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Ea1b5928-f11a-4df1-9290-6aba4b1cf95e - samples

ABSTRACT: ChIP-Seq targeting the cohesin subunit STAG2 in STAG2-mutant or cohesin wildtype adult AMLs.

PROVIDER: EGAD00001011205 | EGA |

REPOSITORIES: EGA

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04e9a0ab-7f31-4dc8-bfa8-9ee1f7d94bcf - samples

Project description:ChIPseq targeting the cohesin subunit STAG1 in STAG2-mutated AMLs or cohesin wildtype AMLs

| EGAD00001011206 | EGA

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Project description:ChIP-Seq targeting CTCF in cohesin-mutated (STAG2 or RAD21 mutations) and wildtype adult AMLs (CTRL-AMLs).

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Project description:ChIP-seq targeting the H3K27ac histone modification in cohesin-mutated (STAG2 or RAD21 mutation) and cohesin wildtype (CTRL-AMLs) AMLs.

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Project description:ChIP-Seq targeting the major cohesin core subunit RAD21 to represent cohesin occupancy and binding sites in cohesin-mutated (STA2 or RAD21 mutations) and wildtpye adult AMLs.

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Project description:ATAC-seq (Illumina TDE1 Transposase) to profile accessible chromatin regions of cohesin-mutated (STAG2 or RAD21 mutations) and -wildtype adult AMLs.

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Project description:High-throughput chromosome conformation capture (Hi-C) data generated for cohesin-mutated (STAG2 or RAD21) and cohesin-wildtype AMLs.

| EGAD00001011198 | EGA

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Project description:Low-pass whole-genome DNA sequencing of cohesin-mutated (STAG2 or RAD21 mutations) and wildtype (CTRL-AML) adult AMLs generated generated from ultrasound-fragmented genomic DNA. Samples were only sequenced shallow (20-40 Mio reads) Used for digital karyotyping and ChIP-seq background/copy-nuber normalization/correction.

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STAG2 Mutations Reshape the Cohesin-Structured Spatial Chromatin Architecture to Drive Gene Regulation in Acute myeloid Leukemia [bulk RNA-Seq]

Project description:Cohesin shapes the chromatin architecture, including enhancer-promoter interactions. Its components, especially STAG2 but not its paralogue STAG1, are frequently mutated in myeloid malignancies. To elucidate the underlying mechanisms of leukemogenesis, we comprehensively characterized genetic, epigenetic, transcriptional, and chromatin conformational changes in acute myeloid leukemia (AML) patient samples. Specific loci displayed altered cohesin occupancy, gene expression and local chromatin activation which were not compensated by STAG1. These changes could be linked to disrupted spatial chromatin looping in cohesin-mutated AMLs. We performed complementary depletion of STAG2 or STAG1 in primary human hematopoietic progenitors (HSPCs). We detected effects overlapping STAG2-mutant AML-specific changes following STAG2 knockdown, not invoked by depletion of STAG1. STAG2-deficient HSPCs displayed impaired differentiation capacity and maintained HSPC-like gene expression. This work establishes STAG2 as a key regulator of chromatin contacts, gene expression and differentiation in the hematopoietic system and identifies candidate target genes that may be implicated in human leukemogenesis.

2024-06-18 | GSE267679 | GEO

STAG2 Mutations Reshape the Cohesin-Structured Spatial Chromatin Architecture to Drive Gene Regulation in Acute myeloid Leukemia [ATAC-Seq]

2024-06-18 | GSE267678 | GEO

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