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SUMOylation regulates daunorubicin-induced changes in the long-range interactions between NFKB2 promoter and distant genomic regions in HL-60 cells

ABSTRACT: SUMOylation regulates daunorubicin-induced changes in the long-range interactions between NFKB2 promoter and distant genomic regions in HL-60 cells

PROVIDER: PRJNA817616 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18352744.fastq.gz	Fastqsanger.gz
	SRR18352745.fastq.gz	Fastqsanger.gz
	SRR18352746.fastq.gz	Fastqsanger.gz
	SRR18352747.fastq.gz	Fastqsanger.gz
	SRR18352748.fastq.gz	Fastqsanger.gz

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SUMOylation regulates daunorubicin-induced changes in the long-range interactions between NFKB2 promoter and distant genomic regions in HL-60 cells

Project description:SUMOylation, a post-translational modification of the ubiquitin family plays key roles in Acute Myeloid Leukemias response to therapies, in particular through the regulation of gene expression. We have found that the NFKB2 gene is rapidly induced by DNR in the HL-60 cell line and inhibition of SUMOylation limits is induction. To decipher how SUMOylation controls DNR-induced NFKB2 expression, we analyzed the dynamic of the 3D conformation of the NFKB2 gene using Circularized Chromosome Conformation Capture (4C). We found that the NFKB2 promoter interacts with four distal regions. DNR induced a loss of one of the interaction and the gain of a new interaction. Inhibition of SUMOylation with ML-792 did not affect the interactions between NFKB2 promoter and distal genomic regions. However, inhibition of SUMOylation prevented DNR-regulated changes in the 3D architecture of the locus.

2023-06-23 | GSE198981 | GEO

SUMOylation controls Daunorubicin-regulated gene expression in the Acute Myeloid Leukemia cell line HL-60

Project description:SUMOylation controls Daunorubicin-regulated gene expression in the Acute Myeloid Leukemia cell line HL-60

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RNA-Seq analysis of HL-60 AML cells resistant to daunorubicin or cytarabine

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SUMOylation controls Daunorubicin-regulated gene expression in the Acute Myeloid Leukemia cell line HL-60

Project description:SUMOylation, a post-translational modification of the ubiquitin family plays key roles in Acute Myeloid Leukemias response to therapies, in particular through the regulation of gene expression. We have investigated here how inhibition of SUMOylation with ML-792 affects gene daunorubicine (DNR-)-regulated gene expression. We found that inhibition of SUMOylation limits DNR-induce up- or down-regulation of gene expression.

2023-06-23 | GSE198982 | GEO

SUMO-2/3 ChIP-Seq in HL-60 cells treated or not with Daunorubicin, Cytarabin and the Nox inhibitor VAS2870

Project description:Acute Myeloid Leukemia cell line HL-60 were treated with 1 M daunorubicin (DNR) or 2M cytarabin (Ara-C) or 1 M DNR + 10 M VAS2870 (NADPH oxidase inhibitor) for 2 hours. ChIP-Seq experiments were carried out with SUMO-2/3 antibodies. Immunoprecipitated DNA and corresponding inputs from 3 independent experiments were pooled and processed for deep-sequencing (Hi-SEq 2000, Illumina).

2023-12-30 | E-MTAB-4947 | biostudies-arrayexpress

RNA-Seq analysis of HL-60 AML cells resistant to daunorubicin or cytarabine

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NFKB1 and NFKB2 differently modulate transcriptional profile of MT-2 cells

Project description:To investigate the effects of NFKB signaling, RNA-seq analysis was performed on both Jurkat and MT-2 cells. It was observed that either NFKB1 or NFKB2 knockout could alter the gene expression profile in MT-2 cells compared to Jurkat cells. Gene expression profiles of NFKB1/NFKB2 knockout Jurkat cells were compared to the mock edited Jurkat cells. On the other hand, it was hypothesized that the gene expression profile of MT-2 cells can be more drastically altered by NFKB1 or NFKB2 knockout. NFKB2 knockout MT-2 cells exhibited a unique gene expression profile compared to those of NFKB1 knockout MT-2 cells and mock edited MT-2 cells.

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2023-12-21 | GSE250065 | GEO

NFKB2 in PDAC

Project description:Role of NFKB2 in pancreatic ductal adenocarcinama (PDAC)

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TNF-induced gene-expressions in Nfkb2-/- MEFs and its derivatives

Project description:As such, TNF triggers the canonical NF-?B pathway to induce a nuclear NF-?B activity composed of the RelA:p50 dimer in WT cells. Nfkb2 encodes p100, which regulates the activity of the RelB NF-?B heterodimers during immune cell-differentiation via the noncanonical pathway. Our biochemical analyses revealed that an absence of p100 instead repositions RelB under the control of the TNF-activated canonical pathway. Indeed, chronic TNF treatment of Nfkb2-/- cells activates the RelA:p50 dimer and an additional RelB:p50 dimer. On the other hand, TNF stimulation of Relb-/-Nfkb2-/- and Rela-/-Nfkb2-/- MEFs exclusively activated the RelA:p50 dimer and the RelB:p50 dimer, respectively. We treated this panel of knockout MEFs with TNF for 6h before being subjected to microarray mRNA analysis. We also included in our analysis WT MEFs and Rela-/-Relb-/-Rel-/- MEFs, which served as a negative control. Our analyses revealed overlapping and distinct gene-expression specificities of RelA:p50 and RelB:p50 dimers activated in mutant cells in response to TNF.

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