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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from Amacr knock-out mouse intestine

ABSTRACT: Bile acids play multiple roles in vertebrate metabolism by facilitating lipid absorption in the intestine and acting as a signaling molecule in lipid and carbohydrate metabolism. Bile acids are also the main route to excrete excess cholesterol out of the body. Alpha-methyl-Coa racemase (Amacr) is one of the enzymes needed to produce bile acids from cholesterol. The mouse model lacking Amacr can produce only minor (less than 10%) amounts of bile acids, but still they are symptomless in normal laboratory conditions. Cholesterol absorption occurs in the jejunum part of the intestine. In this experiment, the intestines from Amacr-/- and wild-type mice were divided into four equal segments and the endothelial layer was collected by scraping. The RNA from these samples was isolated and the gene expression levels in each segment were compared. 3 biological replicates per genotype/segment combination.

ORGANISM(S): Mus musculus

SUBMITTER: Kaija Autio

PROVIDER: E-GEOD-40124 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Phytol is lethal for Amacr-deficient mice.

Selkälä Eija M EM Nair Remya R RR Schmitz Werner W Kvist Ari-Pekka AP Baes Myriam M Hiltunen J Kalervo JK Autio Kaija J KJ

Biochimica et biophysica acta 20150804 10

α-Methylacyl-CoA racemase (Amacr) catalyzes the racemization of the 25-methyl group in C27-intermediates in bile acid synthesis and in methyl-branched fatty acids such as pristanic acid, a metabolite derived from phytol. Consequently, patients with Amacr deficiency accumulate C27-bile acid intermediates, pristanic and phytanic acid and display sensorimotor neuropathy, seizures and relapsing encephalopathy. In contrast to humans, Amacr-deficient mice are clinically symptomless on a standard labor ...[more]

PMID: 26248199

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