory programs governing NK cell differentiation. Through integrative multi-omics, we demonstrate that CD56bright versus CD56dim NK cell subsets have differential distal regulatory element (DRE) landscapes, with fewer accessible DREs in the CD56dim NK cells. We combine epigenetic, chromatin looping, and human genetic data to show mechanisms governing the NCAM1 (encoding CD56) and KIR loci. For example, we identify NCAM1 DREs that bind STAT in most NK cells, while identifying a genetic cohort that has motifs for binding repressive BLIMP1 at the DRE and resulting in less CD56 expression. Together, our findings reveal novel epigenetic and transcriptomic systems for regulation of NK cells cytotoxicity and diversity, deepening our understanding of their function and how transcription factor networks govern CD56bright versus CD56dim phenotypes.

2025-05-27 | GSE298188 | GEO

Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [scATAC-seq]

2025-05-24 | GSE297712 | GEO

Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements

Project description:Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements

| PRJNA1268504 | ENA

Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [scATAC-seq]

Project description:Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements [scATAC-seq]

| PRJNA1265757 | ENA

Neural cell adhesion molecule 1 (NCAM1; CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

Project description:Neural cell adhesion molecule 1 (NCAM1; also known as CD56) is expressed in up to 20% of acute myeloid leukemia (AML) patients. Expression of NCAM1 is widely used as a marker of minimal residual disease; however, the biological function of this cell surface protein in AML remains elusive. In this study we investigated the impact of aberrant NCAM1 expression on leukemogenesis, drug resistance and its role as a biomarker to guide therapy.Gene expression profiling was performed with RNA-seq in three cell lines (SKM-1, NOMO-1, MOLM-14) after doxycycline-mediated induction of scrambled shRNA or shNCAM1 at timepoint 72 hours.

2019-02-22 | GSE123071 | GEO

Isoform-specific regulation of NCAM1 gene expression in ischemic cardiomyopathy

Project description:Although ischemic cardiomyopathy (ICM) is the leading cause of chronic heart failure, one of the most common diseases overall, many aspects of the molecular pathogenesis of ICM still remain to be clarified. It has been We have previously shown that the neural cell adhesion molecule (NCAM1, CD56) is upregulated in ischemic cardiomyopathy by novel isoforms of the transcription factor RUNX1 (AML1) and, in the current study, we show that this upregulation is attributed exclusively to the NCAM1 isoform CD56-140kD. Moreover, we show that the upregulation of CD56-140kD has proapoptotic and antiproliferative effects on cardiomyocytes in vitro as well as inducing mitochondrial damage and reducing the capacity for Ca2+-uptake. As loss of cells and negative inotropy have previously been identified as major components in the development of ischemic cardiomyopathy, these data suggest that the upregulation of CD56-140kD may play a relevant role in the pathogenesis of ICM and therapeutic strategies targeting this molecule may prove to be valuable tools in the management of this very common and often fatal disease in the future.

2014-12-01 | GSE34124 | GEO

Identification of human exTregs as CD16+CD56+ cytotoxic CD4+ T cells.

Project description:In chronic inflammatory diseases with an autoimmune component like atherosclerosis, some regulatory T cells (Tregs) lose their regulatory function and become exTregs. The present study was designed to identify surface markers specific of human exTregs, using an integrated approach from sorted mouse exTregs bulk RNA-Seq to human scRNA-Seq with CITE-Seq, to sort human exTregs and characterize them by transcriptome and function. We crossed inducible Treg lineage tracker mice (FoxP3-eGFP-Cre-ERT2 ROSA26CAG-fl-stop-fl-tdTomato) to atherosclerosis-prone Apoe -/- mice, sorted Tregs and exTregs from lymph nodes and spleens of replicate mice and determined their transcriptomes by bulk RNA sequencing (RNA-Seq). A support vector machine (SVM) approach identified the leading signature genes for exTregs as CST7, NKG7, GZMA, PRF1, TBX21 and CCL4. Projecting these genes onto feature maps of human PBMC single cell (sc)RNA-Seq with CITE-Seq from 61 subjects with and without atherosclerosis showed that CST7, NKG7, GZMA, PRF1, TBX21 and CCL4 mapped to CD4 T cells that expressed CD56 and CD16. This finding was validated in a second, independent scRNA- and CITE-Seq dataset. Even in healthy volunteers, a subpopulation of CD4 T cells expressed both CD56 and CD16. Bulk RNA-Seq identified these cells as cytotoxic CD4 T cells, which was functionally confirmed in a cell killing assay. DNA sequencing for TCRβ showed clonal expansion of Treg CDR3 sequences in CD16 + CD56 + exTregs. Taken together, we identify mouse and human exTregs as cytotoxic CD4 T cells.

2023-07-25 | GSE217010 | GEO

Neural cell adhesion molecule 1 (NCAM1 CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

Project description:Neural cell adhesion molecule 1 (NCAM1 CD56) promotes leukemogenesis and confers drug resistance in acute myeloid leukemia.

| PRJNA507440 | ENA

Gene regulatory programs of NK cells show that NCAM1 (CD56) and KIRs are controlled by genetically polymorphic distal regulatory elements

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-05-28 | GSE298200 | GEO

Gene expression analysis for CD56- T, NK, CD56+ T cells, and iNKT cells

Project description:A small subset of T cells also expresses kiler-cell immunoglobulin-like receptors (KIRs). We find that KIR+ T cells primarily reside in the CD56+ T population. However, little is known on how these cells are different from the conventional CD56- T, NK, and iNKT cells. We used microarray profiling to compare and determine the distinctive differences of CD56+ T cell and its KIR subsets when compared to the conventional CD56- T, NK and iNKT cells. Lymphocyte subsets were sorted from human peripheral blood mononuclear cells with FACSAriaII (BD Biosciences, San Jose, CA) using anti-CD3, anti-CD56, anti-CD14, anti-KIR2DL1, anti-KIR2DL2/3, anti-KIR3DL1 and anti-TCRValpha24 antibodies. The purity of CD3+CD56- T cells, CD3-CD56+ NK cells, CD3+CD56+ T cells, KIR-CD3+CD56+ T cells, and KIR+CD3+CD56+ T cells were more than 98% in all experiments. The purities of iNKT cells for TCRValpha24 and CD1d-tetramer were >95% and >90%, respectively. RNA pre-amplification, labeling and hybridization on Human Genome U133Plus 2.0 GeneChip array were performed in the St. Jude Hartwell Center for Bioinformatics & Biotechnology microarray core facility according to the manufacturer’s instructions (Affymetrix, Santa Clara, CA).

2013-07-01 | E-GEOD-47855 | biostudies-arrayexpress

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