Ask about this productRelated genes to: SPNS1 Blocking Peptide
- Gene:
- SPNS1 NIH gene
- Name:
- sphingolipid transporter 1 (putative)
- Previous symbol:
- -
- Synonyms:
- HSpin1, nrs, SPINL, PP2030, SPIN1, LAT
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-04-12
- Date modifiied:
- 2017-07-21
Related products to: SPNS1 Blocking Peptide
Related articles to: SPNS1 Blocking Peptide
- The lack of reliable diagnostic tools and relapse monitoring for latent tuberculosis infection (LTBI) constitutes a major obstacle to global tuberculosis (TB) control. This highlights an urgent need for robust animal models and predictive biomarkers. To address this, we report the successful establishment of a rapid murine model of recapitulating the active, latent, and relapse phases of TB within a compressed ten-week timeframe-hence termed the rapid multi-stage TB murine model. In this model, mice were first intravenously infected with , followed by a four-week isoniazid (INH) regimen starting at two weeks post-infection. By week six, pulmonary bacterial loads in most mice dropped below the detection limit, signifying the establishment of latency. Reactivation was subsequently triggered by a four-week administration of anti-TNF-α (Tumor Necrosis Factor-α) monoclonal antibody. Leveraging this reproducible and time-efficient model, we performed transcriptomic profiling of peripheral blood and identified a distinct sixteen-gene signature (including , , , , , , , , , , , , , , , ) that dynamically tracks disease progression. Collectively, these findings not only provide a valuable and efficient preclinical tool but also deliver transformable candidate biomarkers with immediate potential to guide the development of novel diagnostic strategies for LTBI surveillance and management. - Source: PubMed
Publication date: 2026/03/11
Li HaifengWang JunfeiWang YuLiu FanTang JunSun MengmengZhan Lingjun - Doxorubicin (DOX) causes cardiotoxicity and heart failure in a significant fraction of patients, but the molecular etiology is poorly understood. - Source: PubMed
McDermott-Roe ChrisLv WenjianShao YengHoshino AtsushiArany ZoltanMusunuru Kiran - To investigate the dynamic genetic regulatory mechanisms of CD4 T cells in the pathogenesis of obstructive sleep apnea (OSA), particularly in the immune and inflammatory response induced by intermittent hypoxia (IH). - Source: PubMed
Publication date: 2025/12/17
Zhang XinyueRen Lingfei - Human enterovirus A71 (EV-A71) is a major cause of hand, foot and mouth disease. Cellular factors critical for EV-A71 infection remain enigmatic. Here, we performed CRISPR/Cas9 screens and identified sphingolipid transporter 1 (SPNS1) as an essential factor for EV-A71. SPNS1 deficiency inhibits infection of EV-A71 and 9 of 11 examined enteroviruses. Mechanistically, the endo/lysosomal localization of SPNS1 and the acidification of the endo/lysosomes are essential for SPNS1 to support EV-A71 infection. SPNS1 deficiency inhibits EV-A71 genomic RNA replication, but barely affects replication of EV-A71 RNA directly transfected into the cytoplasm. SPNS1 interacts with the EV-A71 capsid protein VP1 and entry receptor SCARB2 in the endo/lysosomes, where it acts as a transporter to release the viral pocket factor into the cytosol, leading to uncoating. Animal experiments show that SPNS1 deficiency results in reduced viral loads, pathological effects, and lethality following EV-A71 infection. Our findings collectively identified SPNS1 as a transporter of the EV-A71 viral pocket factor. - Source: PubMed
Publication date: 2025/12/12
Fu Yu-ZhiLuo Fang-FangYang LiuZhang Yu-XiaLi Jing-YangWang Su-YunZhang YongWang Yan-Yi - Mutations in , the gene encoding the lysosomal hydrolase glucocerebrosidase (GCase), are the strongest common genetic risk factor for Parkinson's Disease (PD). However, these mutations are incompletely penetrant, which suggests that there are likely genetic modifiers of GCase function. To identify such genes, we implemented a live cell GCase activity-based CRISPR-platform to enable genome-wide screening for novel regulators of lysosomal GCase activity. Among the screening hits, we find significant enrichment of genes linked to development and progression of PD through genome-wide association studies (GWAS). Moreover, we identify two lysosomal lipid transporter genes, including those encoding the lysosphospholipid transporter SPNS1 and the cholesterol transporter NPC1, and find an allele of SPNS1 that is associated with increased risk of PD. We show that disruption of SPNS1 does not affect GCase protein levels but impairs its lysosomal function. Collectively, these data suggest that dysfunction of many PD-associated genes converge to impact lysosomal GCase activity and thereby contribute to disease pathogenesis. A better understanding of the impacts of these and the other GCase modulators identified here should help unravel the important, yet complex, relationship between and PD. - Source: PubMed
Publication date: 2025/09/03
Udayar VinodGilormini Pierre-AndréBryois JulienGehrlein AlexandraChen XiSonea StephanieZhu ShaDeen Matthew CAnastasi NadiaMurphy Alan ESkene NathanTan Manuela M XTunold Jon-AndersRoudnicky Filipvan de Berg Wilma D JPihlstrøm LasseVocadlo David JJagasia Ravi