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Expression data from Amacr knock-out mouse liver

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. Bile acid synthesis occurs in liver. In this experiment, liver samples from Amacr-/- and wild-type mice were collected and their gene expression levels were compared. 4 biological replicates per genotype.

ORGANISM(S): Mus musculus

SUBMITTER: Kaija Autio

PROVIDER: E-GEOD-40085 | 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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