Ask about this productRelated genes to: SYTL1 Blocking Peptide
- Gene:
- SYTL1 NIH gene
- Name:
- synaptotagmin like 1
- Previous symbol:
- -
- Synonyms:
- SLP1, JFC1, FLJ14996, exophilin-7
- Chromosome:
- 1p36.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-10
- Date modifiied:
- 2016-10-05
Related products to: SYTL1 Blocking Peptide
Related articles to: SYTL1 Blocking Peptide
- The molecular basis of neutrophil-driven immunopathology in severe coronavirus disease 2019 (COVID-19) remains poorly defined. Here, we identify the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) SARS-unique domain (SUD)2core domain as a direct binding partner of the neutrophil-associated protein heme binding protein 2 (HEBP2). We show that HEBP2 normally suppresses azurophilic granule exocytosis, whereas SUD2core recruits the E3 ligase LTN1 to ubiquitinate and degrade HEBP2, thereby activating the Rab27a-Synaptotagmin Like 1 (SYTL1) axis to promote granule release, NETosis, and pro-inflammatory cytokine secretion. In a human immuno-epithelial organoid co-culture model, SUD2core amplifies epithelial damage in an HEBP2-dependent manner. Importantly, two small-molecule compounds that disrupt the SUD2core-HEBP2 interaction effectively attenuate neutrophil-mediated inflammation. These findings reveal a viral strategy that dismantles host restraint on neutrophil effector functions and highlight the SUD2core-HEBP2 interface as a promising therapeutic target for COVID-19. - Source: PubMed
Publication date: 2026/09/02
Li YingShao SongjunLei QianLi ChunjieYu QuanweiLi YuxiangWang ShuiLi LinChen HaiHuang RidongDeng HuiLi WeiminWang Chengdi - Endometrial cancer (EC) is a major reproductive system tumor and a common cancer in women. Polycystic ovary syndrome (PCOS) is one of the most prevalent female reproductive endocrine disorders. The incidence of EC is significantly higher in individuals with PCOS. This study seeks to elucidate the organic correlations and interaction mechanisms between the 2 diseases through series of exploration of key genes with a bioinformatics analysis. The PCOS sample data and the EC single-cell dataset were downloaded from the gene expression omnibus database. The EC sample data were retrieved from the cancer genome atlas public database. The random survival forest method was employed to identify key genes associated with the prognosis of PCOS and EC comorbidity. Corresponding analyses on functional pathway enrichment, regulatory networks, and immune micro-environment are conducted. From a bioinformatics perspective, the association and interaction mechanisms between PCOS and EC comorbidity were explored to provide research and development references for the prevention and control of PCOS and EC comorbidity. Five key genes associated with the prognosis of PCOS and EC comorbidity were identified using the random survival forest method. The identified genes are SYTL1, PARVG, ID4, IL1RN, and S100A9. The abnormal expression of these key genes has impacted various enrichment pathways, including the TGF-β signaling-pathway, motif regulatory networks (such as motif cisbp__M4556), and miRNA regulatory networks, which encompass genes such as ATM, BARD1 and BRCA1. Furthermore, these also influence the immune cell microenvironment, such as T cells regulatory. Collectively, these key genes play a significant role in the occurrence and progression of comorbidities through the pathways mentioned above. The dysregulation of key genes (SYTL1, PARVG, ID4, IL1RN, S100A9) in the context of PCOS-EC comorbidities, along with their associated enrichment pathways, including the TGF-β signaling-pathway and immune microenvironment, plays a significant role in the occurrence and progression of EC. - Source: PubMed
Yao YingshaZhu ShulanZhu Xiaoming - As the major subtypes of esophageal cancer (EC), esophageal adenocarcinoma (EAC) and esophageal squamous cell carcinoma (ESCC) exhibit distinct etiological mechanism, epidemiology, tumor biology, and prognoses. We performed bioinformatics analysis on specific genes related to pathological subtypes to identify potential biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2025/10/29
Lyu QiChai YanfeiChen WeiChen YaoLi Yufei - Os teomyelitis is a severe bone infection characterized by inflammation and destruction of bone and bone marrow, often leading to significant morbidity and challenging treatment strategies. Although it is known that many factors such as autoimmune diseases are related to the progress of osteomyelitis, the relationship between plasma protein and osteomyelitis has not been fully studied. We applied two-sample Mendelian randomization (MR) to evaluate causal effects of 4907 circulating plasma proteins on osteomyelitis risk. Proteomic exposure data were derived from a genome-wide association study (GWAS) of 35,559 Icelandic participants, while outcome statistics incorporated 2125 clinically validated osteomyelitis cases and 429,826 population controls from the FinnGen cohort. To ensure robustness, sensitivity analyses were conducted on the identified causal proteins. Additionally, to deepen our understanding of the biological processes, molecular functions, cellular compositions, and relevant metabolic and signaling pathways implicated in osteomyelitis, we performed Gene Ontology (GO) enrichment analysis, KEGG pathway analysis, and GeneMANIA analysis. The study identified five plasma proteins-SYTL1, DEFA1, MICB, FTMT, and TMEM38B-significantly associated with osteomyelitis, with protective effects indicated (inverse variance weighted p < 0.001, OR < 1). The strong statistical evidence highlights the proteins' potential as osteomyelitis biomarkers, which are crucial for enhancing our molecular insights and guiding future therapeutic development. Our findings provide valuable insights into the role of the plasma proteome in osteomyelitis and underscore the significance of the ferroptosis pathway. By identifying potential therapeutic targets associated with this pathway, we can establish a robust biological foundation for future research and therapeutic development in osteomyelitis. - Source: PubMed
Publication date: 2025/07/14
Chai WeihaoYuan HongruiLiu JiangweiYang Yi - The molecular mechanisms underlying the transport of influenza A virus (IAV) membrane proteins to the cell surface remain largely unclear. In this study, siRNA screening identifies Rab27a as a critical host factor regulating this transport process. GTP-bound Rab27a operates via its effectors, synaptotagmin-like protein 1 (SYTL1) and SYTL4, to facilitate the transport of vesicles carrying viral membrane proteins to the plasma membrane. Absence of Rab27a or SYTL4 does not block the early stages of the IAV life cycle but restricts viral assembly and budding. Notably, silencing SYTL4 provides superior protection in the female mouse IAV infection model. This investigation elucidates the molecular mechanism by which Rab27a and its effectors modulate the transport of IAV membrane proteins, thereby bridging a critical gap in IAV life cycle research and presenting a potential target for the development of antiviral drugs. - Source: PubMed
Publication date: 2025/07/08
Chen TongOuyang AotianZou JiahuiFeng YiWu ChangsongJiang MeijunTu ShaoyuDing LingCheng YanqingHu WenshuoSheng WeiLi YanglinJin MeilinChen HuanchunZhou Hongbo