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
- While atherosclerotic plaque vulnerability drives acute coronary syndrome, the regulatory mechanisms underlying plaque stability remain unclear. Protein kinase Cδ (PKCδ) has been implicated in atherosclerosis progression, but its specific role in plaque vulnerability and the underlying mechanisms require clarification. We analyzed PKCδ expression in human atheroma datas and investigated its role using low-density lipoprotein receptor-knockout mice with global and myeloid-specific PKCδ deletion. Plaque morphology, necrotic core formation, and fibrous cap thickness were evaluated. Macrophage metabolic profiling, mitochondrial function, inflammatory responses, and pyroptosis markers were assessed using biochemical and molecular approaches. Human atheroma analysis revealed elevated PKCδ expression, particularly in macrophages within ruptured plaques. PKCδ deletion in mice reduced necrotic core formation and increased fibrous cap thickness in both global and myeloid-specific models. Mechanistically, macrophage PKCδ deficiency improved mitochondrial fitness by promoting mitochondrial oxidative phosphorylation and elevating α-ketoglutarate (α-KG) levels. This metabolic shift reduced pro-inflammatory responses through PIK3AP1-mTORC2 activation and downregulated NLRP3 inflammasome-mediated pyroptosis. Dimethyl α-ketoglutarate (DKG) supplementation provided similar protective effects. Both human and in vivo analyses revealed PKCδ association with pyroptosis markers, including NLRP3, caspase-1, IL-1β, and GSDMD, whereas PKCδ deficiency reduced their co-localization with CD68⁺ macrophages. In conclusion, PKCδ serves as a key regulator of macrophage inflammation, pyroptosis, and mitochondrial dysfunction in atherosclerotic plaques. PKCδ deficiency promotes metabolic reprogramming that stabilizes plaques through reduced pyroptosis and enhanced mitochondrial function. These findings highlight PKCδ as a potential therapeutic target to reduce acute cardiovascular events by modulating plaque stability. - Source: PubMed
Publication date: 2026/09/10
Lien Chih-FengChang Hsin-YiYu Shu-HanCho Rou-LingChen Sy-JouKuo Tzu-TingChong Patrick Chun-ThengYe Chih-HungLin Feng-YenWu Wan-LinLin Shih-HuaTsai Chien-SungLin Chin-Sheng - Prostate cancer often reaches bone, which poses a challenge in orthopedic oncology since few therapies directly suppress tumor growth in bone. Bruceine D (BD) is a quassinoid from Brucea javanica. It is known anticancer activity but its effects on prostate cancer have not been defined. - Source: PubMed
Publication date: 2026/06/01
Chen ZhiweiHuang QingbinZheng YingmingGaru ALingHu XitaoYu WenchongZhao GuangquanZhang JieyingTian LinTang YuboHuang ShuaiZhao Xiaodong - Ovarian cancer (OC) remains one of the most lethal gynecological cancers worldwide. Despite advances in diagnosis, OC is mostly detected at late stages due to undefined symptoms. Therefore, identifying feasible, reliable, non-invasive biomarkers for early detection and disease stratification of OC is crucial. Tumor-educated platelets (TEPs) have emerged as a promising source for liquid biopsy, harboring oncogenic mRNA signatures that reflect the tumor microenvironment. In this study, we investigated TEP-mRNAs to identify stage-specific biomarkers for OC diagnosis and prognosis, while uncovering disease progression mechanisms and potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/08
Gahin Shaimaa GamalIbrahim Mostafa SBadr Eman - Gouty arthritis (GA) is caused by hyperuricemia and the articular deposition of urate crystals, for which current treatments remain suboptimal. Considering the anti-inflammatory properties of Dendrobium extracts, especially Dendrophenol (Den), this study conducted an in-depth investigation into its effects on GA. - 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