SphKSphingosine Kinase
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In addition, the IPCinduced cardioprotective effect may also result from PKC activation and SPHK activation to enhance intracellular S1P levels in rat heart [80].
Tissues also generate protective S1P, likely by activation of ceramidase and/or SPHK, during very early phases of ischemia, which may cause transient reduction of ceramide and S1P-induced inhibition of SMase.
Cells were first treated with a selective SphK inhibitor (iSK, 5 [micro]M), that blocks S1P synthesis, in order to evaluate the contribution of S1P inside-out signalling or with exogenous S1P (exoS1P, 1 [micro]M).
Activation of various plasma membrane receptors, such as the PDGFR [22, 51], the FceRI, and FcyRI [52] as well as the C5aR [53], was found to rapidly increase intracellular S1P production through the stimulation of the SphK. Inhibition of SphK stimulation strongly reduced or even prevented cellular events such as receptor-stimulated DNA synthesis, [Ca.sup.2+] mobilization, and vesicular trafficking.
The evidence for SphK inducing production of COX-2 during parturition was uncovered by Serrano-Sanchez et al.
En contraparte, los niveles de S-1-P y la actividad de la enzima esfingosina quinasa, son aumentados, entre otros, por el tratamiento con los factores de crecimiento EGF, PDGF y NGF, cuyo efecto proliferativo es inhibido competitivamente por inhibidores de SphK, por lo que se ha asociado este esfingolipido a efectos proliferativos (65).
LEC-specific deletion of SphK1 in the SphK2 knockout mouse inhibited lymphatic vessel maturation, indicating that SphKs and S1P in LECs are required for proper development of lymphatic vessels [3].
Ceramidases promote carcinogenesis by disturbing the ceramide/S1P ratio, permitting phosphorylation of sphingosine by SPHKs, and determine the efficacy of cancer therapy.
Sphingosine kinases (SPHK), including SPHK1 and SPHK2, are a conserved lipid kinase family that catalyzes S1P formation.
FTY720 is now considered as a competitive inhibitor of SphK1 [27], while some showed that FTY720 could inhibit the activities of both SphK1 and SphK2 and suppress the phosphorylation of sphingosine by SphKs, resulting in decreased S1P production [28].
Erythrocytes and platelets are major contributors to blood S1P, as both of these cell types are exposed to circulating sphingosine, contain SphKs activity, and lack most of the S1P-degrading enzymes [30, 62].
Sphingosine is further converted to S1P by SphKs. S1P can be converted back to sphingosine by the S1P phosphatase, or it can be irreversibly degraded by S1P lyase to ethanolamine phosphate and hexadecanal (palmitaldehyde).