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

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

PROVIDER: PRJNA736680 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14778971_1.fastq.gz	Fastqsanger.gz
	SRR14778971_2.fastq.gz	Fastqsanger.gz
	SRR14778972_1.fastq.gz	Fastqsanger.gz
	SRR14778972_2.fastq.gz	Fastqsanger.gz
	SRR14778973_1.fastq.gz	Fastqsanger.gz

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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)

| PRJNA736684 | ENA

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 (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.

2021-06-11 | GSE176546 | GEO

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

2021-06-11 | GSE176545 | GEO

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

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

2021-06-11 | GSE176547 | GEO

Bacterial Heterochromatin Formation Through Liquid-Liquid Phase Separation

Project description:Bacterial Heterochromatin Formation Through Liquid-Liquid Phase Separation

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Homodimer-mediated phosphorylation of C/EBPα-p42 S16 modulates acute myeloid leukaemia differentiation through liquid-liquid phase separation [ChIP-seq]

Project description:CCAAT/enhancer binding protein α (C/EBPα) regulates myeloid differentiation, and its dysregulation contributes to acute myeloid leukaemia (AML) progress. Clarifying its functional implementation mechanism is of great significance for its further clinical application. Here, we show that C/EBPα regulates AML cell differentiation through liquid-liquid phase separation (LLPS), which can be disrupted by C/EBPα-p30. Considering that C/EBPα-p30 inhibits the functions of C/EBPα through the LZ region, a small peptide TAT-LZ that could instantaneously interfere with the homodimerization of C/EBPα-p42 was constructed, and dynamic inhibition of C/EBPα phase separation was observed, demonstrating the importance of C/EBPα-p42 homodimers for its LLPS. Mechanistically, homodimerization of C/EBPα-p42 mediated its phosphorylation at the novel phosphorylation site S16, which promoted LLPS and subsequent AML cell differentiation. Finally, decreasing the endogenous C/EBPα-p30/C/EBPα-p42 ratio rescued the phase separation of C/EBPα in AML cells, which provided a new insight for the treatment of the AML.

2023-11-08 | GSE243423 | GEO

Homodimer-mediated phosphorylation of C/EBPα-p42 S16 modulates acute myeloid leukaemia differentiation through liquid-liquid phase separation [RNA-seq]

2023-11-08 | GSE243422 | GEO

Study on the effect and mechanism of c-Maf liquid-liquid separation in promoting MM cellular proliferation and drug resistance through Mtbp/c-Myc axis

Project description:Previous experiments have demonstrated that c-Maf can undergo liquid-liquid phase separation (LLPS) in MM. In order to search for the downstream target genes of c-Maf based on its LLPS regulation, we successfully constructed three kinds of cells with EV, c-Maf and already c-Maf-IDR mutation, and simultaneously subjected the three kinds of cells to ChIP sequencing (selecting the FLAG-tagged antibody), and then analysed them for the differential genes, thus screening the downstream targets of c-Maf based on its LLPS regulation.

2024-08-31 | GSE264392 | GEO

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