anti-Ceramide Synthase 2 (CERS2) Antibodies

Human Ceramide Synthase 2 (CERS2) interaction partners

1. The study demonstrates that miR-98 targets LASS2 and regulates bladder cancer chemoresistance through modulation of mitochondrial function.

2. Data indicate that miR-3658 regulates tumor biological behavior and its downstream molecule signaling pathways through longevity assurance 2 protein (LASS2).

3. Data show that mRNA expression of Cer metabolizing enzyme CERS2 was significantly increased in multiple sclerosis (MS) patients.

4. G0/G1 ratio in LASS2/TMSG1 S248A group was obviously higher than that in LASS2/TMSG1 wild group

5. Study findings suggest that LASS2 inhibits proliferation and induces apoptosis in HepG2 hepatoblastoma cells through the mitochondrial apoptotic, NFkappaB and cell cycle signaling pathways.

6. results indicate that miR-3622a promotes the proliferation and invasion of bladder cancer cells by downregulating LASS2.

7. As potential molecular markers for bladder carcinoma, both TWIST1 and LASS2 transcripts seem to play role during the tumorigenesis and development of bladder cancer.

8. Results show that silencing of ATP6V0C in highly metastatic prostate cancer (PC) cell lines, inhibited V-ATPase activity, which coincided with the inhibition of cell migration and invasion in vitro, as well as a marked decrease in the expression of LASS2/TMSG1 probably through positive feedback.

9. CerS2-knockdown via CRISPR-Cas9 technology in cultured colon epithelial cells impaired barrier function.

10. Low expression of LASS2 and TGFB1 contributes to the aggressiveness and poor prognosis of hepatocellular carcinoma, and may represent a novel prognostic biomarker for hepatocellular carcinoma patients.

11. ASGR1 can inhibit the activity of V-ATPase by interacting with LASS2, thereby suppressing the metastatic potential of hepatoma cells.

12. 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.

13. Data show that 1-acylglycerol-3-phosphate O-acyltransferase 9 (AGPAT9) inhibit cell growth by regulating expression of KLF4/LASS2/V-ATPase proteins in breast cancer.

14. these results indicate that miR-9 upregulation might be associated with malignant phenotype of bladder cancer. miR-9 promotes chemoresistance of bladder cancer cells by target LASS2.

15. Data show that CERS2 expression was markedly different between various breast cancer cells and inversely correlated with cell invasion.

16. silencing of TMSG1 increased V-ATPase activity, decreased extracellular pH and in turn the activation of secreted MMP-2, which ultimately promoted metastasis capacity of breast cancer cell.

17. Results confirmed that TMSG1 is a potential metastasis suppressor gene, and suggested that the mechanism involved the induction of apoptosis and inhibition of cell proliferation via a caspase-dependent mitochondrial pathway.

18. the vacuolar ATPase (V-ATPase) activity and extracellular hydrogen ion concentration were significantly decreased and the activity of secreted matrix metalloproteinase-2 (MMP-2) was downregulated in MCF-7 cells overexpressing LASS2/TMSG1

19. the inhibitory effect of the LASS2 on growth, invasion and metastasis of prostate cancer cells

20. 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.

Mouse (Murine) Ceramide Synthase 2 (CERS2) interaction partners

1. Our findings indicate that LASS2 plays an important role in the pathogenesis of diet-induced hepatic steatosis

2. Gene expression analyses in livers of transgenic mouse mutants revealed that inactivation of CerS2 catalytic activity largely affects transcription of genes involved in lipid metabolism and cell division and is associated with the formation of hepatocellular carcinoma in 6 to 8-week-old mice.

3. Deficiency of CerS2 influences intestinal barrier function and the severity of experimental colitis and may represent a potential mechanism for inflammatory bowel disease pathogenesis.

4. LASS2 plays an important role in efficient liver regeneration in response to partial hepatectomy.

5. Deletion of CerS2 strongly reduced very long-chain ceramides (Cer24:0, 24:1) but concomitantly increased long-chain ceramides and sphinganine in plasma and colon tissue. In naive CerS2(-/-) mice, the expression of tight junction proteins including ZO-1 was almost completely lost in the colon epithelium, leading to increased membrane permeability. Ceramide synthase 2 deficiency aggravates dextran induced colitis in mice.

6. this study shows that Cers2 limits the levels of S1P in thymus and blood to maintain functional S1P gradients that mediate thymocyte emigration into the circulation

7. that only LCBs, the substrates common for all of the CerS isoforms, but not ceramides and complex sphingolipids, were restored to the wild-type levels in the Cers2-rescued Cers1 mutant mouse brains.

8. CerS1, -2, and -6 are hyperacetylated in the mitochondria of SIRT3-null mice.

9. 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.

10. Haploinsufficiency for this enzyme altered the pattern of ceramide acylation in the liver without affecting total ceramide levels, replacing very-long-chain ceramides with long-chain C16-ceramides.

11. Development of pheochromocytoma in ceramide synthase 2 null mice

12. our data strongly indicate that G-CSF-induced CXCR2 expression is regulated in a CerS2-dependent manner and that CerS2 thereby promotes the migration of neutrophils, thus, contributing to inflammation and the development of EAE and MS.

13. study is the first comparison of spatial distribution between SM molecular species and CerS isoforms, and revealed their distinct association in the brain.

14. Data indicate that the augmented rate of death of ceramide synthase 2 (CerS2) null mice is due to elevated levels of tumor necrosis factor alpha (TNFalpha) secretion as a result of enhanced activity of TNFalpha-converting enzyme (TACE).

15. CerS2-deficient kidneys were completely depleted of phytosphingosine-containing cortical sulfatides without any compensatio

16. we first report that Lass2 deficiency caused the downregulation of miR-694 and the upregulation of its target gene Tnfaip3 in vivo in mice, which may be related to a high risk of occurrence of hepatocellular carcinoma

17. The identification of specific cell types in which CerS2 protein is expressed is prerequisite to further mechanistic characterization of phenotypic abnormalities exhibited by CerS2-deficient mice.

18. Lass2 is a protective gene against diethylnitrosamine-induced liver tumorigenesis; and upregulation of the TGF-beta1-Smad4-PAI-1 axis may contribute to the vulnerability of Lass2-knockout mice to diethylnitrosamine.

19. Data indicate that oxidized phospholipids (OxPLs)-induced ceramide synthases (CerS1-Cers6) activity in macrophages is responsible for the accumulation of ceramide.

20. Protection of a ceramide synthase 2 null mouse from drug-induced liver injury: role of gap junction dysfunction and connexin 32 mislocalization.