anti-Ceramide Synthase 2 (CERS2) Antibodies

Human Ceramide Synthase 2 (CERS2) interaction partners

1. Results show that silencing of ATP6V0C (show ATP6V0C Antibodies) in highly metastatic prostate cancer (PC) cell lines, inhibited V-ATPase (show ATP6V1H Antibodies) 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.

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

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

4. ASGR1 (show ASGR1 Antibodies) can inhibit the activity of V-ATPase (show ATP6V1H Antibodies) by interacting with LASS2, thereby suppressing the metastatic potential of hepatoma cells.

5. Data show that 1-acylglycerol-3-phosphate O-acyltransferase 9 (AGPAT9 (show AGPAT9 Antibodies)) inhibit cell growth by regulating expression of KLF4 (show KLF4 Antibodies)/LASS2/V-ATPase (show ATP6V1H Antibodies) proteins in breast cancer.

6. these results indicate that miR (show MLXIP Antibodies)-9 upregulation might be associated with malignant phenotype of bladder cancer. miR (show MLXIP Antibodies)-9 promotes chemoresistance of bladder cancer cells by target LASS2.

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

8. silencing of TMSG1 increased V-ATPase (show ATP6V1H Antibodies) activity, decreased extracellular pH and in turn the activation of secreted MMP-2 (show MMP2 Antibodies), which ultimately promoted metastasis capacity of breast cancer cell.

9. 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 (show CASP3 Antibodies)-dependent mitochondrial pathway.

10. the vacuolar ATPase (V-ATPase (show DNAH8 Antibodies)) activity and extracellular hydrogen ion concentration were significantly decreased and the activity of secreted matrix metalloproteinase-2 (MMP-2 (show MMP2 Antibodies)) was downregulated in MCF-7 cells overexpressing LASS2/TMSG1

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

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

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

3. 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 (show TJP1 Antibodies) was almost completely lost in the colon epithelium, leading to increased membrane permeability. Ceramide synthase 2 deficiency aggravates dextran induced colitis in mice.

4. this study shows that Cers2 limits the levels of S1P (show S1PR1 Antibodies) in thymus and blood to maintain functional S1P (show S1PR1 Antibodies) gradients that mediate thymocyte emigration into the circulation

5. 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 (show CERS1 Antibodies) mutant mouse brains.

6. CerS1 (show CERS1 Antibodies), -2, and -6 are hyperacetylated in the mitochondria of SIRT3 (show SIRT3 Antibodies)-null mice.

7. 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.

8. Development of pheochromocytoma in ceramide synthase 2 null mice

9. our data strongly indicate that G-CSF (show CSF3 Antibodies)-induced CXCR2 (show CXCR2 Antibodies) 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.

10. 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 (show TNF Antibodies)) secretion as a result of enhanced activity of TNFalpha (show TNF Antibodies)-converting enzyme (TACE (show ADAM17 Antibodies)).