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The protein encoded by SMPD1 is a lysosomal acid sphingomyelinase that converts sphingomyelin to ceramide. Additionally we are shipping Sphingomyelin phosphodiesterase 1, Acid Lysosomal Antibodies (72) and Sphingomyelin phosphodiesterase 1, Acid Lysosomal Kits (34) and many more products for this protein.
Showing 10 out of 12 products:
results provide evidence that translocated lysosomal V1 H(+)-ATPase (show ATP6AP1 Proteins) contributes to formation of local acid microenvironment to facilitate activation of ASM and consequent membrane raft(MR) aggregation, forming MR redox signalosomes and mediating redox signaling in coronary endothelial cells
Acid sphingomyelinase activation serves as a triggering mechanism, leading to fusion of membrane proximal lysosomes into lipid rafts clusters on the cell membrane of coronary arterial endothelial cells.
Report lysosomal targeting and trafficking of acid sphingomyelinase to lipid raft platforms in coronary endothelial cells.
this is the largest study on mutation analysis of patients with ASM-deficient Niemann-Pick disease reported in literature and also the first study on the SMPD1 gene mutation spectrum in India.
ASM and ceramides, together with STX6 (show STX6 Proteins) and cholesterol, constitute a new regulatory mechanism for the exit of Met from the Golgi during its biosynthetic route.
the p.Ala359Asp mutation causes structural alterations in the hydrophobic environment where ASM is located, decreasing its enzymatic activity
Airway cells with lower SMPD1 activity increases neutrophil chemotaxis towards them.
The results identify acid sphingomyelinase as a novel target of Lycium Chinense berries to decrease saturated/unsaturated fatty acid sphingomyelin ratio, known to be useful for cell health. Consistent with these data, the berries regulate specifically gene expression to protect cells from apoptosis.
ASMase mediated the 50-Hz MF-induced EGFR (show EGFR Proteins) clustering via ceramide which was produced from hydrolyzation on lipid rafts
ASM is a negative regulator of regulatory T Cell development.
We report on an infant with a new frameshift mutation (c.575dupG) of the SMPD1 gene.
Seven novel mutations (c.518-519insT, c.562_563insC, c.792Gdel, c.949G>A, c.1487_1499delACCGTGTGTACCA, c.1495T>C and c.1670T>C) of the SMPD1 gene were identified in four patients. Only one fetus had two mutations of the SMPD1 gene of amniocytes
The results show that mice lacking acid sphingomyelinase had a significant increase in myelin recovery and a significantly higher oligodendrocyte cell count after 2 weeks remyelination compared to wildtype littermates.
These findings suggest that the paradoxical antidepressant effects of alcohol in depressed organisms are mediated by ASM and its control of sphingolipid homeostasis
this study shows that Asm-deficient mice develop brain measles virus infection that is consistent with an enhanced Treg frequency and/or activity
K8/K18 (show KRT18 Proteins)-dependent PKCdelta (show PKCd Proteins)- and ASMase-mediated modulation of lipid raft size can explain the more prominent FasR-mediated signaling resulting from K8/K18 (show KRT18 Proteins) loss.
Aged platelets elicit lung injury in primed recipient mice, which can be alleviated by pharmacological inhibition or genetic deletion of acid sphingomyelinase.
Transgenic ASM female, but not male, mice showed an impaired social preference and a depressive- and anxiogenic-like phenotype, which could be normalized by amitriptyline treatment.
this study shows decreased T cell numbers in Asm-deficient, burn-injured, and microbiota-depleted mice
These findings indicate a novel pathway in tumor metastasis, i.e., tumor cell mediated activation of P-selectin (show SELP Proteins) in platelets, followed by activation and secretion of Asm and in turn release of ceramide and tumor metastasis. The data suggest that p38 MAPK (show MAPK14 Proteins) acts downstream from P-selectin (show SELP Proteins) and is necessary for the secretion of Asm.
Inhibition of ASM in diabetic CACs improved membrane fluidity and homing of these cells to damaged retinal vessels. Collectively, these findings indicate that selective modulation of sphingolipid metabolism in BM-derived cell populations in diabetes normalizes the reparative/proinflammatory cell balance and can be explored as a novel therapeutic strategy for treating diabetic retinopathy.
Inhibition of the smpd1 by antidepressants prevents stress-induced phosphorylation/activation of p38K indicating that antidepressants indirectly target p38K via the acid sphingomyelinase/ceramide system.
The protein encoded by this gene is a lysosomal acid sphingomyelinase that converts sphingomyelin to ceramide. The encoded protein also has phospholipase C activity. Defects in this gene are a cause of Niemann-Pick disease type A (NPA) and Niemann-Pick disease type B (NPB). Multiple transcript variants encoding different isoforms have been identified.
, acid sphingomyelinase
, sphingomyelin phosphodiesterase 1, acid lysosomal (acid sphingomyelinase)
, sphingomyelin phosphodiesterase 1, acid lysosomal
, sphingomyelin phosphodiesterase 1
, sphingomyelin phosphodiesterase-like