Detection of Human Adenosylhomocysteinase/AHCY by Western Blot.
Western blot shows lysates of Bowes human melanoma cell line and HeLa human cervical epithelial carcinoma cell line. PVDF Membrane was probed with 1 µg/mL of Human Adenosylhomocysteinase/AHCY Antigen Affinity-purified Polyclonal Antibody (Catalog # AF6466) followed by HRP-conjugated Anti-Sheep IgG Secondary Antibody (Catalog # HAF016). A specific band was detected for Adenosylhomocysteinase/AHCY at approximately 48 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 8.
Preparation and Storage
Sterile PBS to a final concentration of 0.2 mg/mL.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
Human S‑Adenosylhomocysteinase (AHCY) is a cytoplasmic tetramer with a tightly bound NAD co‑factor for each subunit (1, 2). It is the only known enzyme to catalyze the breakdown of S‑adenosylhomocysteine (AdoHcy) to homocysteine and adenosine. AdoHcy hydrolysis is a reversible reaction with an equilibrium favoring AdoHcy formation, but hydrolysis prevails under physiological conditions due to the rapid removal of adenosine and homocysteine. Thus, AHCY’s activity in mammals is directly related to homocysteine level, an independent risk factor for vascular disease (3). It also functions as a regulator of biological transmethylation by controlling the concentration of AdoHcy, a potent competitive inhibitor of all S‑adonosyl-L-methionine methyltransferases (1). A mutation in the human AHCY results in AHCY deficiency with increase of plasma creatine kinase, methionine, S‑adenosylmethionine and AdoHcy, delay of myelination, myopathy and psychomotor retardation (4, 5).
Turner, M. A. et al. (2000) Cell Biochem. Biophys. 33:101.
Takata, Y. et al. (2002) J. Biol. Chem. 277:22670.
Gellekink, H. et al. (2004) Eur. J. Hum. Genet. 12:942.
Baric, I. et al. (2004) Proc. Natl. Acad. Sci. USA. 101:4234.
Fumic, K. et al. (2007) Eur. J.Hum. Genet. 15:347.
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