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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 Kits (34) and Sphingomyelin phosphodiesterase 1, Acid Lysosomal Proteins (11) and many more products for this protein.
Showing 10 out of 69 products:
Cow (Bovine) Polyclonal SMPD1 Primary Antibody for WB - ABIN2776371
Zeidan, Jenkins, Hannun: Remodeling of cellular cytoskeleton by the acid sphingomyelinase/ceramide pathway. in The Journal of cell biology 2008
Human Polyclonal SMPD1 Primary Antibody for FACS, IHC (p) - ABIN656161
Ullio, Casas, Brunk, Sala, Fabriàs, Ghidoni, Bonelli, Baccino, Autelli: Sphingosine mediates TNF?-induced lysosomal membrane permeabilization and ensuing programmed cell death in hepatoma cells. in Journal of lipid research 2012
results provide evidence that translocated lysosomal V1 H(+)-ATPase (show ATP6AP1 Antibodies) 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.
A comprehensive updated review of already reported and newly identified SMPD1 variants of Niemann-Pick Types A and B disease has been presented. (Review)
a conserved haplotype and shared 280 Kb region around the SMPD1 gene was observed in the patients analyzed, indicating that the variant originated from a common ancestor
ASM activation may be involved in the pathophysiology of Kawasaki disease
These results indicate that increased EGR1 (show EGR1 Antibodies)/3 and ASMase expression play an important role in cellular ceramide increase by RSV treatment.
The results of this study suggested that disruptive mutations in SMPD1 constitute a risk factor for parkindon disease.
This is the first evidence that supports the possibility that sphingolipid metabolism is affected via the induction of ASMase by the Nrf2 (show GABPA Antibodies) pathway.
ASM has a pivotal role in adaptive immune T-cell responses.
Patterns of alternatively spliced SMPD1 transcripts are significantly different in patients with systemic inflammatory response syndrome and severe sepsis/septic shock compared to control subjects allowing discrimination of respective disease entity.
The mechanisms by which pyocyanin induces the release of mitochondrial ROS (show ROS1 Antibodies) and by which ROS (show ROS1 Antibodies) induce neutrophil death via mitochondrial acid sphingomyelinase was identified.
Results show four novel mutations in SMPD1 in Iranian patients with type A or B Niemann-Pick disease extending the genotypic spectrum of the disease.
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 reduction of membrane sphingomyelin (SM)is due to transcriptional upregulation of neutral sphingomyelinase (show SMPD2 Antibodies) (NSM) through active RhoA (show RHOA Antibodies).
Intravenous injection of B16F10 melanoma cells into wild-type mice resulted in multiple lung metastases, while Asm-deficient mice (Smpd1(-/-) mice) were protected from pulmonary tumor spread.
Acid sphingomyelinase deficiency reduces S. aureus-induced lung edema.
Ceramide production in M-CSF (show CSF1R Antibodies)-deprived macrophages arises from a combination of ASMase activity and de novo synthesis.
aSMase-deficient mouse is the first example in which microglial lipid inclusions are directly related to a loss of retinal function
ASMase deficiency determined resistance to hepatic steatosis mediated by a high fat diet.
results provide the mechanism for dysferlin (show DYSF Antibodies)-mediated repair of skeletal muscle sarcolemma and identify ASM as a potential therapy for dysferlinopathy
Acid sphingomyelinase (ASM) controls autophagy maturation in smooth muscle cells. ASM maintains smooth muscle cell homeostasis and its contractile phenotype. ASM plays a protective role in smooth muscle dysfunction and atherosclerosis.
The action of A-SMase is mediated by the activation of the extracellular signal-regulated kinase, the subsequent proteasomal degradation of the Microphtalmia-associated transcription factor (Mitf (show MITF Antibodies)).
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