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Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ATAC-Seq)

ABSTRACT: Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during drug resistance, but the underlying mechanisms are not fully understood. Here we demonstrate that HP1g coordinates histone H3 lysine 9 trimethylation (H3K9me3) to regulate chromatin dynamic and gene transcription during bortezomib resistance.Mechanistically, HP1g can interact with H3K9me3, its CD domain is responsible to read H3K9me3 to serve its function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE176545 | GEO | 2021/06/11

REPOSITORIES: GEO

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Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ChIP-seq)

Project description:Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during drug resistance, but the underlying mechanisms are not fully understood. Here we demonstrate that HP1g coordinates histone H3 lysine 9 trimethylation (H3K9me3) to regulate chromatin dynamic and gene transcription during bortezomib resistance.Mechanistically, HP1g can interact with H3K9me3, its CD domain is responsible to read H3K9me3 to serve its function.

2022-12-01 | GSE218772 | GEO

Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (RNA-Seq)

Project description:Functional crosstalk between histone modifications and chromatin remodeling has emerged as a key regulatory mode of transcriptional control during drug resistance, but the underlying mechanisms are not fully understood. Here we demonstrate that HP1g regulates chromatin dynamic and gene transcription during drug resistance in multiple myeloma. To study the cellular and molecular function of HP1g during bortezomib resistance, we used RNA sequencing (RNA-seq) to generate gene expression profiling under HP1g steady overexpression in LP-1. We identified multiple genes whose expression is significantly affected by HP1g levels.

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Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation

Project description:Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation

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Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-11 | GSE176547 | GEO

Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (RNA-Seq)

Project description:Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (RNA-Seq)

| PRJNA736685 | ENA

Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ChIP-seq)

Project description:Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ChIP-seq)

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Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ATAC-Seq)

Project description:Deacetylation of HP1g enhances multiple myeloma drug resistance through DNA damage repair and liquid-liquid phase separation (ATAC-Seq)

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Gene expression signatures in Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors

2014-08-01 | GSE48897 | GEO

Gene expression signatures in Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors

Project description:Gene expression analyses of Tif1b, Hp1a or Hp1g knockdown hematopoietic progenitors. Growth of hematopoietic stem cells (HSCs) are significantly impaired upon knockdown of Hp1a and Hp1g. Results provide insight into the role of these factors in hematopoiesis. HSCs (CD34- c-Kit+ Sca1+ Lineage- ) were transduced with lentivirus expressing shRNA against Tif1b, Hp1a or Hp1g, and cultured for 14 days. Then, GFP+ c-Kit+ Lineage- hematopoietic progenitors were sorted and subjected into microarray analysis

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Genome-wide mapping of Cbx3/HP1g deposition in wild-type CD8+ effector T cells

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