| First Author | Tadano-Aritomi K | Year | 2003 |
| Journal | J Lipid Res | Volume | 44 |
| Issue | 9 | Pages | 1737-43 |
| PubMed ID | 12810822 | Mgi Jnum | J:120657 |
| Mgi Id | MGI:3707622 | Doi | 10.1194/jlr.M300119-JLR200 |
| Citation | Tadano-Aritomi K, et al. (2003) Seminolipid and its precursor/degradative product, galactosylalkylacylglycerol, in the testis of saposin A- and prosaposin-deficient mice. J Lipid Res 44(9):1737-43 |
| abstractText | Sphingolipid activator proteins (saposins A, B, C, and D) are derived from a common precursor protein (prosaposin) and specifically activate in vivo degradation of glycolipids with short carbohydrate chains. A mouse model of prosaposin deficiency (prosaposin-/-) closely mimics the human disease with an elevation of multiple glycolipids. The recently developed saposin A-/- mice showed a chronic form of globoid cell leukodystrophy, establishing the essential in vivo role of saposin A as an activator for galactosylceramidase to degrade galactosylceramide. Seminolipid, the principal glycolipid in spermatozoa, and its precursor/degradative product, galactosylalkylacylglycerol (GalEAG), were analyzed in the testis of the two mouse mutants by electrospray ionization mass spectrometry. Saposin A-/- mice showed the normal seminolipid level, while that of prosaposin-/- mice was approximately 150% of the normal level at the terminal stage. In contrast, GalEAG increased up to 10 times in saposin A-/- mice, whereas it decreased with age in the wild-type as well as in prosaposin-/- mice. These analytical findings on the two saposin mutants may shed some light on the physiological function of seminolipid and GalEAG. |
