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ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

ABSTRACT: ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

PROVIDER: PRJNA1036664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26705605_1.fastq.gz	Fastqsanger.gz
	SRR26705605_2.fastq.gz	Fastqsanger.gz
	SRR26705606_1.fastq.gz	Fastqsanger.gz
	SRR26705606_2.fastq.gz	Fastqsanger.gz
	SRR26705607_1.fastq.gz	Fastqsanger.gz

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ANP32B promotes colorectal cancer cell progression and reduces cell sensitivity to PRAP1 inhibitor through up-regulating HPF1

Project description:The aim of this work is to explore the role of ANP32B on CRC development

2023-11-24 | GSE247230 | GEO

ANP32B-mediated repression of p53 contributes to maintenance of normal and CML stem cells

Project description:we demonstrate that conditional deletion of acidic leucine-rich nuclear phosphoprotein 32B (ANP32B) in hematopoietic cells impairs repopulation capacity and postinjury regeneration of HSCs. Mechanistically, ANP32B forms a repressive complex with and thus inhibits the transcriptional activity of p53 in hematopoietic cells, and p53 deletion rescues the functional defect in Anp32b-deficient HSCs. Of great interest, ANP32B is highly expressed in leukemic cells from patients with chronic myelogenous leukemia (CML). Anp32b deletion enhances p53 transcriptional activity to impair LSC function in a murine CML model and exhibits synergistic therapeutic effects with tyrosine kinase inhibitors in inhibiting CML propagation. In summary, our findings provide a novel strategy to enhance p53 activity in LSCs by inhibiting ANP32B and identify ANP32B as a potential therapeutic target in treating CML.

2021-09-27 | GSE184474 | GEO

RNA-seq for MV4-11 cell line in either the absence or presence of ANP32B

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for MV4-11 cell line in either the absence or presence of ANP32B

2023-09-12 | GSE242849 | GEO

RNA-seq for Kasumi-1 cell line in either the absence or presence of ANP32B

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare RNA-seq results for Kasumi-1 cell line in either the absence or presence of ANP32B

2023-09-12 | GSE242848 | GEO

The histone chaperone ANP32B regulates chromatin incorporation of the atypical human histone variant macroH2A

Project description:Eukaryotic chromatin structure is highly conserved, with the canonical histone proteins revealing only small sequence changes across species. Yet, all vertebrates exhibit three much larger histone H2A variants, macroH2A. A distinctive feature of these atypical histones is the globular macrodomain module, which can bind metabolites and is connected to the histone fold through a flexible linker. MacroH2A variants impact heterochromatin organization, transcription regulation and establish a barrier for cellular reprogramming. However, the mechanisms of how these large H2A variants are incorporated into chromatin and the identity of any chaperones required for histone deposition have remained elusive. Here, we developed a split-GFP-based cellular readout for histone incorporation and conducted a genome-wide mutagenesis screen in haploid human cells to identify proteins that regulate macroH2A dynamics. We identified and validated the histone chaperone ANP32B as a regulator of macroH2A chromatin deposition. ANP32B associates with macroH2A in cells and in vitro binds to histones with low nanomolar affinity. In vitro nucleosome assembly assays show that ANP32B stimulates deposition of macroH2A-H2B and not of H2A-H2B onto tetraso me. In cells, depletion of ANP32B in cells strongly affects global macroH2A deposition, revealing ANP32B as a macroH2A chaperone. Our study highlights the power of haploid cell functional genomics coupled with cellular imaging to identify factors that are required for chromatin plasticity and diversity.

2023-11-07 | GSE241387 | GEO

Cell lines with either no treatment or ANP32B knockdown

Project description:Cell lines with either no treatment or ANP32B knockdown

| PRJNA1015158 | ENA

Histone Deacetylase 6 inhibition restores leptin sensitivity and reduces obesity

Project description:Histone Deacetylase 6 inhibition restores leptin sensitivity and reduces obesity

| PRJNA785995 | ENA

CUT-TAG for AML cell lines with either no treatment or ANP32B knockdown

Project description:CUT-TAG for AML cell lines with either no treatment or ANP32B knockdown

| PRJNA1013815 | ENA

Amiloride reduces FN3K expression to restore sunitinib sensitivity in renal cell carcinoma

Project description:The kidney is a vital organ responsible for water and sodium metabolism, while the primary function of amiloride is to promote the excretion of water and sodium. We investigated amiloride enhanced the sunitinib sensitivity in RCC. We found both sunitinib and amiloride displayed cytotoxicity and exerted the synergy effect in RCC cells in vivo and in vitro arrays. Protein expression profiles were screened via MS/TMT, revealing that FN3K was upregulated in sunitinib group, and rescued in amiloride and the combination administration. Exogenous FN3K could promote proliferation, invasion and metastasis and decrease the sensitivity of Caki-1 cells to sunitinib, also, exogenous FN3K up-regulated VEGFR2 expression and activated AKT/mTOR signal pathway. More FN3K and VEGFR2 accumulated in R-Caki-1 cells and rescued by amiloride treatment. Co-IP and IF confirmed the interaction between FN3K and VEGFR2. In conclusion, FN3K depletion mediated VEGFR2 disruption promotes amiloride synergized the anti-RCC activity of sunitinib.

2024-05-07 | PXD052100 |

Loss of tetraspanin-7 expression reduces pancreatic beta-cell exocytosis Ca2+ sensitivity but has limited effect on systemic metabolism

Project description:Loss of tetraspanin-7 expression reduces pancreatic beta-cell exocytosis Ca2+ sensitivity but has limited effect on systemic metabolism

| PRJNA882124 | ENA

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