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

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

PROVIDER: PRJNA512203 | ENA |

REPOSITORIES: ENA

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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+ 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.

2019-10-17 | GSE124495 | GEO

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: Not available

| S-EPMC6853375 | biostudies-literature

npm

Project description:Re-sequencing of npm mutants and siblings

| PRJEB32642 | ENA

Expression data from NPM-ALK T cell lymphoma in WT or WASP-deficient background

Project description:Total RNA was extracted from primary T cell lymphoma that spontaneously developed in either NPM-ALK or NPM-ALK/WASP-deficent transgenic mice

2018-11-08 | GSE102889 | GEO

Effect of oocyte-enriched histones Th2a, Th2b, and histone chaperone Npm on mouse iPS cell generation

Project description:Expression of key transcription factors Klf4, Oct3/4, Sox2, and c-Myc (KOSM) in embryonic stem cells can reprogram somatic cells into pluripotent cells. We found that two histone variants, TH2A and TH2B, and histone chaperone Npm enhance the KOSM-dependent generation of induced pluripotent cells (iPSCs) and produce iPSCs only with Klf4 and Oct3/4. To identify directly affected genes by these histone variants during reprogramming, we carried out gene expression profiling of MEFs overexpressing TH2A/TH2B/Npm and TH2A/TH2B deficient MEFs after infection with retroviruses expressing KOSM. A total of 21 Affymetrix Mouse Gene ST array were done for mRNA expression profiling of ES cells, iPS cells induced by Klf4, Oct4, Sox2, and c-Myc (KOSM) or Klf4, Oct4, Th2a, Th2b, and p-Npm (KOBAN), wild-type MEFs infected with retrovirus vectors expressing KOSM, KOSMBAN, or empty vector and Th2a/Th2b-deficient MEFs infected with retrovirus vector expressing KOSM.

2013-12-25 | E-GEOD-53637 | biostudies-arrayexpress

Gene expression profiling in acute myeloid leukemia with mutated NPM

Project description:Approximately one third of acute myeloid leukemias (AMLs) are characterized by aberrant cytoplasmic localization of Nucleophosmin (NPMc+ AML), consequent to mutations in the NPM putative nucleolar localization signal. These events are mutually exclusive with the major AML-associated chromosomal rearrangements, and are frequently associated with normal karyotype, Fms-like tyrosine kinase (FLT3) mutations and multilineage involvement. We report the gene expression profiles of 78 de novo AMLs (72 with normal karyotype; 6 with non-major chromosomal abnormalities) that were characterized for the subcellular localization and mutation status of NPM. Unsupervised clustering clearly separated NPMc+ from NPMc- AMLs, regardless of the presence of FLT3 mutations or non-major chromosomal rearrangements, supporting the concept that NPMc+ AML represents a distinct entity. The molecular signature of NPMc+ AML includes up-regulation of several genes putatively involved in the maintenance of a stem cell phenotype, suggesting that NPMc+ AML may derive from a multipotent hematopoietic progenitor. 78 de novo AMLs, negative for AML-associated chromosomal translocations at the cytogenetic and/or molecular level.

2012-01-05 | E-GEOD-34860 | biostudies-arrayexpress

The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

Project description:The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

| PRJNA496616 | ENA

The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

Project description:The scaffolding role of RNA in ribonucleoprotein complexes: TRA2A recruitment in FXTAS disease

| PRJNA422212 | ENA

Effect of oocyte-enriched histones Th2a, Th2b, and histone chaperone Npm on mouse iPS cell generation

2013-12-25 | GSE53637 | GEO