Редактирование: ACSL5

Long-chain-fatty-acid--CoA ligase 5 (EC 6.2.1.3) (Arachidonate--CoA ligase) (EC 6.2.1.15) (Long-chain acyl-CoA synthetase 5) (LACS 5) [ACS5] [FACL5] [UNQ633/PRO1250]

==Publications==

{{medline-entry
|title=Ageing sensitized by iPLA β deficiency induces liver fibrosis and intestinal atrophy involving suppression of homeostatic genes and alteration of intestinal lipids and bile acids.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/28888832
|abstract=Ageing is a major risk factor for various forms of liver and gastrointestinal (GI) disease and genetic background may contribute to the pathogenesis of these diseases. Group VIA phospholipase A2 or iPLA β is a homeostatic PLA  by playing a role in phospholipid metabolism and remodeling. Global iPLA β  mice exhibit aged-dependent phenotypes with body weight loss and abnormalities in the bone and brain. We have previously reported the abnormalities in these mutant mice showing susceptibility for chemical-induced liver injury and colitis. We hypothesize that iPLA β deficiency may sensitize with ageing for an induction of GI injury. Male wild-type and iPLA β  mice at 4 and 20-22months of age were studied. Aged, but not young, iPLA β mice showed increased hepatic fibrosis and biliary ductular expansion as well as severe intestinal atrophy associated with increased apoptosis, pro-inflammation, disrupted tight junction, and reduced number of mucin-containing globlet cells. This damage was associated with decreased expression of intestinal endoplasmic stress [[XBP1]] and its regulator HNF1α, FATP4, [[ACSL5]], bile-acid transport genes as well as nuclear receptors LXRα and FXR. By LC/MS-MS profiling, iPLA β deficiency in aged mice caused an increase of intestinal arachidonate-containing phospholipids concomitant with a decrease in ceramides. By the suppression of intestinal FXR/FGF-15 signaling, hepatic bile-acid synthesis gene expression was increased leading to an elevation of secondary and hydrophobic bile acids in liver, bile, and intestine. In conclusions, ageing sensitized by iPLA β deficiency caused a decline of key intestinal homeostatic genes resulting in the development of GI disease in a gut-to-liver manner.
|mesh-terms=* Aging
* Animals
* Bile Acids and Salts
* Ceramides
* Group VI Phospholipases A2
* Intestinal Diseases
* Liver Cirrhosis
* Mice
* Mice, Knockout
* Phospholipids
|keywords=* Ageing
* FXR
* Intestinal homeostasis
* Lipidomics
* Pla2G6
* XBP1
|full-text-url=https://sci-hub.do/10.1016/j.bbalip.2017.09.001
}}