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Status |
Public on Feb 09, 2021 |
Title |
Tumor methionine metabolites reprograms chromatin accessibilities of CD8+ T cells linking to T cell dysfunction. |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
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Summary |
T-cell exhaustion denotes a hypofunctional state of T lymphocytes commonly found in cancer, but how tumor cells drive T-cell exhaustion remains elusive. We found oncogenic reprograming of HCC methionine recycling with elevated 5-methylthioadenosine (MTA) and S-adenosylmethionine (SAM) to be tightly linked to T-cell exhaustion. We used an assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq) to assay the genome-wide chromatin accessibility of T cells during activation and SAM/MTA treatment.
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Overall design |
ATAC-sequencing was performed on non-activated CD8+ T cell and activated CD8+ T cells with and without SAM or MTA treatment.
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Contributor(s) |
Wang XW |
Citation(s) |
33674593 |
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Submission date |
Feb 04, 2021 |
Last update date |
Apr 06, 2021 |
Contact name |
Xin Wei Wang |
E-mail(s) |
[email protected]
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Phone |
2407606858
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Organization name |
National Institutes of Health
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Department |
Center for Cancer Research
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Lab |
Laboratory of Human Carcinogenesis
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Street address |
37 Convent Drive, Bldg 37 Rm 3050
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City |
Bethesda |
State/province |
Maryland |
ZIP/Postal code |
20892 |
Country |
USA |
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Platforms (1) |
GPL20301 |
Illumina HiSeq 4000 (Homo sapiens) |
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Samples (12)
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Relations |
BioProject |
PRJNA699597 |
SRA |
SRP304779 |