Acylation stimulating protein

Complement 3 (C3) through its interaction with factors B and D (adipsine) generates C3a. In human body, C3a is rapidily cleaved by carboxypeptidase B or carbxyopeptidase N that remove the carboxyl-terminal arginine to generate C3adesArg.[1] Thus, most of plasmatic C3a is present in C3adesArg form. C3adesArg is more commonly named ASP or acylation-stimulating-protein due to its marked stimulating action on triacylglycerol synthesis in human adipocytes and skin fibroblasts.[2] ASP is also known for its augmentation of glucose transport and inhibiting action on hormone-sensitive lipase. Because of these actions, it is linked to the pathogenesis of obesity.[3] ASP has also been demonstrated to be present at increased levels in patients with obesity,[4] type II diabetes melitus[5] and coronary artery disease.[6]

ASP ligate a specific receptor named C5L2 which is coupled with a G-protein.[7]

References

  1. ^ (Baldo et al. 1993, pp. 1543–1547)
  2. ^ (Cianflone, Sniderman & Walsh Vu1989, pp. 426–430)
  3. ^ (Sniderman, Maslowska & Cianflone 2000, pp. 291–296)
  4. ^ (Maslowska et al. 1999, pp. 679–686)
  5. ^ (Koistinen et al. 2001, pp. 1034–1039)
  6. ^ (Cianflone et al. 1997, pp. 1239–1244)
  7. ^ (Cui et al. 2009, pp. 3207–3217)

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