Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A Drug-Elicitable Alternative-Splicing Module (DreAM) for Tunable AAV Expression and Controlled Myocardial Regeneration

ABSTRACT: A Drug-Elicitable Alternative-Splicing Module (DreAM) for Tunable AAV Expression and Controlled Myocardial Regeneration

PROVIDER: PRJNA1126649 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR29488100_1.fastq.gz	Fastqsanger.gz
	SRR29488100_2.fastq.gz	Fastqsanger.gz
	SRR29488101_1.fastq.gz	Fastqsanger.gz
	SRR29488101_2.fastq.gz	Fastqsanger.gz
	SRR29488102_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 72

Similar Datasets

A Drug-Elicitable Alternative-Splicing Module (DreAM) for Tunable AAV Expression and Controlled Myocardial Regeneration

Project description:RNA Seq datasets from WT or AAV-injected mice treated with 10 mg/kg risdiplam or solvent. RNA Seq datasets from plasmid-transfection HEK293T cells treated with 1uM risdiplam or DMSO.

2025-04-13 | GSE270445 | GEO

The DREAM complex functions as conserved master regulator of somatic DNA repair capacities

Project description:Mutations in the DREAM complex induce germline-like gene expression patterns including the increase of multiple mechanisms of DNA repair in the soma of Caenorhabditis elegans. This confers mutants of the DREAM complex resistance to a wide range of DNA damage types during development and aging.

2023-01-31 | PXD033836 | Pride

VLDL Proteome in Control-AAV and PSS1(Q353R)-AAV

Project description:Fractionated VLDL from Control-AAV and PSS1(Q353R)-AAV.

2024-10-21 | PXD047916 | Pride

DREAM On, DREAM Off: A Review of the Estrogen Paradox

Project description:DREAM On, DREAM Off: A Review of the Estrogen Paradox

| PRJNA1114009 | ENA

Transcriptional linkage analysis with in vivo AAV-Perturb-seq

Project description:The ever-growing compendium of genetic variants associated with human pathologies demands novel methods to study genotype-phenotype relationships in complex tissues in high-throughput. Here, we introduce AAV-mediated direct in vivo single-cell CRISPR screens, termed AAV-Perturb-seq, a tunable and broadly applicable method for high-throughput and high-resolution phenotyping of genetic perturbations in vivo. We applied AAV-Perturb-seq using gene editing and transcriptional inhibition to systematically dissect the phenotypic landscape underlying 22q11.2 deletion syndrome genes in the adult mouse brain prefrontal cortex. We identified three 22q11.2-linked genes involved in known and novel pathways orchestrating neuronal functions in vivo that explain approximately 40% of the transcriptional changes observed in a 22q11.2 deletion mouse model. Our findings suggest that the 22q11.2 deletion syndrome transcriptional phenotype found in mature neurons may in part be due to the broad dysregulation of a class of disease susceptibility genes important for dysfunctional RNA processing and synaptic function. Our work establishes a flexible and scalable direct in vivo method to facilitate causal understanding of biological and disease mechanisms with potential applications to identify genetic interventions and therapeutic targets for treating disease.

2023-09-20 | GSE236519 | GEO

DREAM in pain mechanisms in the trigeminal ganglia

Project description:Expression of DREAM in dorsal root ganglia and spinal cord is related to endogenous control mechanisms of acute and chronic pain. In primary sensory trigeminal neurons high levels of endogenous DREAM protein are preferentially localized in the nucleus, suggesting a major transcriptional role. Here, we show that DREAM participates in the control of trigeminal pain perception through the regulation of prodynorphin and BDNF. Furthermore, genome-wide analysis of trigeminal neurons in daDREAM transgenic mice revealed that cathepsin L (CTSL) and the monoglyceride lipase (MGLL) are new DREAM downstream targets and have a role in the regulation of trigeminal nociception.

2016-04-22 | GSE69619 | GEO

Drosophila Myb-MuvB/dREAM

Project description:Drosophila Myb-MuvB/dREAM

| PRJNA102609 | ENA

DREAM On, DREAM Off: A Review of the Estrogen Paradox

Project description:It is generally assumed that all estrogen receptor positive (ER+) breast cancers proliferate in response to estrogen and therefore examples of estrogen-induced regression of ER+ cancers are paradoxical. This review reexamines the estrogen regression paradox for the Luminal A subtype of ER+ breast cancers. The proliferative response to estrogen is shown to depend on the level of ER. Mechanistically, a window of opportunity study of pre-operative estradiol suggested that with higher levels of ER, estradiol could activate the DREAM-MMB (Dimerization partner, Retinoblastoma-like proteins, E2F4, and MuvB – MYB-MuvB) pathway to decrease proliferation. The response of breast epithelium and the incidence of breast cancers during hormonal variations that occur during the menstrual cycle and at the menopausal transition respectively suggest that a single hormone, either estrogen, progesterone or androgen could activate the DREAM pathway leading to reversible cell cycle arrest. Conversely, the presence of two hormones, could switch the DREAM-MMB complex to a pro-proliferative pathway. Using publicly available data, we examine the gene expression changes after aromatase inhibitors and ICI 182,780 to provide support for the hypothesis. This review suggests that it might be possible to integrate all current hormonal therapies for Luminal A tumors within a single theoretical schema.

2024-07-03 | GSE268001 | GEO

DREAM silencing is part of a neuroprotective mechanism in Huntington's disease

Project description:Deregulated intracellular Ca2+ homeostasis underlies synaptic dysfunction and is a common feature in neurodegenerative processes, including Huntington's disease (HD). DREAM/calsenilin/KChIP-3 is a multifunctional Ca2+ binding protein that controls the expression level and/or the activity of several proteins related to Ca2+ homeostasis, neuronal excitability and neuronal survival. We found that expression of endogenous DREAM (DRE antagonist modulator) is reduced in the striatum of R6 mice, in STHdh-Q111/111 knock in striatal neurons and in HD patients. DREAM down regulation in R6 striatum occurs early after birth, well before the onset of motor coordination impairment, and could be part of an endogenous mechanism of neuroprotection, since i) R6/2 mice hemizygous for the DREAM gene (R6/2xDREAM+/-) showed delayed onset of locomotor impairment and prolonged lifespan, ii) motor impairment after chronic administration of 3-NPA was reduced in DREAM knockout mice and enhanced in daDREAM transgenic mice and, iii) lentiviral-mediated DREAM expression in STHdh-Q111/111 knock in cells sensitizes them to oxidative stress. Transcriptomic analysis showed that changes in gene expression in R6/2 striatum were notably reduced in R6/2xDREAM+/- striatum. Chronic administration of repaglinide, a molecule able to bind to DREAM in vitro and to accelerate its clearance in vivo, delayed the onset of motor dysfunction, reduced striatal loss and prolonged the lifespan in R6/2 mice. Furthermore, exposure to repaglinide protected STHdh-Q111/111 knock in striatal neurons sensitized to oxidative stress by lentiviral-mediated DREAM overexpression. Thus, genetic and pharmacological evidences disclose a role for DREAM silencing in early neuroprotective mechanisms in HD.

2016-02-01 | GSE48104 | GEO

In Vivo Direct Reprogramming by AAV Improves Cardiac Function after Myocardial Infarction. [RNA-seq]

Project description:The overexpression of cardiac transcription factors, Gata4/Hand2/Tbx5, and Mef2c (GHT/M) has been indicated that directly reprogram cardiac fibroblasts (CFs) into induced cardiomyocytes (iCMs) in vivo, and improve cardiac function after MI in mice. Previous studies demonstrated in vivo reprogramming by using Sendai virus vectors. Here we show that in vivo reprogramming by using Adeno-associated virus (AAV) vectors. Additionally, we use Mef2cM3 (M3), a fusion of Mef2c with a strong MyoD transcriptional activation domain. RNA-seq revealed that directly cardiac reprogramming of GHT/M3 by AAV vector activated the cardiac program and concomitantly suppressed fibroblast and inflammatory signatures.

2024-09-05 | GSE246524 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data