Cryo-EM in combination with biochemistry, flow cytometry and fluorescence microscopy reveals the activation of S1PR1 by CD69, a type II membrane protein, in cis to induce receptor internalization and thereby disrupt cellular responsiveness to S1P gradients.

Inflammatory S1P signaling is dynamically regulated in chick Müller glia after retinal injury and suppresses Müller glia reprogramming into neuron-like cells.

Impairment of the autocrine S1PR1-Gi signaling on HEVs results in high-endothelial cell apoptosis, reduced CCL21-secretion from HEVs, and cessation of HEV-DC interactions and lymphocyte immigration across the high-endothelial barrier.

Constitutive sphingosine 1-phosphate signaling via the G-protein coupled receptor S1PR3 in mechanonociceptive somatosensory neurons is required for normal behavioral responses to noxious mechanical stimuli.

RNA-Seq analysis and molecular biological approaches reveal a novel mechanism and provide a promising preventive and therapeutic molecular target for vulnerability to chronic pain-related memory impairment.

Mir155 showed a catabolic effect on osteogenesis and bone mass phenotype via interaction with the S1pr1 gene, suggesting inhibition of Mir155 as a potential approach to bone regeneration and bone defect healing.

Shortage of blood-borne apolipoprotein-M–bound sphingosine-1-phosphate, which accompanies various brain disorders, causes paracellular leak and increase in transcytosis at the blood–brain barrier, which can be reversed, thus is of clinical relevance.

The sphingosine 1-phosphate receptor-1 (S1PR1) signals in heterogenous populations of mouse adventitial lymphatic (LEC) and arterial endothelial cells (aEC1, aEC2) to regulate chromatin and the transcriptome, thus affecting their phenotypes.

Sphinganine-1-phosphate (SA1P) is linked to paclitaxel-induced peripheral neuropathy, offering a potential target for reducing this severe side effect of paclitaxel treatment.

Progesterone mediates nongenomic signaling in Xenopus oocyte meiosis by activating a PLA2 activity that requires two membrane receptors ABDH2 and mPRß.