DAP12 Blocking Peptide
- Known as:
- DAP12 Blocking Peptide
- Catalog number:
- 33r-11048
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- DAP12 Blocking Peptide
Related genes to: DAP12 Blocking Peptide
- Gene:
- TYROBP NIH gene
- Name:
- TYRO protein tyrosine kinase binding protein
- Previous symbol:
- PLOSL
- Synonyms:
- DAP12, PLO-SL, KARAP
- Chromosome:
- 19q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2019-04-23
Related products to: DAP12 Blocking Peptide
Related articles to: DAP12 Blocking Peptide
- Beyond cognitive impairment, Alzheimer's disease (AD) is frequently accompanied by apathy, the most prevalent and burdensome neuropsychiatric symptom (NPS). Apathy significantly impacts AD onset and progression, yet its molecular underpinnings remain unclear. Our previous RNA-sequencing analysis revealed abnormal immune gene expression uniquely associated with apathy in AD patients. In this study, we investigated whether changes in these immune related genes are also linked to apathy-like behavior, and whether administration of C3a receptor antagonist SB290157, alone or with methylphenidate, modifies apathy-like behaviors in 5xFAD mice. We first validated the apathy-related immune hub genes identified in human AD in the prefrontal cortex (PFC) of 16-18 month-old 5xFAD mice using RT-qPCR. Then separate cohorts of similarly aged 5xFAD mice received SB290157 and/or methylphenidate for three weeks. Our results showed that elevated immune hub genes Tyrobp, C3, C3ar, C1qa, C1qb, and C1qc were strongly correlated with apathy-like behavior in 5xFAD mice. Combined SB290157 and methylphenidate treatment improved nest-building behavior, reduced C3 and C3ar expression as well as restored dendritic spine density in the PFC. Our results confirm complement-mediated immune dysregulation is linked to apathy and suggest that co-targeting complement and catecholaminergic pathways may offer a novel therapeutic strategy for alleviating apathy in AD. - Source: PubMed
Publication date: 2026/04/25
Monteiro RaisaDunn Jeffrey TRodriguez GuadalupeFisher Daniel WDong Hongxin - Helicobacter pylori (H. pylori) infection and atrial fibrillation(AF) are major global health concerns. Emerging evidence has suggested a potentially chronic inflammation-mediated link between them, but the shared genetic mechanisms remain unclear. - Source: PubMed
Publication date: 2026/04/10
Deng AojianWang Wei - Diabetic kidney disease (DKD) is a common diabetes complication that increases global morbidity and mortality. To identify DKD biomarkers and explore autophagy-related mechanisms to find potential therapeutic targets for DKD treatment. - Source: PubMed
Wang QinLi XiaoqiYe WenWang QiBi Xianjin
- Source: PubMed
- Status epilepticus (SE) is a severe type of epileptic seizure and induces molecular and cellular changes in the brain tissues which contribute to neuron injury. Here we used RNA sequencing to determine changes in hippocampal gene expression in pilocarpine-induced SE mice at 3-hour (SE-3h) and 24-hour (SE-24h) time points, a crucial stage of SE-induced brain acute damage. A total of 366 differentially expressed genes (DEGs) were identified from the SE-3h hippocampus and 570 DEGs from the SE-24h hippocampus, and most of them were up-regulated upon SE induction. Bioinformatical analyses showed that, compared to SE-3h up-regulated genes with poor scores in functional and pathway enrichment, the SE-24h up-regulated genes were predominantly enriched in inflammatory and immune response, positive regulation of response to external stimuli and inflammatory response (GO function), and Microglia pathogen phagocytosis pathway and Tyrobp causal network in microglia (WikiPathway). Specifically, a subset of DEGs such as Tyrobp, C1qc, Itgb2, Ncf2, and Nckap1l involved in the two pathways are present in the inflammatory and immune cascades. Therefore, this study delineates early altered transcriptional profiles in the hippocampus after SE, and highlights up-regulation of a subset of genes might be involved in the activation of microglia-mediated inflammatory and immune responses linked to the early pathogenesis of SE-induced brain injury. - Source: PubMed
Publication date: 2026/03/20
Tang Hui-LingMin YuLong Yue-Sheng