PE(15:0/20:0) is a lipid of Glycerophospholipids (GP) class. Pe(15:0/20:0) is associated with abnormalities such as Exanthema, Infection, Painful Bladder Syndrome, Obesity and Fatty Liver. The involved functions are known as conjugation, Transcription, Genetic, Sinking, Autophagy and Protein Biosynthesis. Pe(15:0/20:0) often locates in membrane fraction, soluble, Membrane, Body tissue and Tissue membrane. The associated genes with PE(15:0/20:0) are GABARAPL2 gene, ATG10 gene, ATG12 gene, SLC33A1 gene and GABARAP gene. The related lipids are Liposomes, Lipopolysaccharides, Phosphatidylserines, Membrane Lipids and Cardiolipins. The related experimental models are Knock-out and Cancer Model.
To understand associated biological information of PE(15:0/20:0), we collected biological information of abnormalities, associated pathways, cellular/molecular locations, biological functions, related genes/proteins, lipids and common seen animal/experimental models with organized paragraphs from literatures.
PE(15:0/20:0) is suspected in Infection, CONE-ROD DYSTROPHY 1 (disorder), Diabetes, Obesity, Malaria, Atherosclerosis and other diseases in descending order of the highest number of associated sentences.
Disease | Cross reference | Weighted score | Related literature |
---|
We collected disease MeSH terms mapped to the references associated with PE(15:0/20:0)
There are no associated biomedical information in the current reference collection.
Associated locations are in red color. Not associated locations are in black.
Location | Cross reference | Weighted score | Related literatures |
---|
Function | Cross reference | Weighted score | Related literatures |
---|
Lipid concept | Cross reference | Weighted score | Related literatures |
---|
Gene | Cross reference | Weighted score | Related literatures |
---|
Knock-out are used in the study 'Sequential synthesis and methylation of phosphatidylethanolamine promote lipid droplet biosynthesis and stability in tissue culture and in vivo.' (Hörl G et al., 2011) and Knock-out are used in the study 'An Atg4B mutant hampers the lipidation of LC3 paralogues and causes defects in autophagosome closure.' (Fujita N et al., 2008).
Cancer Model are used in the study 'Improving penetration in tumors with nanoassemblies of phospholipids and doxorubicin.' (Tang N et al., 2007).
Model | Cross reference | Weighted score | Related literatures |
---|
Authors | Title | Published | Journal | PubMed Link |
---|---|---|---|---|
Nair U et al. | A role for Atg8-PE deconjugation in autophagosome biogenesis. | 2012 | Autophagy | pmid:22622160 |
Alirezaei M et al. | Coxsackievirus can exploit LC3 in both autophagy-dependent and -independent manners in vivo. | 2015 | Autophagy | pmid:26090585 |
Kuma A et al. | LC3, an autophagosome marker, can be incorporated into protein aggregates independent of autophagy: caution in the interpretation of LC3 localization. | 2007 Jul-Aug | Autophagy | pmid:17387262 |
Mizushima N and Yoshimori T | How to interpret LC3 immunoblotting. | 2007 Nov-Dec | Autophagy | pmid:17611390 |
Yu ZQ et al. | Dual roles of Atg8-PE deconjugation by Atg4 in autophagy. | 2012 | Autophagy | pmid:22652539 |
Mitroi DN et al. | SGPL1 (sphingosine phosphate lyase 1) modulates neuronal autophagy via phosphatidylethanolamine production. | 2017 | Autophagy | pmid:28521611 |
Nivon M et al. | Autophagy activation by NFkappaB is essential for cell survival after heat shock. | 2009 | Autophagy | pmid:19502777 |
Shao Y et al. | Stimulation of ATG12-ATG5 conjugation by ribonucleic acid. | 2007 Jan-Feb | Autophagy | pmid:16963840 |
Nakatogawa H et al. | Lipidation of Atg8: how is substrate specificity determined without a canonical E3 enzyme? | 2008 | Autophagy | pmid:18690009 |
Park JM et al. | The ULK1 complex mediates MTORC1 signaling to the autophagy initiation machinery via binding and phosphorylating ATG14. | 2016 | Autophagy | pmid:27046250 |