Cell Signaling Technology

Product Pathways - Ca / cAMP / Lipid Signaling

ASM Antibody #3687

Applications Reactivity Sensitivity MW (kDa) Source
W H (Mk) Endogenous 57, 70 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

ASM Antibody detects endogenous levels of total human ASM protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues at the carboxyl terminus of human ASM. Antibody was purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from THP-1 and HL-60 cells, untreated (-) or treated overnight with TPA #9905 (+), using ASM Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from COS-7 cells, untransfected (-) or transfected with a human ASM construct (+), using ASM Antibody.

Background

Sphingomyelinases (SMases) catalyze the hydrolysis of sphingomyelin to produce ceramide and phosphocholine (1). Ceramide is an important bioactive lipid triggering signal transduction involved in cell proliferation, apoptosis and differentiation (1,2). A number of SMases have been described and categorized based on their optimum pH activity, cation dependence, tissue distribution, and subcellular localization (1). These include a lysosomal acid SMase, a Zn++-dependent secreted acid SMase, a membrane-bound Mg++-dependent neutral SMase, a Mg++-independent neutral SMase, and an alkaline SMase.

Acid sphingomyelinase (ASM or SMPD1) is a lysosomal enzyme responsible for the hydrolysis of sphingomyelin to ceramide and phosphocholine. The ASM gene encodes three proteins, ASM-1, ASM-2, and ASM-3, of which ASM-1 is the only catalytically active enzyme (3,4). ASM-1 can exist as a 70 kDa form as well as a 57 kDa proteoytic product (5). Expression of ASM is induced during monocytic cell differentiation (6). Defects in the ASM gene are associated with type A and type B Niemann-Pick disease (7).

  1. Marchesini, N. and Hannun, Y.A. (2004) Biochem Cell Biol 82, 27-44.
  2. Ruvolo, P.P. (2001) Leukemia 15, 1153-60.
  3. Quintern, L.E. et al. (1989) EMBO J 8, 2469-73.
  4. Schuchman, E.H. et al. (1991) J Biol Chem 266, 8531-9.
  5. Ferlinz, K. et al. (1994) Biochem J 301 ( Pt 3), 855-62.
  6. Langmann, T. et al. (1999) J Lipid Res 40, 870-80.
  7. Levran, O. et al. (1991) Proc Natl Acad Sci USA 88, 3748-52.

Application References

Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!

Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

Products