Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fasting wildtype, tfeb -/- knockout, and lmna -/- knockout metabolite profiling of adult zebrafish

ABSTRACT: Inhibition of mechanistic target of rapamycin (mTOR) activity exerts cardioprotective functions. We propose to assess the metabolite profile in zebrafish cardiomyopathy models to test the cardioprotective role of mTOR-TFEB-autophagy and mTOR-lmna- autophagy signaling in heart, liver, muscle, brain, and kidney tissue. In addition mTOR signaling among zebrafish 2 hour post feeding, 24 hour post feeding, and 48 hour post feeding will be profiled. These studes will be used as a baseline and for protocol development before we assess changes in DOX-induced cardiomyopathy.

ORGANISM(S): Danio Rerio Zebrafish

TISSUE(S): Heart, Brain, Liver, Muscle, Kidney

DISEASE(S): Heart Disease

SUBMITTER: Xiaolei Xu

PROVIDER: ST000584 | MetabolomicsWorkbench | Fri Mar 10 00:00:00 GMT 2017

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

mTOR activity is essential for retinal pigment epithelium regeneration in zebrafish

Project description:Zebrafish is capable of endogenously regenerating functional retina pigment epithelium (RPE) after widespread genetic ablation which involves a series of cellular and molecular events that remain to be defined. Here, using the RPE genetic ablation model in zebrafish, we observed that mTOR signaling was activated in the RPE cells post-ablation. Pharmacological and genetic inhibition of mTOR signaling impaired RPE regeneration, while activation of mTOR signaling benefited RPE recovery, suggesting mTOR signaling was required and sufficient for RPE regeneration post-ablation in zebrafish. We further identified an interesting crosstalk between mTOR signaling and microglia/macrophages during RPE regeneration that mTOR acts as an upstream regulator of microglia/macrophage infiltration to the injury site while microglia/macrophage, in turn, rainenforce mTOR activity.

2022-03-01 | GSE174538 | GEO

Real-time quantitative PCR analysis of WT and NOD1 knockout zebrafish (mTor)

Project description:Zebrafish larvae from WT and NOD1-1IS-/- collected at 10 dpf were used for Zebrafish mTOR Signaling RT² Profiler™ PCR Array.

2017-06-23 | GSE80621 | GEO

Galectins control mTOR in response to endomembrane damage

Project description:The Ser/Thr protein kinase mTOR controls metabolic pathways, including the catabolic process of autophagy. Autophagy plays additional, catabolism-independent roles in homeostasis of cytoplasmic endomembranes and whole organelles. How signals from endomembrane damage are transmitted to mTOR to orchestrate autophagic responses is not known. Here we show that mTOR is inhibited by lysosomal damage. Lysosomal damage, recognized by galectins, leads to association of Gal8 with mTOR apparatus on the lysosome. Gal8 inhibits mTOR activity through its Ragulator-Rag signaling machinery. Thus, a novel galectin-based signal-transduction apparatus, termed here GALTOR, controls mTOR in response to lysosomal damage.

2017-12-07 | MSV000081788 | MassIVE

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts [total RNA]

Project description:Diabetes leads to cardiomyopathy and heart failure, the leading cause of death for diabetic patients. Monoamine oxidase (MAO)-dependent reactive oxygen species (ROS) formation contributes to the development of diabetic cardiomyopathy by inducing mitochondrial and cardiomyocyte dysfunction. Yet, it is unclear whether, in addition to the direct effects exerted by MAO-dependent ROS on mitochondria, MAO activity is able to post-transcriptionally regulate cardiomyocyte function and survival in diabetes. To this aim, we performed gene and miRNA expression profiling in cardiac tissue from a mouse model of type 1 diabetes (T1D) with or without pharmacological MAO inhibition. We found that MAO-dependent ROS generation in T1D hearts leads to profound transcriptomic changes, affecting autophagy and pro-survival pathways activation. MAO activity in T1D hearts affected expression levels of miR-133a-3p, -193a-3p, and -27a-3p that target insulin-like growth factor receptor 1 (Igf1r), growth factor receptor bound protein 10 and inositol polyphosphate 4 phosphatase type 1A, respectively, all components of the Igf1r/PI3K/Akt signaling pathway. Indeed, Akt activation was significantly downregulated in T1D hearts, whereas MAO inhibition restored the activation of this pro-survival pathway. The present study provides an important link between MAO activity, transcriptomic changes, and activation of pro-survival signaling and autophagy in diabetic cardiomyopathy.

2022-09-20 | GSE210611 | GEO

Monoamine oxidase-dependent pro-survival signaling in diabetic hearts is mediated by miRNAs

2022-09-20 | GSE210036 | GEO

Autophagy is essential for cardiac morphogenesis during vertebrate development

Project description:This study examined the effects of genetic knockdown of autophagy genes on vertebrate cardiac development We performed microarray studies comparing the hearts of control zebrafish embryos to the hearts of embryos with decreased expression of the autophagy genes atg5, becn1 or atg7. The results provide insight into the role of autophagy in developmental morphogenesis. Hearts were purified from 3 day-old zebrafish embryos injected with control or autophagy gene-specific morpholino oligonucleotides. RNA was prepared from all samples and hybridized to zebrafish-specific Affymetricx arrays.

2014-03-01 | E-GEOD-51541 | biostudies-arrayexpress

Gene expression profiling of zebrafish embryos at 1 hour post injection of PAMPs

Project description:We use the zebrafish embryo model to study the transcriptome responses to flagellin and Pam3CSK4. Therefore, we injected these PAMPs into the caudal vein at the 27 hours post fertilization and took samples at 1 hour post injection.

2015-11-18 | GSE64570 | GEO

Gene expression profile at Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mice, Gcn2 Knockout mice, and Hri Knockout mice

Project description:To study the mitochondrial stress response HRI-eIF2a-ATF4 signaling pathway in mitochondrial cardiomyopathy , we generated Ptpmt1 cardiomyocytes-specific Knockout mcie, Eif2a mutant mcie, Gcn2 Knockout mcie, and Hri Knockout mcie

2022-04-21 | GSE201042 | GEO

Let-7 coordinately suppresses components of the amino acid sensing pathway to induce autophagy

Project description:Macroautophagy (hereafter autophagy) is the major pathway by which macromolecules and organelles are degraded. Autophagy is regulated by the mTOR signaling pathway, which is the focal point for integration of metabolic information, with mTORC1 playing a central role in balancing biosynthesis and catabolism. Of the various inputs to mTORC1, the amino acid sensing pathway is among the most potent. Based upon transcriptome analysis of neurons subjected to nutrient deprivation, we identified let-7 as a microRNA capable of promoting neuronal autophagy. We found that let-7 activates autophagy by coordinately down-regulating the amino acid sensing pathway to prevent mTORC1 activation. Let-7 induced autophagy in the brain and greatly reduced protein aggregates in a lentivirus model of polyglutamine disease, establishing the physiological relevance of let-7 for in vivo autophagy modulation. Moreover, peripheral delivery of let-7 anti-miR repressed autophagy in muscle and white fat, suggesting that let-7 autophagy regulation extends beyond the CNS. Hence, let-7 plays a central role in nutrient homeostasis and proteostasis regulation in higher organisms. Using sets of wild-type C57BL/6J mice, we established primary cortical neuron cultures from P0 littermates, and cultured these neurons (n = 3 / set) in CM or NLM for 4 hrs.

2015-08-03 | E-GEOD-60452 | biostudies-arrayexpress

Versatile regulation of autophagy by the deubiquitinase USP11

Project description:Ubiquitination is a versatile post-translational modification known to regulate autophagy. Here, we show that loss of the deubiquitinase USP11 leads to an increase in the autophagic flux. To investigate the molecular details of how USP11 impacts autophagy, we determined interaction partners of USP11 using an affinity purification-mass spectrometry approach. GFP-tagged, catalytically inactive USP11(C318S) was overexpressed in 293 cells. After 4 hour treatment with Torin 1, an inhibitor of mTOR that induces autophagy, cells were lysed and samples further processed for analysis. Catalytically inactive USP11 was used to increase the chances of capturing both interaction partners and potential substrates. We identified many autophagy-related proteins that co-precipitated with USP11, suggesting that USP11 does not regulate autophagy via a single substrate, but that the observed phenotype is the sum of many interactions, each of which should be independently investigated in more detail. Our work focused on elucidating the regulation of autophagy via the lipid kinase complex PI3KC3 complex I, as one of its components (VPS15) was identified in our USP11 interactome data. PI3KC3 complex I is crucial for initiation of autophagosome formation at the endoplasmatic reticulum. USP11 knockout caused an increase in complex activity, which could explain enhanced autophagy in these cells.

2022-02-16 | PXD022143 | Pride

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