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RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RIP-seq]

ABSTRACT: RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RIP-seq]

PROVIDER: PRJNA1044024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26916074_1.fastq.gz	Fastqsanger.gz
	SRR26916074_2.fastq.gz	Fastqsanger.gz
	SRR26916075_1.fastq.gz	Fastqsanger.gz
	SRR26916075_2.fastq.gz	Fastqsanger.gz
	SRR29633821_1.fastq.gz	Fastqsanger.gz

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RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RIP-seq]

Project description:The cardiomyocyte-specific deletion of Ddx5 in mice resulted in heart failure characterized by diminished cardiac function, enlarged heart chambers, and heightened fibrosis. Proteomic analysis unveiled the involvement of DDX5 in RNA splicing within cardiomyocytes. Our study identified DDX5 as a regulator of the abnormal splicing of CamkIIδ, preventing the generation of CaMKIIδA. This isoform activates LTCC through serine phosphorylation of Cacna1c, disrupting Ca2+ homeostasis. Consistently, DDX5-depleted cardiomyocytes exhibited elevated intracellular Ca2+ transients and increased sarcoplasmic reticulum Ca2+ content.

2024-12-02 | GSE248444 | GEO

RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RNA-seq]

Project description:RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RNA-seq]

| PRJNA1044023 | ENA

RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RNA-seq]

2024-12-02 | GSE248443 | GEO

Alternative splicing signatures in apoptosis related genes of human HeLa cells with RNAi targeting p68 RNA helicase-DDX5

Project description:Alternative splicing profiling of apopotosis related genes in human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs targetting p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5) cloned into the pSuper expression vector compared to empty vector. Keywords: treated vs. untreated comparison; alternative splicing Two-condition experiment, where the p68 DDX5 gene product levels was inhibited by siRNA transfection and compared to transfection with the negative control (scrambled siRNA). Biological replicates: 2, all independently grown and harvested. A dye swapping technical duplicate was performed for each biological replicate. Samples were hybridized onto a 44290 feature array designed by ExonHit to detect splicing events in apopotosis related genes and manufactured by Agilent using in situ synthesis of oligonucleotides by SurePrint technology.

2011-01-21 | E-GEOD-20010 | biostudies-arrayexpress

RIP-seq of DDX5 in rhabdomyosarcoma cells

Project description:Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma of childhood characterized by the inability to exit the proliferative myoblast-like stage. Here, we identified the DEAD box RNA helicase 5 (DDX5) as a potential therapeutic target to inhibit alveolar rhabdomyosarcoma (ARMS) growth. We show that DDX5 is overexpressed in alveolar RMS cells, demonstrating that its depletion drastically decreases ARMS viability and slows tumor growth in xenograft models. Mechanistically, we provide evidence that DDX5 functions upstream the G9a/AKT survival signalling pathway, by modulating G9a protein stability

2022-08-22 | GSE175455 | GEO

Alternative splicing signatures in apoptosis related genes of human HeLa cells with RNAi targeting p68 RNA helicase-DDX5

2011-01-21 | GSE20010 | GEO

BRCA2 promotes DNA-RNA hybrid resolution by DDX5 helicase at DNA breaks to facilitate their repair

Project description:The BRCA2 tumor suppressor is a DNA double-strand break repair factor essential to maintain genome integrity. BRCA2-deficient cells spontaneously accumulate DNA-RNA hybrids, a known source of genome instability. However, the specific role of BRCA2 on these structures remains poorly understood. Here we identified the DEAD-box RNA helicase DDX5 as a BRCA2 interacting partner. We show that DDX5 associates with DNA-RNA hybrids that form in the vicinity of DSBs and this association is enhanced by BRCA2. Notably, BRCA2 stimulates the DNA-RNA hybrid helicase activity of DDX5. Impaired BRCA2-DDX5 interaction, as observed in cells bearing the breast cancer variant BRCA2-T207A, reduces DDX5 association with DSBs, decreases the number of RPA foci upon irradiation and impairs RAD51 repair foci formation. Our findings are consistent with DNA-RNA hybrids being an impediment for the repair of DSBs by homologous recombination and reveal BRCA2 and DDX5 as active players in their removal.

2021-02-26 | GSE150163 | GEO

RIP-seq of DDX5 in rhabdomyosarcoma cells

Project description:RIP-seq of DDX5 in rhabdomyosarcoma cells

| PRJNA732419 | ENA

The RNA helicase DDX5 supports mitochondrial function in small cell lung cancer

Project description:DDX5 is a founding member of the DEAD-box RNA helicase family, which are a group of enzymes that regulate ribonucleoprotein (RNP) formation and function in every aspect of RNA metabolism. Our lab previously found that DDX5 is involved in energy homeostasis, a process altered in many cancers. Small cell lung cancer (SCLC) is an understudied cancer type that lacks effective treatment. Therefore, we investigated the roles of DDX5 in SCLC. We show here that DDX5 is overexpressed in SCLC cell lines. Depletion of DDX5 results in reduced growth and mitochondrial dysfunction in the chemoresistant SCLC cell line H69AR. The latter is evidenced by downregulation of genes involved in oxidative phosphorylation and impaired oxygen consumption,. Interestingly, depletion of DDX5 specifically leads to reduction of intracellular succinate, a TCA intermediate that serves as a direct electron donor to mitochondrial complex II. Taken together, we propose that the oncogenic role of DDX5 is at least in part manifested through upregulation of respiration to support the energy demands of cancer cells. This also suggests that defects in RNP remodeling are connected to energy metabolism and carcinogenesis.

2020-05-06 | GSE142024 | GEO

RNA helicase DDX5-induced circPHF14 promotes gastric cancer cell progression

Project description:RNA helicase DDX5-induced circPHF14 promotes gastric cancer cell progression

| PRJNA856484 | ENA