SPHK2 antibody
- Known as:
- SPHK2 (anti-)
- Catalog number:
- orb101571
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- SPHK2 antibody
Related genes to: SPHK2 antibody
- Gene:
- SPHK2 NIH gene
- Name:
- sphingosine kinase 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-05
- Date modifiied:
- 2018-03-13
Related products to: SPHK2 antibody
Related articles to: SPHK2 antibody
- Opaganib is a proprietary, host-directed, potentially broadly potent, first-in-class oral sphingosine kinase 2 (SphK2) selective inhibitor developed by RedHill Biopharma Tel Aviv, Israel. It is currently the most widely used selective SphK2 inhibitor. It simultaneously inhibits three sphingolipid-metabolizing enzymes in human cells-SphK2, dihydroceramide desaturase (DES1), and glucosylceramide synthase (GCS)-leading to depletion of sphingosine 1-phosphate (S1P), accumulation of ceramides and dihydroceramides, and suppression of key pro-survival pathways including pERK, pAKT, and NF-κB. These events promote autophagy, apoptosis, and disruption of viral replication. A large body of evidence indicates that SphK plays an important role in health and disease. This study reviews the role and mechanisms of opaganib effects as anticancer, anti-inflammatory, and antiviral agent. The latest research directions for opaganib are described as gastrointestinal acute radiation syndrome (GI-ARS), chemical exposure indications, and COVID-19, Ebola, and other viruses, providing new therapeutic ideas and considerations for future research and clinical trials. - Source: PubMed
Publication date: 2026/05/22
Huang FuxunZhan PengShi XiujuanSun YueyangSong XingboSun PeiluLiu Bo - Myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment (TME) limit the efficacy of adoptive T cell therapies, highlighting the need to overcome tumor-associated immunosuppression. Sphingosine-1-phosphate (S1P), is an abundant signaling lipid in the TME. Here, we show that inhibition of sphingosine kinase-2 (SphK2), the enzyme generating S1P in MDSCs, reduces the suppressive activity of monocytic MDSCs (M-MDSCs) while promoting their differentiation toward a mature, immunogenic phenotype characterized by enhanced antigen presentation. Pharmacological SphK2 inhibition enhances the response to anti-PD-1 therapy in preclinical models of checkpoint-resistant breast, bladder, and melanoma cancers by mitigating MDSC-mediated suppression and limiting tumor progression. Mechanistically, S1P directly binds acetyl-CoA carboxylase-1 (ACC1) to inhibit its activity, thereby rewiring fatty-acid metabolism. Lowering intracellular S1P restores ACC activity, promotes phosphatidylcholine synthesis, and reduces MDSC immunosuppression. These findings identify the SphK2-ACC-phospholipid axis as a metabolic checkpoint controlling the immunogenicity of MDSCs and a potential therapeutic target for enhancing cancer immunotherapy. - Source: PubMed
Publication date: 2026/06/02
Chakraborty ParamitaChatterjee ShilpakKassir Mohamed FaisalWofford WyattChoi SeunghoOleinik NataliaSaatci OzgeDarawshi OdaiDas SatyajitOberhoeltzer NathanielGautam AnupamMills StephanieDeMass ReidHedley ZachariaLiu YueyingParikh Rasesh YPaul SandipSeal SouvikSmith Charles DLilly Michael BGangaraju Vamsi KPeterson YuriMehrotra MeenalHill ElizabethSahin OzgurLeitinger NorbertRodriguez Paulo COgretmen BesimMehrotra Shikhar - Targeting Sphingosine kinase (SphK1/2) has become a novel strategy for the treatment of cancer. However, potent ATP competitive inhibitors are rare. Herein, a series of novel SphK1 and SphK2 inhibitors were identified through virtual screening and structural optimization. The structure-activity relationship revealed compound 9d had excellent inhibitory activity and selectivity on SphK1. 9d can increase the level of Sph while reducing the content of S1P in vivo and in vitro. Moreover, 9d demonstrated anti-tumor effect on various cell lines and mouse models. In addition, another compound 6a was found to have good inhibitory activity and selectivity on SphK2 and showed potent anti-proliferative activity on tumor cells. It can be studied as an inhibitor of SphK2 in the future. - Source: PubMed
Publication date: 2026/05/22
Zhang MeiyanHuo YidanSong YaliLi LongfeiMeng MingGuo JianshuangCao FeiYang Kan - The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. To assess the de novo mutation (DNM) hypothesis, we performed a nationwide recruitment of 37 novel sEOAD patients-unaffected parents trios. After assessing known monogenic genes, we performed trio-based exome sequencing and jointly analyzed novel trios with 12 previously reported ones. Of these, we selected 16 trios for genome sequencing. We identified three patients with a pathogenic DNM in APP or PSEN1. Then, from the 46 remaining trios, we identified 38 non-synonymous coding DNM and 4 de novo copy number variants (CNVs) in exome data. Four DNM (2 novel, in SPHK2 and DDR1) and bi-allelic inherited variants in two genes affected Alzheimer disease-related genes. No significant burden of rare coding variants in exome/genome data from 5643 EOAD cases and 16097 controls was identified using nested windows centered on each DNM position, at the transcript level. From genome data, one non-coding DNM was predicted to affect splicing in an AD-associated gene, PINX1. Overall, 48% probands carried ≥1 inherited risk factor with odds ratio (OR) > 1.5 and GWAS-defined Genetic Risk Scores (GRS) distribution was more consistent with random distribution than enrichment in higher scores in probands. We confirm that DNMs in known monogenic genes explain sEOAD in a minority of cases, while candidate DNMs in other genes might account for a small proportion of additional cases. The majority of sEOAD patients may have a complex etiology including multiple inherited variants, however, GRS might not explain most of its genetic component. - Source: PubMed
Publication date: 2026/05/29
Zarea AlineCassinari KevinLecoquierre FrançoisQuenez OlivierCharbonnier CamilleSchramm CatherineLacour MorganeRousseau StéphaneRichard Anne-ClaireRovelet-Lecrux AnneLecourtois MagalieOlaso RobertBoland AnneDeleuze Jean-FrançoisGilissen ChristianVeltman Joris AVissers Lisenka ElmBellenguez CélineDols-Icardo OrioHardy JohnHolstege HenneHulsman MarcLambert Jean-CharlesMead SimonRamirez AlfredoSims Rebeccavan Swieten JohnWagner MichaelWilliams JulieBombois StéphanieBoutoleau-Bretonniere ClaireCharmard-Witkowski Ludivinede la Sayette VincentDeramecourt VincentEtcharry-Bouyx FrédériqueGabelle AudreyGueriot ClaudeLe Guyader GwenaëlLe Ber IsabelleLebouvier ThibaudMartinaud OlivierMichon AgnèsQuelin ChloéSarazin MarieSévin MathieuThauvin-Robinet ChristelWallon DavidNicolas Gaël - Women living with HIV face an increased burden of spontaneous preterm birth (sPTB); however, the underlying immunological mechanisms of sPTB and its association with HIV infection are poorly understood. Although the limited earlier literature implicates sphingosine-1-phosphate (S1P), a lysosphingolipid signaling molecule, in reproductive biology, the association of S1P signaling with HIV and sPTB has not been investigated. We examined whether two S1P signaling components, S1P receptors and sphingosine kinases, are expressed in the female reproductive tract and whether levels are associated with HIV status or spontaneous preterm birth. We quantified the mRNA expression of sphingosine-1-phosphate receptors 1 and 3 (/) and sphingosine kinases 1 and 2 (/) in 167 banked vaginal swab specimens collected between 14 and 26 weeks of gestation in a longitudinal pregnancy cohort in Lusaka, Zambia. We evaluated the expression of , , , and by real-time quantitative reverse transcription PCR (RT-qPCR) in four groups (n = 41-42 each): women without HIV (WWoH) with term birth (≥37 weeks of gestation; TB), WWoH with spontaneous preterm birth (<37 weeks of gestation, sPTB), women with HIV (WWH) with TB, and WWH with sPTB. We found that S1P receptors and sphingosine kinases are expressed in the female reproductive tract. and mRNA expression were generally comparable among women independent of HIV status or birth outcome, though trended toward higher expression in women with HIV and women with sPTB. In contrast, mRNA trended toward higher expression in WWH vs. WWoH overall, as well as in WWH vs. WWoH among women with sPTB. Similarly, mRNA expression was greater in women with HIV than in women without HIV, and WWH, both with TB and sPTB, had higher mRNA expression than WWoH with TB. Perturbations in and mRNA expression may be associated with inflammation related to HIV infection and spontaneous preterm birth, suggesting that further studies of S1P signaling in pregnancy, especially among women with HIV, are warranted. - Source: PubMed
Publication date: 2026/05/14
Resop Rachel SMwape InnocentSebastião Yuri VRittenhouse Katelyn JSindano NtazanaMwape HumphreyKasaro Margaret PVwalika BellingtonPrice Joan TStringer Jeffrey S ADe Paris Kristina