Product nameAnti-AMACR antibody
See all AMACR primary antibodies
DescriptionRabbit polyclonal to AMACR
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human
Recombinant full length protein corresponding to Human AMACR aa 1-382.
MALQGISVVELSGLAPGPFCAMVLADFGARVVRVDRPGSRYDVSRLGRGK RSLVLDLKQPRGAAVLRRLCKRSDVLLEPFRRGVMEKLQLGPEILQRENP RLIYARLSGFGQSGSFCRLAGHDINYLALSGVLSKIGRSGENPYAPLNLL ADFAGGGLMCALGIIMALFDRTRTGKGQVIDANMVEGTAYLSSFLWKTQK LSLWEAPRGQNMLDGGAPFYTTYRTADGEFMAVGAIEPQFYELLIKGLGL KSDELPNQMSMDDWPEMKKKFADVFAEKTKAEWCQIFDGTDACVTPVLTF EEVVHHDHNKERGSFITSEEQDVSPRPAPLLLNTPAIPSFKRDPFIGEHT EEILEEFGFSREEIYQLNSDKIIESNKVKASL
Database link: Q9UHK6
- PC3, SW480, HeLa, ES-2 and liver cell lysates.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.30
Preservative: 0.02% Sodium azide
Constituents: 49% PBS, 50% Glycerol
Concentration information loading...
PurityProtein A purified
- Pathways and Processes
- Metabolic signaling pathways
- Lipid and lipoprotein metabolism
- Lipid metabolism
Our Abpromise guarantee covers the use of ab175280 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/2000. Predicted molecular weight: 42 kDa.|
|IHC-P||1/50 - 1/200.
ab171870 - Rabbit polyclonal IgG, is suitable for use as an isotype control with this antibody.
FunctionRacemization of 2-methyl-branched fatty acid CoA esters. Responsible for the conversion of pristanoyl-CoA and C27-bile acyl-CoAs to their (S)-stereoisomers.
PathwayLipid metabolism; bile acid biosynthesis.
Lipid metabolism; fatty acid metabolism.
Involvement in diseaseDefects in AMACR are the cause of alpha-methylacyl-CoA racemase deficiency (AMACRD) [MIM:614307]. AMACRD results in elevated plasma concentrations of pristanic acid C27-bile-acid intermediates. It can be associated with polyneuropathy, retinitis pigmentosa, epilepsy.
Defects in AMACR are the cause of congenital bile acid synthesis defect type 4 (CBAS4) [MIM:214950]; also known as cholestasis, intrahepatic, with defective conversion of trihydroxycoprostanic acid to cholic acid or trihydroxycoprostanic acid in bile. Clinical features include neonatal jaundice, intrahepatic cholestasis, bile duct deficiency and absence of cholic acid from bile.
Sequence similaritiesBelongs to the CaiB/BaiF CoA-transferase family.
Cellular localizationPeroxisome. Mitochondrion.
- Information by UniProt
- 2 arylpropionyl CoA epimerase antibody
- 2 methylacyl CoA racemase antibody
- 2-methylacyl-CoA racemase antibody
ab175280 has not yet been referenced specifically in any publications.