Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 1000

Cardiolipin

ABSTRACT: Cardiolipin( 1',3'-bis[1,2-dimyristoyl-sn-glycero-3-phospho]-glycerol (sodium salt)) and bovine heart cardiolipin Standards.

INSTRUMENT(S): Xevo G2-S QTOF from Waters

ORGANISM(S): Diphosphatidylglycerol Lipid

SUBMITTER: Dale Nagle

PROVIDER: MSV000083086 | MassIVE | Wed Oct 31 14:30:00 GMT 2018

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Similar Datasets

GNPS - Cardiolipin

Project description:Cardiolipin( 1',3'-bis[1,2-dimyristoyl-sn-glycero-3-phospho]-glycerol (sodium salt)) and bovine heart cardiolipin Standards.

2018-10-31 | MSV000083086 | GNPS

GNPS Cardiolipin

Project description:Cardiolipin( 1',3'-bis[1,2-dimyristoyl-sn-glycero-3-phospho]-glycerol and bovine heart cardiolipin Standards.

2018-10-31 | MSV000083087 | GNPS

GNPS Cardiolipin standard

Project description:Cardiolipin bovine heart C18:2 and cardiolipin C14:0 standards were purchased from Sigma and dissolved in i-PrOH 10ug/ml ,1ug/ml respectively.

2018-02-16 | MSV000082075 | GNPS

Defective mitochondrial cardiolipin remodeling dampens HIF-1a expression in hypoxia

Project description:Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin-remodeling, upon loss of the cardiolipin acyl transferase Tafazzin, mutes HIF-1a signaling in hypoxia. Tafazzin-deficiency does not affect posttranslational HIF-1a regulation but rather HIF-1a gene-expression, a dysfunction recapitulated in iPSCs-derived cardiomyocytes from Barth Syndrome patients with Tafazzin-deficiency. RNAseq analyses confirmed drastically altered signaling in Tafazzin mutant cells. In hypoxia, Tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-kB activation and concomitantly HIF-1a gene-expression. In agreement, Tafazzin-deficient mice hearts display reduced HIF-1a levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondrial cardiolipin-remodeling dampens HIF-1a signaling through inactivation of a non-canonical signaling pathway: Lack of NF-kB activation through reduced mitochondrial ROS production diminishes HIF-1a transcription.

2018-09-12 | GSE119775 | GEO

Genome-wide analysis of gene transcription in myocardium of mice transgenically expressing human cardiolipin synthase 1 (hCLS1) in cardiac tissue

Project description:Analysis of the transcriptome of cardiac tissue from mice transgenically expressing human cardiolipin synthesis. The hypothesis tested was that cardiac specific transgenic expression of cardiolipin synthase alters myocardial lipidomic flux resulting in compensatory metabolic gene transcriptional changes that will attenuate pathological environmental and dietary insults on bioenergetics. Total RNA obtained from cardiac tissue from transgenic cardiac specific expressing human cardiolipin synthase 1 (hCLS1) mouse model at 4 months of age compared to wildtype littermates

2011-11-05 | E-GEOD-33451 | biostudies-arrayexpress

Cardiolipin Synthesis Governs Systemic Energy Homeostasis through Thermogenic Fat Mitochondria

Project description:Here we show that synthesis of the mitochondrial phospholipid cardiolipin is an indispensable driver of thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response by overexpressing cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency diminishes mitochondrial uncoupling in brown and beige adipocytes and elicits a nuclear transcriptional response through ER stress-mediated retrograde communication. Cardiolipin depletion in brown and beige fat abolishes adipose thermogenesis and glucose uptake and renders animals strikingly insulin resistant. We further identify a rare human CRLS1 variant associated with insulin resistance and show that adipose CRLS1 levels positively correlate with insulin sensitivity. Thus, adipose cardiolipin is a powerful regulator of organismal energy homeostasis through thermogenic fat bioenergetics.

2018-07-19 | GSE110297 | GEO

Cardiolipin is required for membrane docking of mitochondrial ribosomes and protein synthesis

Project description:The mitochondrial inner membrane contains a unique phospholipid known as cardiolipin (CL), which stabilises the protein complexes embedded in the membrane and supports its overall structure. Recent evidence indicates that the mitochondrial ribosome may associate with the inner membrane to facilitate co-translational insertion of the hydrophobic oxidative phosphorylation (OXPHOS) proteins into the inner membrane. We generated three mutant knockout cell lines for the cardiolipin biosynthesis gene Crls1 to investigate the effects of cardiolipin loss on mitochondrial protein synthesis. Reduced CL levels caused altered mitochondrial morphology and transcriptome-wide changes that were accompanied by reduced uncoordinated mitochondrial translation rates and impaired respiratory supercomplex formation. Aberrant protein synthesis was caused by impaired formation and distribution of mitochondrial ribosomes. Reduction or loss of cardiolipin resulted in resulted in different mitochondrial and endoplasmic reticulum stress responses. We show that cardiolipin is required to stabilise the interaction of the mitochondrial ribosome with the membrane via its association with OXA1 during active translation. This interaction facilitates insertion of newly synthesised mitochondrial proteins into the inner membrane and stabilises the respiratory supercomplexes.

2020-07-08 | GSE148178 | GEO

Genome-wide analysis of gene transcription in myocardium of mice transgenically expressing human cardiolipin synthase 1 (hCLS1) in cardiac tissue

2011-11-05 | GSE33451 | GEO

Zc3h10 controls mitochondrial function coupling iron and cardiolipin homeostasis.

Project description:Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we have identified the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is a nuclear RNA binding protein that controls the fate of Slc25a37 and Prelid3a mRNA transcripts, two nuclear-encoded mitochondrial proteins central for iron and cardiolipin homeostasis. Depletion of Zc3h10 results in mitochondrial dysfunction and reduced TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with decreased mitochondrial function, increased body mass index, fat mass, fasting glucose and triglycerides. Cells from Cys105 homozygotes display alterations in Slc25a37 and Prelid3a levels and defects in mitochondrial iron and cardiolipin homeostasis that derive in mitochondrial dysfunction.

2023-05-22 | GSE99138 | GEO

GNPS Cardiolipin standards

Project description:liquid chromatography-mass spectroscopy analysis of Cardiolipin standards C14:0 and C18:2

2018-02-26 | MSV000082109 | GNPS