EC Number   |
General Information |
Reference |
|---|
    2.3.1.24 | evolution |
Lass proteins are known to contain a TLC [TRAM/Lag1p/ CLN8 (ceroid-lipofuscinoses, neuronal 8)] homology domain with the Lag1 motif. Lass family members Lass2, Lass4 and Lass5, but not Lass1, also contain a HOX (homeobox) domain |
752700 |
| 2.3.1.24 | evolution |
murine Lass6 is a member of the mouse Lass family. It exhibits the highest identity with Lass5 (61.7% identity and 68.2% similarity) and the lowest identity with Lass1 (16.0% identity and 27.4%similarity). Lass proteins are known to contain a TLC [TRAM/Lag1p/ CLN8 (ceroid-lipofuscinoses, neuronal 8)] homology domain with the Lag1 motif. Lass family members Lass2, Lass4 and Lass5, but not Lass1, also contain a HOX (homeobox) domain |
752700 |
| 2.3.1.24 | evolution |
schlank belongs to the ceramide family, schlank falls into the Lass family, phylogenetic tree of Lass family members and TRAM proteins, overview |
753417 |
| 2.3.1.24 | malfunction |
ceramide synthase-specific inhibitor fumonisin B1 suppresses hypoxia-reoxygenation-induced ceramide generation and provides protection against hypoxia-reoxygenation-induced EndoG release, DNA fragmentation, and cell death |
752435 |
| 2.3.1.24 | malfunction |
CerS6 knockdown might decrease apoptosis compared to normal irradiated HeLa cells |
753223 |
| 2.3.1.24 | malfunction |
decreased enzyme expression induces endoplasmic reticulum stress and apoptosis in head and neck squamous carcinoma cells but not in A-549, MCF-7, or SW-480 cells, which are derived from lung, breast, and colon cancer, respectively, detailed overview |
736471 |
| 2.3.1.24 | malfunction |
disruption of the de novo pathway of sphingolipid biosynthesis may be a critical in the diseases that have been associated with consumption of fumonisins. Fusarium moniliforme causes equine leucoencephalomalacia, porcine pulmonary edem syndrome, and liver cancer in rats |
-, 754040 |
| 2.3.1.24 | malfunction |
inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Combined knockdown of CerS5 and CerS6 is able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation, CerS6 knockdown clearly decreases C14:0- and C16:0-Cer basally and reduces their accumulation following UV-C irradiation, CerS5 knockdown has no appreciable effects on Cer levels. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells |
754096 |
| 2.3.1.24 | malfunction |
inhibition of CerS is able to protect from cell death. Moreover, this protection occurs downstream or independently of mitochondrial permeabilization. Inhibition of CerS greatly inhibits plasma membrane permeabilization. Combined knockdown of CerS5 and CerS6 is able to decrease long-chain ceramide accumulation and plasma membrane permeabilization. Individual CerS knockdown does not significantly inhibit total ceramide accumulation, knockdown of CerS6 actually even increases total ceramide levels. CerS5 knockdown has no appreciable effects on Cer levels. Inhibition of CerS but not de novo synthesis inhibits plasma membrane rupture that is not specific to UV-C irradiation or MCF-7 cells |
754096 |
| 2.3.1.24 | malfunction |
knockdown using fumonisin B 1 or LASS5 small, interfering RNA reduced ceramide synthase activity by 78% or 45%, respectively. Exogenously expressed LASS5 in lung epithelia is membrane-associated, triggering increased ceramide synthesis. Compared with control cells, cells transfected with LASS5 siRNA exhibit a 43% increase in rates of phosphatidylcholine synthesis |
-, 754360 |
