AMACR Antibody (Rabbit mAb) [F7A19] Datasheet

Biological Description

Specificity	AMACR Antibody (Rabbit mAb) [F7A19] detects endogenous levels of total AMACR protein.
Background	Alpha-methylacyl-CoA racemase (AMACR) is a peroxisomal enzyme that is essential for breaking down branched-chain fatty acids and bile acid intermediates. It converts pristanoyl-CoA and C27-bile acyl-CoAs into their (S)-stereoisomers, the only forms that the peroxisomal β-oxidation machinery can degrade. AMACR therefore acts as a gatekeeper that routes these substrates into β-oxidation, so lipid breakdown and bile acid synthesis depend directly on its racemase activity. When AMACR is deficient, pristanic acid and C27 bile acid intermediates build up in plasma. Mutations in the AMACR gene that cause this deficiency lead to adult-onset sensory motor neuropathy. In some patients this is accompanied by pigmentary retinopathy that resembles Refsum disease, and in others by upper motor neuron signs in the legs that resemble adrenomyeloneuropathy. Affected children can show the biochemical deficiency without neuropathy. AMACR is also strongly overexpressed in prostate cancer. Gene expression profiling, RT-PCR and immunoblotting confirm higher AMACR levels in malignant tissue. Immunohistochemistry shows stronger AMACR protein expression in malignant prostate epithelium than in benign epithelium, with the most intense staining in localized prostate cancer across benign, atrophic and neoplastic tissue. In prostate needle biopsies, AMACR staining is highly sensitive and specific for detecting cancer, which makes it a tissue marker for diagnostically difficult biopsies.

Specificity

AMACR Antibody (Rabbit mAb) [F7A19] detects endogenous levels of total AMACR protein.

Background

Alpha-methylacyl-CoA racemase (AMACR) is a peroxisomal enzyme that is essential for breaking down branched-chain fatty acids and bile acid intermediates. It converts pristanoyl-CoA and C27-bile acyl-CoAs into their (S)-stereoisomers, the only forms that the peroxisomal β-oxidation machinery can degrade. AMACR therefore acts as a gatekeeper that routes these substrates into β-oxidation, so lipid breakdown and bile acid synthesis depend directly on its racemase activity. When AMACR is deficient, pristanic acid and C27 bile acid intermediates build up in plasma. Mutations in the AMACR gene that cause this deficiency lead to adult-onset sensory motor neuropathy. In some patients this is accompanied by pigmentary retinopathy that resembles Refsum disease, and in others by upper motor neuron signs in the legs that resemble adrenomyeloneuropathy. Affected children can show the biochemical deficiency without neuropathy. AMACR is also strongly overexpressed in prostate cancer. Gene expression profiling, RT-PCR and immunoblotting confirm higher AMACR levels in malignant tissue. Immunohistochemistry shows stronger AMACR protein expression in malignant prostate epithelium than in benign epithelium, with the most intense staining in localized prostate cancer across benign, atrophic and neoplastic tissue. In prostate needle biopsies, AMACR staining is highly sensitive and specific for detecting cancer, which makes it a tissue marker for diagnostically difficult biopsies.

Usage Information

Application

WB, IP, IHC

Dilution

WB	IP	IHC
1:1000	1:200	1:400-1:1600

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

42 kDa

Storage Buffer

PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage
(from the date of receipt)

-20°C (avoid freeze-thaw cycles), 2 years

References

https://pubmed.ncbi.nlm.nih.gov/10655068/
https://pubmed.ncbi.nlm.nih.gov/11926890/

AMACR Antibody (Rabbit mAb) [F7A19]

Biological Description

Usage Information

References

Application Data