Редактирование: ABHD12

Lysophosphatidylserine lipase ABHD12 (EC 3.1.-.-) (2-arachidonoylglycerol hydrolase ABHD12) (Abhydrolase domain-containing protein 12) (hABHD12) (Monoacylglycerol lipase ABHD12) (EC 3.1.1.23) (Oxidized phosphatidylserine lipase ABHD12) (EC 3.1.-.-) [C20orf22]

==Publications==

{{medline-entry
|title=Elevated Levels of Arachidonic Acid-Derived Lipids Including Prostaglandins and Endocannabinoids Are Present Throughout [[ABHD12]] Knockout Brains: Novel Insights Into the Neurodegenerative Phenotype.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/31213981
|abstract=Derived from arachidonic acid (AA), the endogenous cannabinoid (eCB) 2-arachidonoyl glycerol (2-AG) is a substrate for α/β hydrolase domain-12 ([[ABHD12]]). Loss-of-function mutations of [[ABHD12]] are associated with the neurodegenerative disorder polyneuropathy, hearing loss, ataxia, retinitis pigmentosa, and cataract (PHARC). [[ABHD12]] knockout (KO) mice show PHARC-like behaviors in older adulthood. Here, we test the hypothesis that [[ABHD12]] deletion age-dependently regulates bioactive lipids in the CNS. Lipidomics analysis of the brainstem, cerebellum, cortex, hippocampus, hypothalamus, midbrain, striatum and thalamus from male young (3-4 months) and older (7 months) adult [[ABHD12]] KO and age-matched wild-type (WT) mice was performed on over 80 lipids via HPLC/MS/MS, including eCBs, lipoamines, 2-acyl glycerols, free fatty acids, and prostaglandins (PGs). Aging and [[ABHD12]] deletion drove widespread changes in the CNS lipidome; however, the effects of [[ABHD12]] deletion were similar between old and young mice, meaning that many alterations in the lipidome precede PHARC-like symptoms. AA-derived lipids were particularly sensitive to [[ABHD12]] deletion. 2-AG increased in the striatum, hippocampus, cerebellum, thalamus, midbrain, and brainstem, whereas the eCB [i]N[/i]-arachidonoyl ethanolamine (AEA) increased in all 8 brain regions, along with at least 2-PGs. Aging also had a widespread effect on the lipidome and more age-related changes in bioactive lipids were found in [[ABHD12]] KO mice than WT suggesting that [[ABHD12]] deletion exacerbates the effects of age. The most robust effects of aging (independent of genotype) across the CNS were decreases in [i]N[/i]-acyl GABAs and [i]N[/i]-acyl glycines. In conclusion, levels of bioactive lipids are dynamic throughout adulthood and deleting [[ABHD12]] disrupts the wider lipidome, modulating multiple AA-derived lipids with potential consequences for neuropathology.

|keywords=* ABHD12
* PHARC
* aging
* arachidonic acid
* endogenous cannabinoid
* lipidomics
* mouse brain
* neurodegeneration
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6555221
}}