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

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

PROVIDER: PRJNA1044023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26915779_1.fastq.gz	Fastqsanger.gz
	SRR26915779_2.fastq.gz	Fastqsanger.gz
	SRR26915780_1.fastq.gz	Fastqsanger.gz
	SRR26915780_2.fastq.gz	Fastqsanger.gz
	SRR26915781_1.fastq.gz	Fastqsanger.gz

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

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

| PRJNA1044024 | ENA

RNA helicase DDX5 maintains cardiac function by regulating CamkIIδ alternative splicing [RNA-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 | GSE248443 | GEO

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

2024-12-02 | GSE248444 | 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

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

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

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

2011-01-21 | GSE20010 | 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

The m6A reader YTHDC1 and the RNA helicase DDX5 control the production of rhabdomyosarcoma-enriched circRNAs

Project description:N6-Methyladenosine (m6A) is well-known for controlling different processes of linear RNA metabolism. Conversely, its role in the biogenesis and function of circular RNAs (circRNAs) is still poorly understood. Here, we characterize circRNA expression in the pathological context of rhabdomyosarcoma (RMS), observing a global increase when compared to wild-type myoblasts. For a set of circRNAs, such an increase is due to the raised expression of the m6A machinery, which we also find to control the proliferation activity of RMS cells. Furthermore, we identify the RNA helicase DDX5 as a novel mediator of the back-splicing reaction and as a co-factor of the m6A regulatory network. DDX5 and the m6A reader YTHDC1 are shown to interact and to promote the production of a common subset of circRNAs in RMS. In line with the observation that YTHDC1/DDX5 depletion reduces RMS proliferation, our results provide proteins and RNA candidates for the study of rhabdomyosarcoma tumorigenicity.

2023-03-20 | GSE207453 | GEO

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

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

| PRJNA595593 | ENA