Ask about this productRelated genes to: TPPP3 antibody
- Gene:
- TPPP3 NIH gene
- Name:
- tubulin polymerization promoting protein family member 3
- Previous symbol:
- -
- Synonyms:
- CGI-38, p25gamma, p20
- Chromosome:
- 16q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-05-02
- Date modifiied:
- 2016-03-24
Related products to: TPPP3 antibody
Related articles to: TPPP3 antibody
- Lithium is the mainstay treatment for bipolar disorder, improving brain white matter microstructure and regulating genes involved in immune response and cell signaling. In 116 patients affected by a major depressive episode in the course of bipolar disorder, we investigated the effect of long-term lithium treatment on gene expression in peripheral blood mononuclear cells and their association with white matter microstructure. Differential gene expression analysis identified three genes significantly upregulated in lithium-treated compared to nontreated patients: SEPTIN11, DGKK, and TPPP3; and two downregulated genes: LEF1-AS1 and PLXDC1. At tract-based spatial statistics, significant lithium-by-gene expression interactions were observed for SEPTIN11, LEF1-AS1, PLXDC1, and DGKK, indicating that the relationship between gene expression and white matter microstructure differed depending on lithium treatment status. Only in lithium-treated participants, LEF1-AS1 and PLXDC1 expression were associated with increased fractional anisotropy and decreased radial diffusivity and mean diffusivity, while SEPTIN11 expression was associated with increased axial diffusivity, mean diffusivity, and radial diffusivity. These genes are widely expressed in the brain, and their peripheral expression correlates with white matter microstructure measures associated with lithium treatment. This observation supports the potential usefulness of peripheral transcriptomic signatures to mark the individual biological impact of lithium treatment on the brain. - Source: PubMed
Publication date: 2026/09/04
Betelli DianaFurno SerenaBravi BeatriceDi Carlo CarloLorenzi CristinaSpadini SaraFinardi AnnamariaColombo CristinaFurlan RobertoPoletti SaraBenedetti Francesco - Nasopharyngeal carcinoma (NPC) arises in an immune-suppressive milieu that frequently undermines treatment efficacy. TPPP3 has been implicated as a negative regulator of NPC aggressiveness, yet its relevance to immune modulation or chaperone networks remains poorly defined. We therefore sought to determine how TPPP3 shapes the NPC immune landscape and to identify its interacting protein partners. Public single-cell RNA-sequencing datasets from head and neck squamous cell carcinoma and nasopharyngeal carcinoma were analyzed using R. HK-1 and C666-1 cells stably overexpressing TPPP3 were established. These cells were used to construct humanized xenograft tumor models, with intratumoral immune cell infiltration evaluated by immunohistochemistry. In vitro, the same cells and their controls were indirectly co-cultured with peripheral blood mononuclear cells. Cellular lysates from TPPP3-overexpressing cells were subjected to immunoprecipitation-mass spectrometry and immunofluorescence staining, which identified HSPA8 as a TPPP3-interacting protein. Three groups-control, TPPP3-overexpressing, and TPPP3-overexpressing plus the HSPA8 inhibitor VER155008-were then compared in wound healing, colony formation, cell-cycle, and xenograft assays, with immunohistochemical staining for Ki67, TPPP3, and CD3 performed on tumor sections. TPPP3 transcripts were barely detectable across most tumor cell subsets but showed preferential enrichment in NPC epithelial clusters. Enforced TPPP3 expression curtailed xenograft outgrowth while increasing intratumoral abundance of CD3 T cells, CD8 T cells, and CD11c dendritic cells. Pharmacological blockade of HSPA8 with VER155008 further enhanced TPPP3-driven suppression of migration, clonogenicity, and tumor expansion, and also altered cell-cycle progression while boosting CD3 T-cell accumulation within grafts. These findings suggest a functional association between TPPP3 and HSPA8 that may contribute to tumor growth suppression and immune microenvironment remodeling in NPC. Pharmacological disruption of HSPA8-dependent proteostasis enhanced TPPP3-associated antitumor activity in both in vitro and in vivo models, indicating that this chaperone pathway represents a candidate mechanism worthy of further mechanistic investigation and therapeutic exploration. - Source: PubMed
Publication date: 2026/09/03
Li ShengweiLiao JiejunYang JiaweiHan YanfengLei ZixiaoYang Zheng - Exposure to ambient particulate matter (PM) has been linked to renal dysfunction, particularly in diabetic populations, but the underlying mechanisms remain unclear. We performed bidirectional Mendelian randomization to assess causal relationships between PM exposure and estimated glomerular filtration rate (eGFR), integrated transcriptomic datasets to identify PM-related genes overlapping with diabetic kidney disease (DKD) differentially expressed genes, and applied machine learning approaches to select key feature genes and construct diagnostic models. Single-cell and spatial transcriptomic analyses were used to characterize cell-type and region-specific expression patterns, while in silico knockout analysis explored potential functional associations. PM2.5-10 exposure was causally associated with decreased eGFR, particularly among individuals with diabetes, with no evidence of reverse causality. Transcriptomic integration identified 168 shared PM-DKD genes enriched in inflammatory, immune, and metabolic pathways, including AGE-RAGE, IL-17, TNF, and PI3K-Akt signaling. Seven feature genes (AVPI1, DUSP1, FOSB, JUNB, PDK2, TPPP3, and VIM) showed good diagnostic performance across training and external validation cohorts, and machine learning models and nomogram analyses demonstrated consistent predictive performance. Single-cell and spatial transcriptomic analyses revealed distinct cell-type and region-specific expression patterns, with VIM enriched in interstitial and fibrotic regions, TPPP3 mainly detected in podocytes, and other genes distributed across tubular or immune cell populations. In silico knockout analysis suggested potential associations of these genes with mitochondrial metabolism, oxidative stress, tubular function, and inflammatory processes. Database-based therapeutic exploration identified VIM as a potential candidate target, with sanguinarine showing favorable predicted binding affinity. Collectively, these findings suggest that PM2.5-10 exposure may contribute to DKD susceptibility through inflammatory, metabolic, and oxidative stress-related mechanisms, and provide candidate molecular markers for further investigation. - Source: PubMed
Publication date: 2026/08/25
Tan JiangChen YuqinHu Jiliang - APOE ε4 is the strongest common genetic risk factor for Alzheimer's disease (AD), yet many carriers remain cognitively unimpaired into late life. We tested whether protected ε4-first plasma proteomics could identify proteins associated with delayed clinical onset. - Source: PubMed
Le Guen YannPark JunyoungPeña-Tauber AndrésGreicius Michael D - The toxic mechanisms of norgestrel (NGT), an emerging marine pollutant, on the sperm from externally fertilized invertebrates remain elusive. This study employed an integrated physiological and multi-omics framework to elucidate how NGT (10 and 1000 ng/L) disrupts acrosome reaction (AR) signaling machinery, thereby impairing the functional integrity of Pacific oyster (Crassostrea gigas, also known as Magallana gigas) sperm. Exposure to NGT triggered a significant, dose-dependent premature AR, characterized by elevated acrosin activity and a loss of acrosomal integrity. Multi-omics integration supports a model in which this premature exocytosis is linked to signaling disturbances, including disruption of calcium signaling and reduced transcript abundance of calmodulin (CaM) and the primary recognition protein zonadhesin (Zan). This signaling interference induced an premature AR, subsequently driving a cascade of bioenergetic and structural failures. At the mitochondrial level, NGT induced abnormal mitochondrial permeability transition pore (mPTP) opening and elevated the transcript levels of antioxidant defense genes (e.g., peroxiredoxin-5, PRDX5). These alterations indicate the occurrence of mitochondrial collapse. Concurrently, scanning electron microscopy verified localized plasma membrane wrinkling and pore formation in sperm. In addition, NGT exposure decreased the transcript abundance of cytoskeleton-related genes, including solute carrier family 26 member 6 (SLC26A6), actin (ACT), and tubulin polymerization promoting protein family member 3 (TPPP3). These molecular changes further disrupted membrane phospholipid homeostasis, as represented by altered glycerophospholipid metabolism. At the same time, cumulative cellular stress was associated with decreased transcript abundance of cytoprotective factors (e.g., baculoviral IAP repeat-containing proteins, birc2) and changes in apoptosis-related genes consistent with activation of a caspase-8-mediated apoptotic programme. In conclusion, NGT, as a representative synthetic progestin, exerts reproductive toxicity by interfering with signaling mediators to induce premature AR, which subsequently exhausts metabolic energy and triggers plasma membrane impairment. These findings provide a critical mechanistic basis for the aquatic ecological risk assessment of synthetic progestins. - Source: PubMed
Publication date: 2026/07/28
Zheng TaoZhong HaoyangChen ChangkunXu DazhongZhang YunlingXu JinchaoLi DaFang YanYang Chunyan