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

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

PROVIDER: PRJNA905432 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22408879_1.fastq.gz	Fastqsanger.gz
	SRR22408879_2.fastq.gz	Fastqsanger.gz
	SRR22408880_1.fastq.gz	Fastqsanger.gz
	SRR22408880_2.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

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

| PRJNA736680 | ENA

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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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

Bacterial Heterochromatin Formation Through Liquid-Liquid Phase Separation

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

| PRJNA730564 | ENA

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

HSD17B13 liquid-liquid phase separation activates autocrine platelet-activating factor signaling in NASH

Project description:HSD17B13 liquid-liquid phase separation activates autocrine platelet-activating factor signaling in NASH

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HSD17B13 liquid-liquid phase separation activates autocrine platelet-activating factor signaling in NASH

Project description:Loss-of-function variants in 17-beta hydroxysteroid dehydrogenase 13 (HSD17B13) are associated with decreased inflammation in human chronic liver disease. The underlying mechanism by which HSD17B13 promotes liver inflammation remains largely elusive. Here we find that HSD17B13 undergoes liquid-liquid phase separation (LLPS) around lipid droplets (LDs) in the liver of NASH patients. Dimerization of HSD17B13 drives LLPS formation and regulates its enzyme activity. HSD17B13 LLPS promotes leukocyte adhesion and fibrinogen expression in hepatocytes via activating autocrine platelet activating factor (PAF) signaling. Importantly, adeno-associated viral (AAV)-mediated xeno-expression of human HSD17B13 promotes liver inflammation in Hsd17b13-/- mice induced by high fat diet/carbon tetrachloride treatment. In conclusion, HSD17B13 LLPS triggers liver inflammation via promoting PAF-mediated leukocyte adhesion. Targeting HSD17B13 phase transition would be a promising approach to treat liver inflammation in chronic liver disease.

2024-12-19 | GSE238060 | GEO

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