Catalog: YM6658
Size
Price
Status
Qty.
200μL
$600.00
3 weeks
0
100μL
$340.00
3 weeks
0
40μL
$190.00
3 weeks
0
Add to cart
Collected
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Main Information
Target
AMACR
Host Species
Mouse
Reactivity
Human
Applications
IHC, ELISA
MW
42kD (Calculated)
42kD (Observed)
Conjugate/Modification
Unmodified
Detailed Information
Recommended Dilution Ratio
IHC 1:50-200; ELISA 1:500-5000
Formulation
PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA
Specificity
The antibody can specifically recognize human AMACR protein.
Purification
The antibody was affinity-purified from ascites by affinity-chromatography using specific immunogen.
Storage
-15°C to -25°C/1 year (Do not lower than -25°C)
MW(Calculated)
42kD
MW(Observed)
42kD
Modification
Unmodified
Clonality
Monoclonal
Clone Number
ABT-AMACR
Isotype
Mouse IgG1/Kappa
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Antigen&Target Information
Immunogen:
Synthesized peptide derived from human AMACR AA range: 300-382
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Specificity:
The antibody can specifically recognize human AMACR protein.
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Gene Name:
AMACR
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Protein Name:
AMACR
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Background:
This gene encodes a racemase. The encoded enzyme interconverts pristanoyl-CoA and C27-bile acylCoAs between their (R) - and (S) -stereoisomers. The conversion to the (S) -stereoisomers is necessary for degradation of these substrates by peroxisomal beta-oxidation. Encoded proteins from this locus localize to both mitochondria and peroxisomes. Mutations in this gene may be associated with adult-onset sensorimotor neuropathy , pigmentary retinopathy , and adrenomyeloneuropathy due to defects in bile acid synthesis. Alternatively spliced transcript variants have been described. Read-through transcription also exists between this gene and the upstream neighboring C1QTNF3 (C1q and tumor necrosis factor related protein 3) gene. [provided by RefSeq , Mar 2011] ,
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Function:
Catalytic activity: (2S) -2-methylacyl-CoA = (2R) -2-methylacyl-CoA. ,Disease:Defects in AMACR are the cause of alpha-methylacyl-CoA racemase deficiency (AMACRD) [MIM:604489]. AMACRD results in elevated plasma concentrations of pristanic acid C27-bile-acid intermediates. It can be associated with polyneuropathy , retinitis pigmentosa , epilepsy. ,Disease: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. ,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. ,pathway:Lipid metabolism; fatty acid metabolism. ,similarity:Belongs to the caiB/baiF CoA-transferase family. ,similarity:Contains 1 C1q domain. ,similarity:Contains 1 collagen-like domain. ,
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Cellular Localization:
Cytoplasmic
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Tissue Expression:
Research Areas:
>>Primary bile acid biosynthesis ;
>>Metabolic pathways ;
>>Peroxisome
>>Metabolic pathways ;
>>Peroxisome
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Signaling Pathway
Reference Citation({{totalcount}})
Catalog: YM6658
Size
Price
Status
Qty.
200μL
$600.00
3 weeks
0
100μL
$340.00
3 weeks
0
40μL
$190.00
3 weeks
0
Add to cart
Collected
Collect
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