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Investigate the effect of cardiomyocyte-specific deletion of Trbp in transaortic constriction model in mice

ABSTRACT: Investigate the effect of cardiomyocyte-specific deletion of Trbp in transaortic constriction model in mice

PROVIDER: PRJNA1212044 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32034064_1.fastq.gz	Fastqsanger.gz
	SRR32034064_2.fastq.gz	Fastqsanger.gz
	SRR32034065_1.fastq.gz	Fastqsanger.gz
	SRR32034065_2.fastq.gz	Fastqsanger.gz
	SRR32034066_1.fastq.gz	Fastqsanger.gz

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Investigate the effect of cardiomyocyte-specific deletion of Trbp in transaortic constriction model in mice

Project description:Cardiac remodeling in response to disease or tissue damage severely impairs heart function. Therefore, the description of the molecular mechanisms responsible is essential for the development of effective therapies. Trbp (Tarbp2) is a multi-functional RNA-binding protein (RBP) that is essential during heart development but its role in the adult heart and cardiac remodeling are unknown. We generated inducible conditional knockout mice to delete Trbp from cardiomyocytes in young adults (Trbp-cKOs). While Trbp-cKO mice did not display a detectable phenotype, under stress conditions induced by transverse aortic constriction (TAC) pressure overload, they rapidly developed severe heart failure; this was associated with maladaptive cardiac remodeling and increased interstitial fibrosis.

2025-01-31 | GSE287292 | GEO

Effects of Trbp deletion on gene expession in mice hearts

Project description:We generated the cardiac-specific knockout of Trbp (Trbp-cKO) in mice. We profiled the transcriptome in both wild-type and Trbp-cKO hearts, and found numerous genes were deregulated by deletion of Trbp. We also profiled miRNA expression both wild-type and Trbp-cKO hearts, and found expression of a subset of miRNA species was altered in Trbp-cKO hearts.

2015-04-27 | GSE67658 | GEO

Effects of Trbp deletion on gene expession in mice hearts

2015-04-27 | E-GEOD-67658 | biostudies-arrayexpress

Deletion of human tarbp2 reveals cellular microRNA targets and cell cycle function of TRBP

Project description:TRBP has two known functions as Dicer co-factor and PKR inhibitor. However, the role of TRBP in miRNA biogenesis is controversial and its regulation of PKR in mitosis remains unexplored. Here, we generate TRBP KO HeLa cells and find that TRBP depletion alters Dicer processing sites of a subset of miRNAs, but does not affect Dicer stability, miRNA abundance, or Argonaute loading. By generating PACT, another Dicer interactor, and TRBP/PACT double-KO cells, we further show that TRBP and PACT do not functionally compensate each other and that only TRBP contributes to Dicer processing. We also report that TRBP is hyperphosphorylated by JNK in M phase when PKR is activated by cellular dsRNAs. Hyperphosphorylation potentiates the inhibitory activity of TRBP on PKR, suppressing PKR in M-G1 transition. By generating the first human TRBP KO, our study clarifies the role of TRBP and unveils negative feedback regulation of PKR through TRBP phosphorylation.

2014-09-16 | GSE61458 | GEO

Deletion of human tarbp2 reveals cellular microRNA targets and cell cycle function of TRBP

2014-09-16 | E-GEOD-61458 | biostudies-arrayexpress

Effect of cardiomyocyte-specific deletion of Gch1 on gene expression

Project description:To investigate the physiological role of BH4 in cardiac function, we developed mice with cardiomyocyte-specific deletion of (cm)Gch1, the gene that encodes for GTPCH, which responsible for de novo synthesis of BH4. We performed RNA sequencing in heart tissues from cmGch1 KO and WT mice.

2024-04-24 | GSE206063 | GEO

RNA-seq data in cardiac tissues from cardiomyocyte-specific Acsl4 knockout mice after transverse aortic constriction

Project description:In order to investigate the differentially expressed genes in Acsl4 knockout after TAC (Transverse aortic constriction) or sham surgery. The experiment was divided to four groups including sham-operated Acsl4 flox/flox mice (FS), sham-operated Acsl4 knockout mice (KS), TAC-operated Acsl4 flox/flox mice (FT), TAC-operated Acsl4 knockout mice (KT) n=3 mice/group. The heart tissue was isolated after 21 days after performing TAC or sham surgery.

2024-08-26 | E-MTAB-14383 | biostudies-arrayexpress

RNA sequencing of adult cardiomyocyte cyclin C deletion

Project description:RNA sequencing of adult cardiomyocyte cyclin C deletion

| PRJNA605429 | ENA

Gene Expression Following Transaortic Constriction in Cardiomyocyte Specific Insulin Receptor Substrate Knockout Mice

Project description:Gene Expression Following Transaortic Constriction in Cardiomyocyte Specific Insulin Receptor Substrate Knockout Mice

| PRJNA549670 | ENA

Caspase-mediated processing of TRBP regulates apoptosis during viral infection

Project description:RNA silencing is a post-transcriptional gene-silencing mechanism mediated by microRNAs (miRNAs). However, the regulatory mechanism of RNA silencing during viral infection is unclear. TAR RNA-binding protein (TRBP) is an enhancer of RNA silencing that induces miRNA maturation by interacting with the ribonuclease Dicer. TRBP interacts with a virus sensor protein, laboratory of genetics and physiology 2 (LGP2), in the early stage of viral infection of human cells. Next, it induces apoptosis by inhibiting the maturation of miRNAs, thereby upregulating the expression of apoptosis regulatory genes. In this study, we show that TRBP undergoes a functional conversion in the late stage of viral infection. Viral infection resulted in the activation of caspases that proteolytically processed TRBP into two fragments. The N-terminal fragment did not interact with Dicer but interacted with type I interferon (IFN) signaling modulators, such as protein kinase R (PKR) and LGP2, and induced ER stress. The end results were irreversible apoptosis and suppression of IFN signaling. Our results demonstrate that the processing of TRBP enhances apoptosis, reducing IFN signaling during viral infection.

2024-04-19 | GSE234549 | GEO

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