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MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (circRNA-Seq)

ABSTRACT: MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (circRNA-Seq)

PROVIDER: PRJNA1147770 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30226223_1.fastq.gz	Fastqsanger.gz
	SRR30226223_2.fastq.gz	Fastqsanger.gz
	SRR30226224_1.fastq.gz	Fastqsanger.gz
	SRR30226224_2.fastq.gz	Fastqsanger.gz
	SRR30226225_1.fastq.gz	Fastqsanger.gz

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MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (RNA-Seq)

Project description:MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (RNA-Seq)

| PRJNA1147769 | ENA

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (miRNA-Seq)

Project description:MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (miRNA-Seq)

| PRJNA1147768 | ENA

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (miRNA-Seq)

Project description:Mechanical overload is essential to cartilage degeneration during osteoarthritis (OA) development. Recent studies have confirmed that circular RNAs (circRNAs) are mechanically sensitive and that the circRNA-associated competitive endogenous RNA (ceRNA) network regulates cartilage degeneration and OA development. However, the involvement of the circRNA-associated ceRNA network in chondrocyte senescence induced by mechanical overloading remains unestablished.Here,we examined the circRNA, miRNA and mRNA expression of chondrocytes subjected to mechanical overloading.

2024-11-01 | GSE274760 | GEO

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (circRNA-Seq)

2024-11-01 | GSE274761 | GEO

MiR-335-5p escaped from circKIAA0586 adsorption contributes to mechanical overloading-induced cartilage degeneration by targeting HELLS (RNA-Seq)

2024-11-01 | GSE274759 | GEO

Overloading MuSCs

Project description:Overloading MuSCs

| PRJNA560524 | ENA

Decreased chondrocyte features of articular cartilage during short-term repeated overloading: a synovium-cartilage interaction via inhibin subunit beta A

Project description:The primary goal of this study is to investigate the ultrashort-term responses and molecular mechanisms in both the synovium and cartilage under conditions of excessive mechanical loading, a major contributing factor in the pathogenesis of osteoarthritis (OA). While cartilage degeneration is a hallmark of OA, the involvement of the synovium in disease progression and pain, particularly in relation to synovitis, has been increasingly recognized. Despite this, the immediate molecular changes in both tissues following mechanical stress, and the interactions between them, remain unclear. To address these gaps, we developed a mouse model that simulates excessive mechanical loading through treadmill exercise combined with weight attachment. We investigated the ultrashort-term gene expression changes in the synovium and cartilage at 1, 4, and 24 hours post-exercise using RNA sequencing (RNA-seq). Additionally, we examined the effects of repeated overloading by analyzing tissue samples from mice subjected to four consecutive days of overloading. This approach allowed us to capture both the acute and repeated stress responses in these tissues. Through transcriptomic analysis, we aimed to identify key molecular mediators driving both the rapid transcriptional changes in each tissue and the synovium-cartilage interaction.

2025-03-05 | GSE280656 | GEO

Overloading mesenchymal progenitors (FAPs)

Project description:Overloading mesenchymal progenitors (FAPs)

| PRJNA667659 | ENA

Overloading mesenchymal progenitors (FAPs)

Project description:Overloading mesenchymal progenitors (FAPs)

| PRJNA683206 | ENA

The SNF2-like helicase HELLS mediates E2F3-dependent transcription and cellular transformation

Project description:The activating E2F-transcription factors are best known for their dependence on the Retinoblastoma protein and their role in cellular proliferation. E2F3 is uniquely amplified in specific human tumours where its expression is inversely correlated with the survival of patients. Here, E2F3 interaction partners were identified by mass spectrometric analysis. We show that the SNF2-like HELLS interacts with E2F3 in vivo and cooperates with its oncogenic functions. Depletion of HELLS severely perturbs the induction of E2F-target genes, hinders cell cycle re-entry and growth. Using chromatin immmunoprecipitation coupled to sequencing we identified genome-wide targets of HELLS and E2F3. Our analysis revealed that HELLS binds near promoters of active genes, including the trithorax-related MLL1, and co-regulates E2F3-dependent genes. Our analysis is the first to link HELLS with E2F-controlled processes that are critical to establish a proliferative tumour circuitry. Strikingly, just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours. Our work reveals that HELLS is important for E2F3 in tumour cell proliferation. Examination of E2F3, Hells, and H3K27me3 in 2 cell types.

2011-12-19 | E-GEOD-33791 | biostudies-arrayexpress

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