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Gene expression changes in K562 upon USP7 inhibition

ABSTRACT: Gene expression changes in K562 upon USP7 inhibition

PROVIDER: PRJNA616152 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11445511_1.fastq.gz	Fastqsanger.gz
	SRR11445511_2.fastq.gz	Fastqsanger.gz
	SRR11445512_1.fastq.gz	Fastqsanger.gz
	SRR11445512_2.fastq.gz	Fastqsanger.gz
	SRR11445513_1.fastq.gz	Fastqsanger.gz

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Gene expression changes in K562 upon USP7 inhibition

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Chromatin accessibility in T-ALL cells upon USP7 inhibitor with or without dexamethasone (ATAC-Seq)

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USP7 controls the oncogenic transcriptional circuitry and is a novel therapeutic target in T cell leukemia

Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an immature hematopoietic malignancy driven mainly by oncogenic activation of NOTCH1 signaling. In this study we chemically inhibited the deubiquinating enzyme USP7 and assayed for gene expression changes. This piece of data was further integrated to epigenetic changes using ChIP-Sequencing analysis of H3K27me3, H2AUb, H2BUb, H3K27Ac and H3K79me2 upon inhibition of USP7. These results coupled helped to determine the role of USP7 in stabilizing and promoting T-ALL leukemia. We also compared the gene expression and epigenetic changes of USP7 inhibition with inhibition of NOTCH1 pathway and JMJD3.

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Chromatin conformation remains stable upon extensive transcriptional changes driven by heat shock [K562]

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Molecular basis of USP7 inhibition by selective small molecule inhibitors

Project description:Modification by ubiquitin controls the stability of most cellular proteins, and deregulation contributes to a variety of human diseases such as cancer. Deubiquitinases (DUBs) remove ubiquitin from proteins, and the inhibition of DUBs has been recognized as a therapeutic strategy to induce degradation of specific proteins, a concept extendable to ‘undruggable’ targets such as transcription factors. However, this potential has remained untapped; specific small molecule inhibitors for DUBs are scarce and insights into mechanisms of action are limited. Ubiquitin specific protease (USP) 7 stabilises the oncogenic E3 ligase MDM2 that destabilises the tumour suppressor p53 and inhibition of USP7 results in MDM2 degradation and p53 re-activation in a variety of cancers. We here present two small molecule inhibitors, FT671 and FT827, that inhibit USP7 with nanomolar affinity and display exquisite specificity towards USP7 in vitro and in cells. USP7-inhibitor co-crystal structures reveal that both compounds target the auto-inhibited apo-form of USP7 and bind in proximity to the misaligned catalytic triad in a dynamic hydrophobic pocket that serves as the binding site for the ubiquitin C-terminus. The unique auto-inhibited conformation of apo USP7 differs from other USP DUBs, explaining compound selectivity. Consistent with USP7 target engagement in cells, FT671 destabilises MDM2, stabilises p53 and results in transcription of p53 target genes, induction of the tumour suppressor p21, and tumour growth inhibition in vivo.

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