Project description:ChIP-seq analysis of ENL in MOLM-13 human leukemia cells transduced with lentivirus containing CRISPR-Cas9 EV or sgKAT6A for 5 days

2021-10-20 | GSE165076 | GEO

Epigenetic profiling of cells following KAT6A CRISPR targeting

Project description:Epigenetic profiling of cells following KAT6A CRISPR targeting

| PRJNA659930 | ENA

ChIP-seq analysis of ENL following KAT6A CRISPR targeting

Project description:ChIP-seq analysis of ENL following KAT6A CRISPR targeting

| PRJNA693198 | ENA

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domainThe histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domain

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrated that a winged helix domain at the N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A to unmethylated CpG islands (CGIs) genome wide. Mutation of the essential amino acids completely abrogates the enrichment of KAT6A at CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases

2023-01-14 | PXD034833 | Pride

Microarray transcription analysis of MDS/MPN leukocyte samples with and without EZH2 mutations (n = 12, each) and EZH2-downregulated F-36P, MOLM-13 and OCI-M2 cell lines, using 2 shRNAs targeting EZH2 and a non-targeting control shRNA, each

Project description:The aim of this study was to identify EZH2 targets in myeloid malignancies. RNA samples from control F-36P, MOLM-13 and OCI-M2 cells (secondary AML after MDS; EZH2 wild type) treated with random shRNA (n = 4, each) and test F-36P, MOLM-13 and OCI-M2 cells treated with either one of two EZH2-targeting shRNAs (n = 4, each) were screened for differential gene expression. RNA from EZH2 wild type (n = 12) and mutant (n = 12) MDS/MPN patients was also analyzed by microarray transcriptome analysis.

2017-06-15 | E-MTAB-5766 | biostudies-arrayexpress

Mitochondrial Fission 1 (FIS1) knockdown effect on the transcriptome of leukemia cell line MOLM-13 cells

Project description:To explore the function of Mitochondrial Fission 1 (FIS1) in acute myeloid leukemia (AML), we used shRNA to knock down the expression of FIS1 in leukemia cell line MOLM-13 cells and performed RNA-seq experiments to profile transcriptional changes upon FIS1 depletion.

2018-06-01 | GSE114111 | GEO

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