Overview

  • Product name

    Anti-AMACR antibody [AMACR/1723]
    See all AMACR primary antibodies
  • Description

    Mouse monoclonal [AMACR/1723] to AMACR
  • Host species

    Mouse
  • Tested applications

    Suitable for: IHC-Pmore details
  • Species reactivity

    Reacts with: Human
  • Immunogen

    Recombinant full length protein corresponding to Human AMACR aa 1-382.
    Sequence:

    MALQGISVVE LSGLAPGPFC AMVLADFGAR VVRVDRPGSR YDVSRLGRGK RSLVLDLKQP RGAAVLRRLC KRSDVLLEPF RRGVMEKLQL GPEILQRENP RLIYARLSGF GQSGSFCRLA GHDINYLALS GVLSKIGRSG ENPYAPLNLL ADFAGGGLMC ALGIIMALFD RTRTGKGQVI DANMVEGTAY LSSFLWKTQK LSLWEAPRGQ NMLDGGAPFY TTYRTADGEF MAVGAIEPQF YELLIKGLGL KSDELPNQMS MDDWPEMKKK FADVFAEKTK AEWCQIFDGT DACVTPVLTF EEVVHHDHNK ERGSFITSEE QDVSPRPAPL LLNTPAIPSF KRDPFIGEHT EEILEEFGFS REEIYQLNSD KIIESNKVKA SL


    Database link: Q9UHK6

  • Positive control

    • Human prostate carcinoma tissue.
  • General notes

     This product was previously labelled as AMACR, AMCR

     

Properties

Applications

Our Abpromise guarantee covers the use of ab219309 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use a concentration of 1 - 2 µg/ml. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.

(for 30 minutes at RT)

Target

  • Function

    Racemization of 2-methyl-branched fatty acid CoA esters. Responsible for the conversion of pristanoyl-CoA and C27-bile acyl-CoAs to their (S)-stereoisomers.
  • Pathway

    Lipid metabolism; bile acid biosynthesis.
    Lipid metabolism; fatty acid metabolism.
  • Involvement in disease

    Defects 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 similarities

    Belongs to the CaiB/BaiF CoA-transferase family.
  • Cellular localization

    Peroxisome. Mitochondrion.
  • Information by UniProt
  • Database links

  • Alternative names

    • 2 arylpropionyl CoA epimerase antibody
    • 2 methylacyl CoA racemase antibody
    • 2-methylacyl-CoA racemase antibody
    • Alpha methylacyl CoA racemase antibody
    • Alpha methylacyl Coenzyme A racemase antibody
    • Alpha methylacyl-CoA racemase deficiency, included antibody
    • Alpha-methylacyl-CoA racemase antibody
    • Amacr antibody
    • AMACR deficiency, included antibody
    • AMACR_HUMAN antibody
    • CBAS4 antibody
    • Da1-8 antibody
    • EC 5.1.99.4 antibody
    • Macr1 antibody
    • Methylacyl CoA racemase alpha antibody
    • RACE antibody
    • RM antibody
    see all

Images

  • Immunohistochemical analysis of formalin-fixed, paraffin-embedded human prostate carcinoma tissue labeling AMACR with ab219309 at 2 µg/ml.

References

ab219309 has not yet been referenced specifically in any publications.

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