EC Number   |
General Information |
Reference |
|---|
   3.1.3.B4 | malfunction |
disruption of the Sac1-Vps74 interface results in a broader distribution of phosphatidylinositol 4-phosphate within the Golgi apparatus and failure to maintain residence of a medial Golgi mannosyltransferase |
732218 |
| 3.1.3.B4 | malfunction |
genomic ablation of the enzyme causes perturbation on transferrin and integrin recycling as well as defects in cell migration |
751173 |
| 3.1.3.B4 | malfunction |
RNAi-mediated knockdown of SAC1 causes changes in Golgi morphology and mislocalization of Golgi enzymes. Enzymes involved in glycan processing, such as mannosidase II and Nacetylglucosamine transferase I, redistribute to aberrant intracellular structures and to the cell surface in SAC1 knockdown cells. SAC1 depletion also induces a unique pattern of Golgi-specific defects in N- and O-linked glycosylation, phenotype, overview. SAC1 knockdown allows alpha2,6 sialyltransferase to more effectively compete against Core 2 transferase |
716968 |
| 3.1.3.B4 | malfunction |
the rate of biosynthesis of phosphatidylserine in sac1 deleted cells is significantly lower than that in wild-type cells. An abnormal phosphatidylserine distribution in sac1 deleted cells is observed when a specific probe for phosphatidylserine is expressed |
732981 |
| 3.1.3.B4 | metabolism |
the enzyme regulates oxysterol-binding protein activity |
752309 |
| 3.1.3.B4 | physiological function |
deletion of SAC1 encoding a PtdIns(4)P phosphatase, increases levels of most sphingolipid species, including sphingoid bases, sphingoid base phosphates, and phytoceramide. Deletion of SAC1 dramatically reduces inositol phosphosphingolipids, which result from the addition of a PtdIns-derived phosphoinositol head group to ceramides through Aur1p. Deletion of SAC1 decreases PtdIns dramatically in both steady-state and pulse labeling studies, suggesting that the observed effects on sphingolipids may result from modulation of the availability of PtdIns as a substrate for Aur1p |
709078 |
| 3.1.3.B4 | physiological function |
in Drosophila development, the enzyme regulates JNK signaling, attenuates Hedgehog signaling, and regulates axon guidance in the embryonic central nervous system. The enzyme is required for postembryonic synaptic maturation and neuronal cell maintenance |
752310 |
| 3.1.3.B4 | physiological function |
mutant Sac1 C392S is a potent inhibitor of fusion of coat protein complex II, COPII, vesicles with Golgi compartments whereas the Sac1 WT protein does not display an equal inhibitory effect. The inhibitory effects of Sac1 wild-type are likely due to catalytic activity of the enzyme and not due to lipid ligand binding. Pretreatment of acceptor membranes with 50 microM Sac1 wild-type also causes an accumulation of diffusible vesicles in budding reactions and strong inhibition of SNARE complex formation |
716168 |
| 3.1.3.B4 | physiological function |
SAC1 organizes phosphatidylinositol-4-phosphate distribution between the Golgi complex and the trans-Golgi-network, which is instrumental for resident enzyme partitioning and Golgi morphology |
716968 |
| 3.1.3.B4 | physiological function |
the enzyme is crucial for normal eye development and required for promoting microtubule stability |
750385 |
