Cell Signaling Technology

Product Pathways - Ca / cAMP / Lipid Signaling

nSMase1 Antibody #3867

Applications Reactivity Sensitivity MW (kDa) Source
W H Mk Endogenous 50 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

nSMAase Antibody detects endogenous levels of total nSMase1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala200 of human nSMase1.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using nSMase1 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.

nSMase1 (also termed SMPD2) is a Mg++-dependent neutral SMase that is widely expressed and predominantly localized to the endoplasmic reticulum (3,4). This protein has also been shown to have lyso-platelet activating factor (PAF) phospholipase C activity (5). A second neutral SMase, nSMase2 (also termed SMPD3) is predominantly expressed in the brain (6). The activity of neutral SMases is regulated by oxidative stress, chemotherapeutic drugs, inflammatory cytokines, and apoptotic stimuli (1). Analysis of single and double knockouts of the SMPD2 and SMPD3 has revealed that loss of both genes leads to complete loss of neutral SMase activity with developmental defects observed with loss of nSMase2 (7,8).

  1. Marchesini, N. and Hannun, Y.A. (2004) Biochem Cell Biol 82, 27-44.
  2. Ruvolo, P.P. (2001) Leukemia 15, 1153-60.
  3. Tomiuk, S. et al. (1998) Proc Natl Acad Sci U S A 95, 3638-43.
  4. Tomiuk, S. et al. (2000) J Biol Chem 275, 5710-7.
  5. Sawai, H. et al. (1999) J Biol Chem 274, 38131-9.
  6. Hofmann, K. et al. (2000) Proc Natl Acad Sci U S A 97, 5895-900.
  7. Zumbansen, M. and Stoffel, W. (2002) Mol Cell Biol 22, 3633-8.
  8. Stoffel, W. et al. (2005) Proc Natl Acad Sci U S A 102, 4554-9.

Application References

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Companion Products

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

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