Ask about this productRelated genes to: PIK3AP1 antibody
- Gene:
- PIK3AP1 NIH gene
- Name:
- phosphoinositide-3-kinase adaptor protein 1
- Previous symbol:
- -
- Synonyms:
- BCAP, FLJ35564
- Chromosome:
- 10q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-21
- Date modifiied:
- 2016-10-05
Related products to: PIK3AP1 antibody
Related articles to: PIK3AP1 antibody
- - Source: PubMed
Publication date: 2026/03/19
Chen XianjunShi LinPang QingjiangYu RongyaoWang Chenghao - Periodontitis, an inflammatory disease affecting over 45 % of adults globally, causes irreversible alveolar bone loss through immune cells-mediated inflammation, thus necessitating novel regenerative therapies. This study proposes a cold plasma-based nitrogen species implantation (PBNI) technique to regulate the periodontal immune microenvironment and ameliorate periodontal inflammation. This study demonstrates that PBNI, optimizing for nitric oxide (NO) delivery, reprograms macrophage phenotype to resolve inflammation and reduce alveolar bone resorption. The linear correlation between exposure time and NO yield establishes PBNI as a tunable NO delivery approach. In mice with experimental periodontitis, PBNI increased alveolar bone volume, the effects of which were mirrored by the NO donor L-arginine. High-throughput RNA sequencing of bone marrow-derived macrophages (BMDMs) exposed to PBNI identified a cluster of differentially expressed genes responding to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/AMP-activated protein kinase (AMPK) pathways significantly enriched. Mechanistically, PBNI-derived NO activates the canonical soluble guanylate cyclase/Protein Kinase G (sGC/PKG) cascade and a newly identified phosphoinositide-3-kinase adaptor protein 1 (PIK3AP1)/AKT1/AMPKα1 axis, synergistically driving the M2 macrophage repolarization. Crucially, NO scavenging or PI3K pathway inhibition abrogated M2 repolarization and alveolar bone regeneration. This study establishes a tunable NO delivery approach that coordinates sGC/PKG and PIK3AP1/AKT1/AMPKα1 signaling to reprogram periodontal inflammatory microenvironment. By resolving the mechanism of PBNI and enhancing its osteogenic efficacy through controlling NO release, we provide a clinically translatable strategy for immunomodulatory periodontal regeneration therapy. - Source: PubMed
Publication date: 2025/12/24
Liu ZhixinWu LaidiLu XinpeiSong KeCao Yingguang - Bowel resection is required in up to 27% of inflammatory bowel disease (IBD) patients due to severe complications. Identifying reliable predictors for future surgery is crucial for risk stratification and management. - Source: PubMed
Publication date: 2026/01/12
Xu XinyiXu ChenyueZeng NaSun QiXu FangMa JiuyueHuang XuepingZhou MinsiSun JingZhu ShengtaoLi PengZhang ShutianLv HanShi Haiyun - Sepsis is a life-threatening organ dysfunction syndrome caused by a dysregulated host response to infection. As a leading cause of mortality in intensive care units patients, it still lacks sensitive biomarkers. Therefore, this study aimed to develop a diagnostic model for sepsis and identify key driver biomarkers. Using single-cell RNA sequencing (scRNA-seq) data from the GEO database, we constructed a diagnostic model through 113 machine learning (ML) frameworks, supplemented with Shapley additive explanations (SHAP) analysis to identify pivotal genes. Results revealed a significant increase in myeloid cells, particularly neutrophils, in the peripheral blood of sepsis patients. Screening identified 70 upregulated and 762 downregulated neutrophil-associated genes, which were intersected with differentially expressed genes (DEGs) between healthy controls and sepsis patients, yielding 13 overlapping genes - including S100A12 - as potential drivers. These 13 genes were incorporated into 113 ML models. The Random Forest (RF) model, which included S100A12, PIK3AP1, HLA-DMB, and RETN, achieved the highest mean C-index with fewer features. Its robust diagnostic performance was validated using receiver operator characteristic curves, calibration curves, and decision curve analysis. SHAP analysis highlighted S100A12 as the most influential driver gene and identified theophylline, aspirin, and aminophylline as potential targeting compounds. In conclusion, sepsis patients show increased peripheral neutrophils, an RF model based on 4 neutrophil-associated genes demonstrates strong diagnostic ability, and S100A12 serves as a key biomarker for sepsis. - Source: PubMed
Huang XiaopingYu ZiboZhuo Zhifang - Primary cilia have emerged as key regulators in cancer biology, influencing tumor progression and therapeutic response through diverse signaling pathways. In this study, we identify WDR60, a component of the dynein-2 complex essential for retrograde intraflagellar transport, as a novel modulator of pancreatic neuroendocrine tumor (Pa-NET) behavior. Transcriptomic analysis of the GEO dataset GSE73338 revealed that WDR60 is significantly upregulated in both primary and metastatic Pa-NETs compared to normal pancreatic islets. Moreover, WDR60 expression is higher in G2 compared to G1 Pa-NETs. Functional analyses in QGP-1 cells following WDR60 silencing demonstrated broad transcriptional reprogramming with enrichment of pathways related to cell adhesion and extracellular matrix (ECM) remodeling. Notably, WDR60 knockdown reduced cell migration and enhanced adhesion without affecting cell viability or proliferation. Among the key upregulated genes were PIK3AP1, RAP1B, and RFLNA, suggesting that WDR60 is involved in regulating PI3K/AKT signaling and cytoskeletal dynamics. To explore potential therapeutic implications, we examined the effects of Ciliobrevin A (HPI-04), an inhibitor of Hedgehog signaling and ciliogenesis. HPI-04 significantly reduced WDR60 expression, impaired cell migration, and increased adhesion. RT-qPCR confirmed overlapping gene expression changes between HPI-04 treatment and WDR60 silencing, although some differences, such as CD164 regulation, suggest WDR60-independent mechanisms. Collectively, these findings identify WDR60 as a critical regulator of cell motility and adhesion in Pa-NETs via ciliary signaling and cytoskeletal remodeling. They also support the therapeutic potential of targeting cilia-associated pathways, including WDR60 and Hedgehog signaling, in the treatment of Pa-NETs. - Source: PubMed
Publication date: 2025/12/03
Grassi CristinaLaffi AliceZerbi AlessandroLavezzi ElisabettaMazziotti GherardoUccella SilviaLania Andrea GerardoVitali Eleonora