AMACR Antibody [2A10F3] | 32-107

AMACR Antibody [2A10F3] | 32-107 | Gentaur UK, US & Europe Distribution

Host: Mouse

Reactivity: Human

Homology: N/A

Immunogen: Purified truncated recombinant AMACR-His fusion protein expressed in E. Coli strain BL21 (DE3) .

Research Area: Signal Transduction, Neuroscience

Tested Application: E, WB, IHC

Application: Western Blot:1:500 - 1:2, 000
IHC (P) :1:500 - 1:2, 000
ELISA:Propose dilution 1:10, 000.
Determining optimal working dilutions by titration test.

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: N/A

Validation: N/A

Isoform: N/A

Purification: N/A

Clonality: Monoclonal

Clone: 2A10F3

Isotype: IgG2b

Conjugate: Unconjugated

Physical State: N/A

Buffer: Ascitic fluid containing 0.03% sodium azide.

Concentration: N/A

Storage Condition: AMACR monoclonal antibody can be stored at -20˚C, stable for one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: 2-methylacyl-CoA racemaseRM, RACE, CBAS4, AMACRD

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: AMACR (alpha-methylacyl-CoA racemase) has been recently described as prostate cancer-specific gene that encodes a protein involved in the beta-oxidation of branched chain fatty acids. Expression of AMACR protein is found in prostatic adenocarcinoma but not in benign prostatic tissue. It stains premalignant lesions of prostate: high-grade prostatic intraepithelial neoplasia (PIN) and atypical adenomatous hyperplasia. AMACR can be used as a positive marker for PIN. Defects in AMACR are the cause of congenital bile acid synthesis defect type 4 (CBAS4) ; 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.