<HashMap><database>biostudies-arrayexpress</database><scores/><additional><omics_type>Unknown</omics_type><omics_type>Transcriptomics</omics_type><omics_type>Genomics</omics_type><omics_type>Proteomics</omics_type><submitter>SOURA CHAKRABORTY</submitter><instrument_platform>Chromatin IP kit</instrument_platform><instrument_platform>Performed by Novogene; Illumina library preparation instrumentation (provider standard)</instrument_platform><instrument_platform>Immunomagnetic separation system (e.g., Miltenyi MACS separator),  Tissue culture facilities (biosafety cabinet, CO₂ incubator) , Bench centrifuge</instrument_platform><instrument_platform>Illumina NovaSeq 6000</instrument_platform><study_type>ChIP-seq</study_type><organism>Homo sapiens</organism><species>Homo sapiens</species><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/E-MTAB-16594</full_dataset_link><description>To map genome-wide chromatin occupancy of the human glucocorticoid receptor (GR; encoded by NR3C1) in primary activated human CD8⁺ T cells, ChIP–seq was performed following physiological cortisol stimulation. CD8⁺ T cells were isolated from healthy adult donors by immunomagnetic negative selection, activated in vitro with plate-bound anti-CD3 and anti-CD28, expanded in IL-2, and then re-stimulated with anti-CD3/anti-CD28 in the presence of hydrocortisone (cortisol; 100 nM) for 48 hours or vehicle control. GR-bound chromatin was immunoprecipitated and profiled by high-throughput sequencing to identify cortisol-induced GR binding sites and infer direct GR target loci in human CD8⁺ T cells.</description><repository>biostudies-arrayexpress</repository><sample_protocol>Nucleic Acid Extraction - Chromatin immunoprecipitation (ChIP) was performed using the SimpleChIP Enzymatic Chromatin IP Kit (Cell Signaling Technology). Cells were crosslinked with 1% formaldehyde for 10 min at room temperature, quenched with 1× glycine for 5 min, and washed with ice-cold PBS. Nuclei were isolated and chromatin was digested with micrococcal nuclease (0.3 µL in 200 µL ChIP buffer) for 20 min at 37 °C, followed by sonication (Branson 450-D; 36% amplitude; four 5-s pulses; on ice). GR was immunoprecipitated overnight at 4 °C using two anti-GR antibodies (PA1-511A and D6H2L) and immune complexes were captured using ChIP-grade Protein G magnetic beads (2 h, 4 °C). After low- and high-salt washes, chromatin was eluted (1× elution buffer, 30 min, 65 °C), crosslinks were reversed (65 °C, 2 h) in the presence of NaCl and Proteinase K, and DNA was purified for downstream library preparation and sequencing.</sample_protocol><sample_protocol>Library Construction - Purified GR ChIP DNA and matched input DNA were submitted to Novogene (UK) for DNA sample QC and ChIP-seq library preparation using standard Illumina-compatible workflows (end repair/A-tailing, adapter ligation, PCR amplification, and size selection). Final libraries underwent provider QC before sequencing.</sample_protocol><sample_protocol>Sequencing - Sequencing was performed by Novogene (UK) on an Illumina platform using paired-end 150 bp (PE150) sequencing.</sample_protocol><sample_protocol>Sample Collection - Primary human CD8⁺ T cells were obtained from healthy adult donors (with appropriate consent/ethics). CD8⁺ T cells were purified by immunomagnetic negative selection, activated in vitro with plate-bound anti-CD3 and anti-CD28 antibodies, expanded in IL-2, and re-stimulated with anti-CD3/anti-CD28 in the presence of hydrocortisone (cortisol; 100 nM) or vehicle control for 48 h prior to chromatin immunoprecipitation.</sample_protocol><figure_sub>Organization</figure_sub><figure_sub>MINSEQE Score</figure_sub><figure_sub>Assays and Data</figure_sub><figure_sub>MAGE-TAB Files</figure_sub><pubmed_authors>SOURA CHAKRABORTY</pubmed_authors></additional><is_claimable>false</is_claimable><name>Genome wide glucocorticoid receptor (GR) binding sites upon cortisol treatment in human CD8 T cells</name><description>To map genome-wide chromatin occupancy of the human glucocorticoid receptor (GR; encoded by NR3C1) in primary activated human CD8⁺ T cells, ChIP–seq was performed following physiological cortisol stimulation. CD8⁺ T cells were isolated from healthy adult donors by immunomagnetic negative selection, activated in vitro with plate-bound anti-CD3 and anti-CD28, expanded in IL-2, and then re-stimulated with anti-CD3/anti-CD28 in the presence of hydrocortisone (cortisol; 100 nM) for 48 hours or vehicle control. GR-bound chromatin was immunoprecipitated and profiled by high-throughput sequencing to identify cortisol-induced GR binding sites and infer direct GR target loci in human CD8⁺ T cells.</description><dates><release>2026-02-10T00:00:00Z</release><modification>2026-02-10T02:01:58.261Z</modification><creation>2026-01-28T15:19:02.006Z</creation></dates><accession>E-MTAB-16594</accession><cross_references><ENA>ERP188266</ENA><EFO>EFO_0002944</EFO><EFO>EFO_0004170</EFO><EFO>EFO_0002692</EFO><EFO>EFO_0005518</EFO><EFO>EFO_0004184</EFO></cross_references></HashMap>