-
both SphK1 overexpression and S1P addition increased mTOR phosphorylation as shown by ELISA, while S1PR2 inhibition had the inverse effect. These data suggest that CerS6 and SphK1 regulate mTOR signaling in breast cancer cell proliferation. Moreover, mTOR activity can be regulated by the balance between S1P and C16ceramide, which is generated by CerS6.
-
ceramide synthase (CerS)6 was specifically up-regulated in zone 3 hepatocytes in alcoholic steatosis
-
This study has shown that by direct transcriptional activation of CerS6, p53 can regulate specific ceramide biosynthesis, which contributes to the pro-apoptotic cellular response.
-
silencing of CerS6 induced the increased expression of GLUT1, which downregulated the expression of WNT5A and enhanced the invasion and proliferation of melanoma cells.
-
Identification of CerS6 and ceramide pathways as a novel Methotrexate target.
-
These results suggest that the phosphorylation of ceramide synthases may be a key regulatory point in the control of the distribution and levels of sphingolipids of various acyl-chain lengths.
-
stichoposide D inhibits growth of experimental leukemia by activating Fas/ceramide synthase 6/p38 kinase in lipid rafts
-
CERS6-dependent ceramide synthesis and maintenance of ceramide in the cellular membrane are essential for lamellipodia formation and metastasis.
-
Data indicate that ceramide synthase 6 (CerS6) expression is upregulated in leukocytes from multiple sclerosis (MS) patients.
-
On the basis of its pivotal role in regulating cell death upon COX dysfunction, CerS6 might potentially represent a novel target for therapeutic intervention in mitochondrial diseases caused by COX dysfunction.
-
Taken together, these results suggest that increased expression of CerS6 can mediate transcriptional activation of acid ceramidase in a JNK-dependent manner that is independent of CerS6 activity.
-
CerS6 as a novel epithelial-mesenchymal transition-regulated gene that has a pivotal role in the regulation of cell migration.
-
Upregulation of CERS6 in an experimental autoimmune encephalomyelitis model is sex dependent.
-
Co-expression of CerS2 with CerS4/CerS6 reversed the inhibitory effect of long chain ceramides on cell proliferation and the induction of apoptosis. we detected no effect on cell proliferation.
-
folate withdrawal also induced CerS6/C16-ceramide elevation accompanied by p53 accumulation. Overall, these novel findings link folate and de novo ceramide pathways in cellular stress response.
-
The transiently increased expression of ceramide synthase (CerS6) correlates to the clinical finding that C(16:0)-Cer levels are increased 1.9-fold in cerebrospinal fluid of multiple sclerosis patients.
-
Alteration of ceramide synthase 6/C16-ceramide induces activating transcription factor 6-mediated endoplasmic reticulum (ER) stress and apoptosis via perturbation of cellular Ca2+ and ER/Golgi membrane network
-
ionizing radiation induces de novo synthesis of ceramide to influence HeLa cell apoptosis by specifically activating CerS isoforms 2, 5, and 6 that generate opposing anti- and pro-apoptotic ceramides in mitochondrial membranes.
-
CerS2 and CerS6 mRNA was significantly elevated in breast cancer tissue compared to paired normal tissue, with approximately half of the individuals showing elevated CerS2 and CerS6 mRNA.
-
Findings indicate that mda-7/IL-24 induces PERK activation that triggers production of ceramide, ceramide synthase 6 and thioredoxin, which in turn promote glioma cell autophagy and cell death.
