Ask about this productRelated genes to: SELE Blocking Peptide
- Gene:
- SELE NIH gene
- Name:
- selectin E
- Previous symbol:
- ELAM1, ELAM
- Synonyms:
- ESEL, CD62E
- Chromosome:
- 1q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2015-08-25
Related products to: SELE Blocking Peptide
Related articles to: SELE Blocking Peptide
- Gastric cancer (GC) exhibits marked epidemiological differences between European (EUR) and East Asian (EAS) populations, with significantly higher incidence rates in EAS. Circulating proteins represent promising drug targets; however, most proteomic studies have focused primarily on EUR ancestry, leaving EAS-specific targets largely underexplored. This study aims to identify ancestry-specific plasma protein targets for GC using Mendelian randomization (MR). - Source: PubMed
Publication date: 2026/05/01
Zhi PengCui YanXue GuanghuiQiao LingyuGeng JieChang ZhengyaoXu YinmeiYan JuanjuanWang YingliZhao Chenghui - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Given the persistence of the SARS-CoV-2 virus, it is important to understand the proteome associated with breakthrough infections among COVID-19 vaccinated individuals. - Source: PubMed
Publication date: 2026/05/11
Liu YiwenLu EricEllingson Katherine DHollister JamesLiu TuoHamzazai WadanaBeitel Shawn CCaban-Martinez Alberto JGaglani ManjushaNaleway Allison LOlsho Lauren E WPhillips Andrew LSolle Natasha SchaeferTyner Harmony LYoon Sarang KLutrick KarenBurgess Jefferey L - International Classification of Diseases (11th ed.; ICD-11) Complex Posttraumatic Stress Disorder (CPTSD) is a new diagnostic category consisting of PTSD and disturbances of self-organization (DSO) symptoms. This study compares the trajectories of ICD-11 PTSD and DSO symptoms change in three treatments: a phase-based intervention, STAIR Narrative Therapy (SNT), Prolonged Exposure (PE), and skills-training in affect and interpersonal regulation (STAIR). Ninety-two adult patients with ICD-11 CPTSD following childhood abuse were randomly assigned to treatment conditions. Piecewise latent curve models of self-reported symptoms were used to compare the change trajectories. Piece 1 corresponds to phase 1 (SNT) and active treatment (PE/STAIR), and piece 2 corresponds to phase 2 (SNT) and the first two months after treatment (PE/STAIR). In piece 1, PTSD symptom decline was steeper in PE compared to skills-training yielding a difference of d = -0.66, 95% CI [-0.99, -0.32] compared to SNT, and d = -0.56, 95% CI [-0.90, -0.23] compared to STAIR. In piece 2, PTSD symptom decline accelerated in SNT compared to PE, d = -0.25, 95% CI [-0.05, -0.45], but not compared to STAIR. The rate of DSO symptoms decline did not differ among conditions during treatment but decelerated more in PE compared to STAIR after treatment, d = -0.30, 95% CI [-0.08, -0.51]. Trauma-focused interventions may be the preferable treatment approach for PTSD symptoms and comparable to skills-training in reducing DSO symptoms during treatment. Compared to trauma-focused interventions there may be a potential spillover effect of skills-training on DSO symptoms in daily life after treatment. - Source: PubMed
Publication date: 2026/04/21
Sele PeterHoffart AsleHembree ElizabethØktedalen Tuva - Ovarian cancer is the most lethal gynecological malignancy worldwide, largely due to late diagnosis and lack of effective population-level screening tools. Inflammatory cytokines regulate proliferation, apoptosis, angiogenesis, and immune surveillance, making inherited variation in cytokine pathways biologically plausible determinants of ovarian cancer susceptibility and progression. Since the early 2000s, numerous candidate-gene studies have evaluated polymorphisms of genes such as the interleukin () families, tumor necrosis factor alpha (), transforming growth factor beta 1 (), and components of the nuclear factor kappa B () signaling pathway and adhesion pathways, across diverse populations. In this review, we summarize these potential markers to give readers an overview showing accumulated evidence supports a coherent model in which genetically modulated inflammation is an integral driver of epithelial ovarian carcinogenesis. Collectively, studies reveal recurrent patterns of risk-increasing and risk-protective variants. Risky genotypes predicted to enhance pro-inflammatory, pro-angiogenic, or immunosuppressive signaling include rs16944 CC, rs1800795, rs2227306 TT, rs1126647 TT, rs11556218 GT/GG, rs4778889 CT/CC, rs10889677 AC/CC, rs4758680 CA/AA, rs28372698 TT, rs1800629 GA/AA, and peroxisome proliferator-activated receptor gamma () rs1801282 CG genotypes. Conversely, protective variants tend to dampen inflammatory tone or rebalance cytokine networks, including rs17561 GT/TT, rs4848300 CT/CC, rs3783553 insertion/insertion, rs7596684 CT/CC, rs1880242 GT/TT, rs7977932 CG/GG, rs1800469 CT/TT, selectin E () rs5361 AC, intercellular adhesion molecule 1 () rs5498 AG genotypes and specific haplotypes. Beyond risk , several polymorphisms appear predictive of clinical features, including tumor stage, cytoreductive resectability and recurrence, highlighting potential prognostic relevance. Notably, associations are often population-specific, reflecting differences in allelic frequencies and linkage disequilibrium across ethnic groups, underscoring the need for cross-ethnic replication. Further investigations may ultimately enable further improved the prevention, early detection, and personalized management of ovarian cancer. - Source: PubMed
Chang Wen-ShinTsai Chia-WenChen Jaw-ChyunWang Yun-ChiBau DA-Tian