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The deubiquitylating enzyme USP35 restricts regulated cell death to promote survival of renal clear cell carcinoma

ABSTRACT: The deubiquitylating enzyme USP35 restricts regulated cell death to promote survival of renal clear cell carcinoma

PROVIDER: PRJNA892453 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23901639_1.fastq.gz	Fastqsanger.gz
	SRR23901639_2.fastq.gz	Fastqsanger.gz
	SRR23901640_1.fastq.gz	Fastqsanger.gz
	SRR23901640_2.fastq.gz	Fastqsanger.gz
	SRR23901641_1.fastq.gz	Fastqsanger.gz

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The deubiquitylating enzyme USP35 restricts regulated cell death to promote survival of renal clear cell carcinoma

Project description:The ubiquitin proteasome system governs a wide spectrum of cellular events and offers therapeutic opportunities for pharmacological intervention in cancer treatment. Renal clear cell carcinoma represents the predominant histological subtype and accounts for the majority of cancer death related to kidney malignancies. Through a systematic survey in the association of human ubiquitin-specific proteases with patient prognosis of renal clear cell carcinoma and subsequent phenotypic validation, we uncovered the tumor-promoting role of USP35. Biochemical characterizations confirmed the stabilizing effects of USP35 towards multiple members of the IAP family in an enzymatic activity-dependent manner. USP35 silencing led to reduced expression levels of IAP proteins, which were accompanied with increased cellular apoptosis. Further transcriptomic analysis revealed that USP35 knockdown altered expression levels of NRF2 downstream transcripts, which were conferred by compromised NRF2 abundance. USP35 functions to maintain NRF2 levels by catalyzing its deubiquitylation and thus antagonizing degradation. NRF2 reduction imposed by USP35 silencing rendered renal clear cell carcinoma cells increased sensitivity to ferroptosis induction. Finally, induced USP35 knockdown markedly attenuated xenograft formation of renal clear cell carcinoma in nude mice. Hence, our findings identify a number of USP35 substrates and reveal the protecting role of USP35 against both apoptosis and ferroptosis in renal clear cell carcinoma.

2023-06-17 | GSE216154 | GEO

Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11

Project description:Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11

| PRJNA1093404 | ENA

Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 [mRNA-seq]

Project description:Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 [mRNA-seq]

| PRJNA1099387 | ENA

Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 [MeRIP-m6A]

Project description:Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 [MeRIP-m6A]

| PRJNA1106417 | ENA

Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 (MeRIP-m6A-mRNA-seq)

Project description:Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 (MeRIP-m6A-mRNA-seq)

| PRJNA1099641 | ENA

The mitochondrial enzyme pyruvate carboxylase restricts pancreatic β-cell senescence by blocking p53 activation

Project description:The mitochondrial enzyme pyruvate carboxylase restricts pancreatic β-cell senescence by blocking p53 activation

| PRJNA1169324 | ENA

Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 (mRNA-seq db vs. lean)

Project description:Amelioration of nonalcoholic fatty liver disease by inhibiting the deubiquitylating enzyme RPN11 (mRNA-seq db vs. lean)

| PRJNA1099657 | ENA

ABPP-HT - high-throughput activity-based profiling of deubiquitylating enzyme inhibitors in a cellular context

Project description:The potency and selectivity of a small molecule inhibitor are key parameters to assess during the early stages of drug discovery. In particular, it is very informative for characterizing compounds in a relevant cellular context in order to reveal potential off-target effects and drug efficacy. Activity-based probes (ABPs) are valuable tools for that purpose, however, obtaining cellular target engagement data in a high-throughput format has been particularly challenging. Here, we describe a new methodology named ABPP-HT (high-throughput-compatible activity-based protein profiling), implementing a semi-automated proteomic sample preparation workflow that increased the throughput capabilities of the classical ABPP workflow approximately ten times while preserving its enzyme profiling characteristics. Using a panel of deubiquitylating enzyme (DUB) inhibitors, we demonstrate the feasibility of ABPP-HT to provide compound selectivity profiles of endogenous DUBs in a cellular context at a fraction of time as compared to previous methodologies

2021-02-24 | PXD023036 | Pride

METTL3 restricts RIPK1-dependent cell death via the ATF3-cFLIP axis in the intestinal epithelium

Project description:METTL3 restricts RIPK1-dependent cell death via the ATF3-cFLIP axis in the intestinal epithelium

| PRJNA1090958 | ENA

The mitochondrial enzyme pyruvate carboxylase restricts pancreatic β-cell senescence by blocking p53 activation

Project description:Defective glucose-stimulated insulin secretion (GSIS) and β-cell senescence are hallmarks in diabetes. The mitochondrial enzyme pyruvate carboxylase (PC) has been shown to promote GSIS and β-cell proliferation in the clonal β-cell lines, yet its physiological relevance remains unknown. Here, we provide animal and human data showing a role of PC in protecting β-cells against senescence and maintaining GSIS under different physiological and pathological conditions. β-cell-specific deletion of PC impaired GSIS and induced β-cell senescence in the mouse models under either a standard chow diet or prolonged high-fat diet feeding. Transcriptomic analysis indicated that p53-related senescence and cell cycle arrest are activated in PC-deficient islets. Overexpression of PC inhibited hyperglycemia- and aging-induced p53-related senescence in human and mouse islets as well as INS-1E β-cells, whereas knockdown of PC provoked senescence. Mechanistically, PC interacted with MDM2 to prevent its degradation via the MDM2 binding motif, which in turn restricts the p53-dependent senescent program in β-cells. On the contrary, the regulatory effects of PC on GSIS and the tricarboxylic acid (TCA) anaplerotic flux are p53-independent. We illuminate a function of PC in controlling β-cell senescence through the MDM2–p53 axis.

2024-10-10 | GSE278865 | GEO

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