Mitochondrial Fission 1 (FIS1) knockdown effect on the H3K27Ac status of leukemia cell line MOLM-13 cells
Ontology highlight
ABSTRACT: To examine if loss of FIS1 would alter the H3K27Ac status of leukemic cells, we used shRNA to knock down the expression of FIS1 in leukemic cell line MOLM-13 cells and performed H3K27Ac CHIP-seq to characterize any changes in the H3K27Ac marks upon loss of FIS1.
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.
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 primary human AML cells and performed RNA-seq experiments to profile global gene expression changes upon FIS1 depletion.
Project description:The growth arrest and DNA-damage induced 45 gamma (GADD45g) is rapidly induced by various physiological and environmental stresses associated with growth arrest. GADD45g has been observed implicated in cell survival, apoptosis, senescence, cell cycle regulation and DNA repair in a variety of human solid tumor types, acting as either tumor promoter or tumor suppressor. To date, the role of GADD45g in hematopoietic malignancies remains completely unknown. Here, we transduced Molm-13 cells with lentiviral vectors expressing doxycycline-inducible GADD45g. Molm-13 cells with dox administration or not were collected for RNA-seq.
Project description:MOLM-13 acute myeloid leukemia cells were treated with 3 µM FIDAS-5 methionine S-adenosyltransferase 2A (MAT2A) inhibitor or 0.1% DMSO as control for 48 hours