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S1PSphingosine 1-Phosphate
S1PSite-1 Protease
S1PSPH 1-Phosphate
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S1P is a ceramide-induced apoptotic inhibitor, which can prevent chemotherapy induced apoptotic follicle loss in preclinical models, as well as imatinib and granulocyte colony-stimulating factor (G-CSF) (49).
They found that there are already some drugs in use that alter S1P signaling.
Following transplantation, follicles loss is one of the results of non-efficient revascularization of the graft and tissue ischemia; however, these consequences could be prevented by using S1P, Vascular Endothelial Growth Factor (VEGF), Anti Mullerian Hormone (AMH), antioxidants and innovative stem cells therapy approaches (22, 57-61).
"Siponimod reduced the risk of disability progression with a safety profile similar to that of other S1P modulators and is likely to be a useful treatment for SPMS," the authors write.
S1P is known to be a survival factor for a variety of cell types.
Cinamon et al., "Lymphocyte egress from thymus and peripheral lymphoid organs is dependent on S1P receptor 1," Nature, vol.
In the Golgi apparatus, ATF6 is cleaved by site 1 and site 2 proteases (S1P and S2P) at the transmembrane site to generate a transcriptionally active polypeptide.
After dissociation, ATF6 is transferred to the Golgi complex where it is cleaved by site-1 (S1P) and S2P proteases and then translocated to the nucleus as an activated transcription factor.
Peavy et al., "Common signaling pathways link activation of murine PAR-1, LPA, and S1P receptors to proliferation of astrocytes," Molecular Pharmacology, vol.
BS, including sphingosine (SP) and sphingosine-1phosphate (S1P)[9, a biologically important class of compounds, have essential functions including regulation of cell growth, differentiation, proliferation, adhesion, migration, and apoptosis as well as inflammation and angiogenesis [10].
One of the most important breakthroughs in this field was the discovery of the role of sphingosine-1 phosphate (S1P) which acts via its receptors S1PR1 and S1PR2 present on monocytes, as a vital regulator of monocyte bone homing in mice.
Moreover, sphingolipid metabolites, such sphingosine1phosphate (S1P), promote the switching phenotype of mouse macrophages from M1- to M2-like state, by activating S1P1 receptor [208].