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Data suggest that IL-1beta induction of ceramide, cytokine expression, and leukocyte influx are regulated by brain neutral sphingomyelinase II protein (nSMase).
The enzymes involved in sphingolipid metabolism are expressed abnormally in B cells from lupus-prone mice. TLR signaling induced the abnormal expression of sphingomyelin phosphodiesterase 3 (SMPD3). TLR signaling also induced the transport of SMPD3 from the Golgi apparatus. Furthermore, the dysfunction of SMPD3 enhanced TLR-induced inflammatory response of B cells and macrophages in turn.
SMPD3 in the regulation of the protein vesicular secretory pathway may become a diagnostic target in the etiology of unknown forms of juvenile growth and developmental inhibition.
Study provides evidence that Smpd3 expression in both chondrocytes and osteoblasts is required for normal endochondral bone development.
these results highlight the role of nSMase2 in apoptosis evoked by nutrient starvation that could contribute to the delayed apoptosis of hypertrophic chondrocytes in the growth plate, and emphasize the antiapoptotic properties of HAS2
nSMase2 activation is required for the development of infection-induced diaphragm calpain activation and muscle weakness.
These results suggest that OTC is a potent stimulant of nSMase-2 expression and that there may be unanticipated complications of OTC supplementation.
Src and p38 mitogen-activated protein kinase activities are critical for regulating nSMase2 phosphorylation.
Smpd3 was identified as a redox-sensitive enzyme, whose basal activity mediated changes in its oligomeric state.
Data confirms a crucial pro-survival role for SMPD3 during embryonic development.
Smpd3/nSMase2-ceramide-Akt signaling axis negatively regulates BMP-induced chondrocyte maturation.
The H2O2-induced src/PDGFRbeta/SK1 signaling cascade was impaired in nSMase2-deficient fro/fro cells and was rescued by exogenous C2Cer that activated src/PDGFRbeta/SK1.
Neutral sphingomyelinase 2 deficiency is associated with lung anomalies similar to emphysema.
a requirement for nSMase2-mediated cancer cell exosomal miRNAs in the regulation of metastasis through the induction of angiogenesis in inoculated tumors.
Smpd3 expression in odontoblasts is required for tooth mineralization.
Data show that although sphingomyelin (SM) accumulated in both ASMase(-/-) and fro/fro (NSMase2(-/-)) fibroblasts, the reduction of ceramides was more dramatic in fro/fro cells.
NSMase2/Cer are the key mediators of the regulation of HA synthesis, via microdomains and the Akt/mTOR pathway
initial structure/function insights regarding nSMase2 phosphorylation
The Col1a1-Smpd3 mice, in which osteoblast-specific expression of Smpd3 corrected the bone abnormalities observed in fro/fro embryos without affecting the cartilage phenotype.
interactions between nSMase2 and anionic phospholipids
the DK switch regulates ceramide generation by nSMase2 and is governed by an allosteric interdomain interaction at the membrane interface
The enzymes involved in sphingolipid metabolism are expressed abnormally in B cells from SLE patients. TLR signaling induced the abnormal expression of sphingomyelin phosphodiesterase 3 (SMPD3). TLR signaling also induced the transport of SMPD3 from the Golgi apparatus. Furthermore, the dysfunction of SMPD3 enhanced TLR-induced inflammatory response of B cells and macrophages in turn.
ATRA regulates nSMase2 transcriptionally through the retinoic acid receptor-alpha, but this is independent of previously identified transcriptional regulators of nSMase2 (Sp1, Sp3, Runx2) and is not through increased promoter activity.
Overexpression of Smpd3 induced cytodifferentiation of HPDL cells, which could be suppressed by an inhibitor of its protein product, nSMase2. In addition,Smpd3 harboring a SNP (rs145616324) showed no activity and failed to induce cytodifferentiation of HPDL cells. Together, these findings suggest that Smpd3 plays an important role in the osteoblastic differentiation of HPDL cells.
low oxLDL concentration triggers sprouting angiogenesis that involves ROS-induced activation of the neutral sphingomyelinase-2/sphingosine kinase-1 pathway, and is effectively inhibited by GW4869.
nSMase2 is a novel p53 target gene, regulated by the DNA damage pathway to induce cell growth arrest.
nSMase2 involvement in cellular processes including inflammatory signaling, exosome generation, cell growth, and apoptosis, which in turn play important roles in pathologies such as cancer metastasis, Alzheimer's disease
SMPD3 plays an important role in the release of microRNAs into extracellular spaces.
The data shows that nSMase3 acts as a signaling nSMase in skeletal muscle that is essential for TNF-stimulated oxidant activity.
This is the first report on the critical role of ceramide generated by nSMase2 in stem cell ciliogenesis and differentiation.
We found upregulation of specific sphingolipid enzymes, namely sphingomyelin synthase 1 (SMS1), sphingomyelinase 3 (SMPD3), and glucosylceramide synthase (GCS) in the endometrium of endometriotic women.
MMP2 and neutral sphingomyelinase-2 play a role in vasculopathy triggered by a humoral immune response in transplants.
NSMase-2- and PP2A-dependent regulation of IRAK-1 degradation is a novel mechanism to fine tune the magnitude of IL-1beta response.
Neutral sphingomyelinase 2 (nSMase2) is the primary neutral sphingomyelinase isoform activated by tumour necrosis factor-alpha.
nSMase2 is a major component of ATRA-induced growth arrest of MCF-7 cells; S6K is a novel downstream target of nSMase2
Neutral sphingomyelinase 2 (nSMase2) is a phosphoprotein regulated by calcineurin (PP2B)
Data show DA remarkably increased the NSMase2 message and protein, whereas little change in NSMase1 and NSMase3 mRNAs.
Catalyzes the hydrolysis of sphingomyelin to form ceramide and phosphocholine. Ceramide mediates numerous cellular functions, such as apoptosis and growth arrest, and is capable of regulating these 2 cellular events independently. Also hydrolyzes sphingosylphosphocholine. Regulates the cell cycle by acting as a growth suppressor in confluent cells. Acts as a regulator of postnatal development and participates in bone and dentin mineralization. Overexpression enhances cell death, suggesting that it may be involved in apoptosis control. May be involved in IL-1-beta-induced JNK activation in hepatocytes. May act as a mediator in transcriptional regulation of NOS2/iNOS via the NF- kappa-B activation under inflammatory conditions.
sphingomyelin phosphodiesterase 3, neutral membrane (neutral sphingomyelinase II)
, neutral sphingomyelinase 2
, neutral sphingomyelinase II
, sphingomyelin phosphodiesterase 3
, confluent 3Y1 cell-associated 1
, confluent 3Y1 cell-associated protein 1
, neutral sphingomyelin phosphodiesterase 3