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The role of MLF1 on accessible chromatin in AC16 cell line

ABSTRACT: Previous studies found that MLF1 mRNA levels tended to decline in aging hearts. Functional studies found that knockdown of MLF1 ameliorated the drug-induced cellular senescence phenotype. Here, we apply transcriptomics to explore the underlying molecular mechanisms.

ORGANISM(S): Homo sapiens

PROVIDER: GSE207907 | GEO | 2025/01/29

REPOSITORIES: GEO

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Molecular mechanism of MLF1 in AC16 cell line

Project description:Previous studies found that MLF1 mRNA levels tended to decline in aging hearts. Functional studies found that knockdown of MLF1 ameliorated the drug-induced cellular senescence phenotype. Here, we apply transcriptomics to explore the underlying molecular mechanisms.

2025-01-29 | GSE206754 | GEO

Downregulation of MLF1 safeguards cardiomyocytes against senescence-associated chromatin opening

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Molecular mechanism of EP300 in AC16 cell line

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The role of MLF1 on accessible chromatin in AC16 cell line

Project description:The role of MLF1 on accessible chromatin in AC16 cell line

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Molecular mechanism of MLF1 in AC16 cell line

Project description:Molecular mechanism of MLF1 in AC16 cell line

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NPM and NPM-MLF1 interact with chromatin remodeling complexes and influence their recruitment to specific genes

Project description:Nucleophosmin (NPM1) is either frequently mutated or subjected to chromosomal translocation in acute myeloid leukemia (AML). NPM protein is primarily located in the nucleus, but the recurrent NPMc+ mutation is characterized by cytoplasmic localization and leukemogenic properties. Similarly, the NPM-MLF1 translocation product favors the partial cytoplasmic retention of NPM. Regardless of their common cellular distribution, NPM-MLF1 malignancies engender different effects on hematopoiesis compared to NPMc+ counterparts, highlighting possible aberrant nuclear function(s) of NPM in NPMc+ and NPM-MLF1 AML. We performed a proteomics analysis and found that NPM and NPM-MLF1 interact with chromatin remodeling complexes of the ISWI family, as well as with NuRD and P/BAF complexes. Accordingly, NPM and NPM-MLF1 are recruited to transcriptionally active or repressed genes along with NuRD and P/BAF elements. Although the overall gene expression program in NPM knockdown cells is similar to that resulting from NPMc+ and is consistent with loss of nuclear function of NPM, NPM-MLF1 expression differentially altered gene transcription regulated by NPM. The abnormal gene regulation imposed by NPM-MLF1 is characterized by enhanced recruitment of NuRD to gene regulatory regions. Thus, different mechanisms orchestrate the deregulation of NPM function in NPMc+ -versus NPM1-MLF1- associated leukemia.

2019-10-18 | PXD012305 | Pride

NPM and NPM-MLF1 interact with chromatin remodeling complexes and influence their recruitment to specific genes

Project description:Nucleophosmin (NPM1) is either frequently mutated or subjected to chromosomal translocation in acute myeloid leukemia (AML). NPM protein is primarily located in the nucleus, but the recurrent NPMc+ mutation is characterized by cytoplasmic localization and leukemogenic properties. Similarly, the NPM-MLF1 translocation product favors the partial cytoplasmic retention of NPM. Regardless of their common cellular distribution, NPM-MLF1 malignancies engender different effects on hematopoiesis compared to NPMc+ counterparts, highlighting possible aberrant nuclear function(s) of NPM in NPMc+ AML. We performed a proteomics analysis and found that NPM and NPM-MLF1 interact with chromatin remodeling complexes of the ISWI family, as well as with NuRD and P/BAF complexes. Accordingly, NPM and NPM-MLF1 are recruited to transcriptionally active or repressed genes along with NuRD and P/BAF elements. Although the overall gene expression program in NPM knockdown cells is similar to that resulting from NPMc+ and is consistent with loss of nuclear function of NPM, NPM-MLF1 expression differentially altered gene transcription regulated by NPM. The abnormal gene regulation imposed by NPM-MLF1 is characterized by enhanced recruitment of NuRD to gene regulatory regions. Thus, different mechanisms orchestrate the deregulation of NPM function in NPMc+- versus NPM1-MLF1-associated leukemia.

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NPM1-fusion proteins promote myeloid leukemogenesis through XPO1-dependent HOX activation [Cut & Run]

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NPM1-fusion proteins promote myeloid leukemogenesis through XPO1-dependent HOX activation

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RNA sequencing of AC16 and AC16-CAR cells

Project description:The goal of this study was to determine the differences in gene expression due to ectopic CAR overexpression.

2020-12-21 | GSE155312 | GEO