Ask about this productRelated genes to: S1PR5 antibody
- Gene:
- S1PR5 NIH gene
- Name:
- sphingosine-1-phosphate receptor 5
- Previous symbol:
- EDG8
- Synonyms:
- Edg-8
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-02
- Date modifiied:
- 2014-11-19
Related products to: S1PR5 antibody
Related articles to: S1PR5 antibody
- The role of CD8 T cells in Crohn's disease (CD) pathogenesis remains incompletely understood. This study aimed to characterize CD8 T cells in CD and elucidate their potential contribution to intestinal inflammation. T cells from blood and intestinal tissues of 15 patients with CD were analyzed using single-cell RNA and T cell receptor sequencing. Spatial transcriptomics was conducted on inflamed intestinal tissues from two patients. Analysis of 41,699 CD8 T cells identified distinct subsets characterized by differential granzyme expression: granzyme B (GZMB) CD8 T cells, predominantly in blood with high cytotoxic potential, and granzyme K (GZMK) CD8 T cells, enriched in intestinal tissue with lower cytotoxic potential. In the small intestine, GZMKCD8 T cells displayed enhanced tissue residency signatures (for example, CXCR6) and downregulated egress-related genes (S1PR1and S1PR5). GZMKCD8 T cells displayed robust interactions with myeloid cells via the CXCR3-CXCL9/10 axis, coupled with notable colocalization in the small intestine. Pharmacological inhibition of GZMK alleviated intestinal inflammation and tissue damage in a murine model of intestinal injury, supporting its role in modulating inflammatory responses. Together, these findings highlight GZMK as a potential modulator of intestinal inflammation and a candidate for further therapeutic investigation. - Source: PubMed
Publication date: 2026/07/06
Lee YoonhoKim Tae-YoungKim YongjaeBaek JiwonPark HwanYoon Do KyungHwang Sung WookLee Jong LyulPark Sang HyoungKim JihunYang Suk-KyunHan BuhmKweon Mi-NaSong KyuyoungYoon Yong SikYe Byong DukLee Ho-Su - Sphingosine-1-phosphate (S1P) is a pleiotropic bioactive sphingolipid that regulates key cellular processes, like proliferation, apoptosis, inflammation, and vascular homeostasis. S1P acts as a signaling molecule both inside and outside cells by interacting with five G-protein-coupled S1P receptors (S1PR1-S1PR5). Accumulating evidence indicates that dysregulation of S1P signaling is implicated in the pathophysiology of cerebral ischemia/reperfusion (I/R) injury and Alzheimer's disease (AD). In I/R injury, S1P signaling regulates vascular permeability, immune cell infiltration, and neuronal survival and death. In AD, alterations in S1P metabolism are associated with β-amyloid deposition, tau hyperphosphorylation, synaptic dysfunction, and sustained neuroinflammation. S1P receptor (S1PR) modulators represent promising therapeutic agents in both preclinical and clinical studies. Fingolimod was the first oral disease-modifying therapy approved for the treatment of multiple sclerosis and, at the same time, the first S1PR modulator introduced into clinical practice. New selective S1PR-targeting agents, including siponimod and ozanimod (S1PR1 and S1PR5), as well as the S1PR1-selective agent ponesimod, have also been approved for clinical use. In addition to their immunomodulatory properties, S1PR modulators have direct effects in the central nervous system, facilitating the maintenance of blood-brain barrier integrity, reducing microglial activation, and enhancing neuronal survival pathways. Building on this knowledge, we discuss the role of S1P signaling, highlighting recent advances in S1PR modulators as promising therapeutic agents for cerebral I/R injury and AD. - Source: PubMed
Publication date: 2026/06/09
Czubowicz KingaMotyl Joanna AgataWencel AgnieszkaStrosznajder Robert Piotr - Chronic wounds remain a significant clinical challenge due to impaired angiogenesis, persistent inflammation, defective tissue remodeling, and the limited effectiveness of current therapies. Consequently, the development of regenerative approaches capable of modulating multiple stages of wound repair has gained considerable attention. Among emerging therapeutic candidates, sphingosine-1-phosphate (S1P), a bioactive lipid, has shown substantial potential in promoting tissue regeneration. This review summarizes the biological functions of S1P during the hemostasis, inflammation, proliferation, and remodeling phases of wound repair. Particular emphasis is placed on receptor-mediated signaling through S1P receptors (S1PR1-S1PR5) and their downstream pathways, including phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), mitogen-activated protein kinase (MAPK), and Rho GTPase signaling. These pathways regulate key cellular processes such as immune modulation, angiogenesis, fibroblast activation, keratinocyte migration, and extracellular matrix remodeling. S1P also promotes myofibroblast differentiation and vascular maturation while balancing pro- and anti-inflammatory responses, thereby reducing chronic inflammation and excessive fibrosis. Recent advances in biomaterial-based delivery systems have enhanced the therapeutic application of S1P. Hydrogels, nanofibers, decellularized scaffolds, liposomal formulations, and extracellular vesicle-based platforms enable localized and controlled S1P release, leading to improved healing outcomes in diabetic and chronic wounds. Furthermore, biomaterial properties, including surface chemistry, porosity, and mechanical characteristics, significantly influence cell-material interactions and S1P-mediated responses. Despite promising findings, the efficacy of S1P-based therapies depends on receptor selectivity, dosage, release kinetics, and the local wound microenvironment. Future studies should focus on designing bioresponsive, receptor-targeted delivery systems to achieve precise spatiotemporal control of S1P signaling and maximize regenerative outcomes with minimal adverse effects. - Source: PubMed
Publication date: 2026/06/17
Eini MohammadTaghipour NiloofarNaseri MaryamHosseinzadeh SimzarDoudi Shaghayegh - Promoting remyelination is a key therapeutic goal in demyelinating diseases such as multiple sclerosis (MS), yet effective strategies remain limited. Sphingosine-1-phosphate (S1P), a ubiquitous bioactive lipid, has emerged as a key therapeutic target in MS due to its dual roles in immune regulation and neuroprotection; however, the therapeutic efficacy of current S1P-based therapies in remyelination remains unclear. This systematic review evaluated in vivo studies up to July 2025, in accordance with PRISMA guidelines, to assess the efficacy of S1P modulators on remyelination in mammalian models of demyelination. A comprehensive search across three databases identified 24 eligible studies that investigated S1P receptor (S1PR) modulation in both acute and chronic models of demyelination, with or without immune-mediated components. Fingolimod was the most extensively studied compound (16 studies). Of the 18 studies assessing demyelination outcomes, S1P modulation consistently attenuated myelin loss and oligodendrocyte depletion. In contrast, remyelination outcomes were inconsistent: among 15 studies assessing repair, most reported no significant enhancement. While fingolimod showed limited evidence on remyelination, more promising effects were observed with selective S1PR1/5 modulators such as siponimod and ponesimod. Overall, current evidence supports a model in which S1P modulators act primarily through S1PR1-mediated immunomodulation and S1PR5-associated oligodendroglial protection, preserving oligodendrocyte lineage cells rather than driving terminal differentiation or de novo remyelination. Several compounds displayed bell-shaped dose-response patterns, highlighting the importance of dosing and treatment paradigms. Collectively, these findings indicate S1PR-based therapies primarily limit demyelination, with limited evidence of remyelination, emphasising the need for more efficacious S1P modulators to improve MS outcomes. - Source: PubMed
Publication date: 2026/06/10
Vu HarleyGeorge NelsonXiao Junhua - Sphingosine-1-phosphate (S1P) and its five G protein-coupled receptors (S1PR1-S1PR5) regulate a broad range of processes that shape cancer progression, including proliferation, survival, angiogenesis, immune evasion and metastatic dissemination. Under physiological conditions, this signaling axis contributes to vascular integrity, immune cell trafficking and tissue homeostasis. In cancer, however, its output is not solely determined by ligand abundances. Rather, tumors reprogram the S1P-S1PR axis at a number of levels, coupling altered S1P production with receptor-specific changes in expression, localization and the signaling state to generate context-dependent malignant phenotypes. The present review provided a receptor-resolved synthesis of S1PR functions in cancer and examined the mechanisms that underlie pathway dysregulation, including transcriptional activation, epigenetic remodeling, microRNA loss, post-translational modifications and altered receptor trafficking and compartmentalization. It further discussed how metabolic amplification of S1P availability cooperates with receptor-level rewiring to sustain tumor progression, microenvironmental remodeling and therapeutic resistance. This framework positions the S1P-S1PR axis as a dynamically reprogrammed signaling network and highlights therapeutic strategies that concurrently target S1P production and receptor-mediated signaling as promising avenues for more-precise, biomarker-informed cancer treatment. - Source: PubMed
Publication date: 2026/05/04
Chuang Yun-TaWu I-HuiLee Cheng-FanLee Hsinyu