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
- 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 - - Source: PubMed
Publication date: 2026/07/29
Ren ZihanGao WeiLi XinJing YuchenLiu ZheLi XuejieZhang TaoHan Xiangjun - Cisplatin is a mainstay in cancer treatment, but toxicity and resistance limit its potential. Using RNA sequencing (RNA-seq), we show that ovarian cancer cells undergo broad changes in the microtubule cytoskeleton that correlate with resistance. Consistent with this, we find that cisplatin directly impacts microtubule dynamics in vitro and in cells. Paclitaxel counteracts cisplatin and increases resistance. By purifying tubulin from cisplatin-sensitive, -resistant, and -re-sensitized ovarian cancer cells, we demonstrate that resistance acquisition rewires the tubulin code, leading to microtubule stabilization. Furthermore, tubulin polymerization-promoting protein 3 (TPPP3) contributes to resistance. In vitro, TPPP3 synergizes with tubulin isotypes from resistant cells to yield maximal microtubule stabilization in response to cisplatin. Database analysis shows that patients with low TPPP3 levels have improved therapeutic outcome. Our findings implicate TPPP3 and microtubule dysregulation in cisplatin resistance, independent of effects through DNA damage, and have bearing on the etiology of cisplatin-associated neuropathies and ototoxicity. - Source: PubMed
Publication date: 2026/06/04
Horibata SachiMahalingan Kishore KPatel RuchiFan YuHotz Jordan MPonton-Almodovar AdrianaMacRenaris KeithLi YanMeerzaman DaoudGottesman Michael MRoll-Mecak Antonina - Transcriptomic changes in heart failure (HF) patients prior to and following left ventricular assist device (LVAD) support have been extensively studied. Recent studies focused on understanding DNA methylation changes in patients with cardiovascular diseases (CVD) and the role of circulating markers of DNA methylation as clinical predictors of the risk of CVD related morbidity and mortality. In this study, we used paired (pre- and post-LVAD) myocardial samples to examine changes in DNA methylation alongside RNA and protein expression. Our data suggests that patients with no improvement in cardiac function after LVAD therapy, despite showing an improvement in energy production (increased β-oxidation of fatty acid) exhibited persistent activation of profibrotic signaling, increased collagen deposition and cytoskeletal disarray evident from abnormal increase in sarcomeric distance following LVAD support. Contrarily, patients with improvement in cardiac function after LVAD therapy showed activation of pro-inflammatory signaling, collagen degradation and myogenesis. Both RNA sequencing and western blot data showed increased COL1A1 and decreased TPPP3 in post-NR thereby suggesting increased fibrosis and disrupted cytoskeletal signaling as potential barriers to myocardial recovery. Additionally, responders to LVAD therapy showed a significant reversal in myocardial interstitial fibrosis with a preserved sarcomeric architecture. Mice model of HF and recovery also confirmed our human findings, with reduced fibrotic signaling and improved cytoskeletal remodeling signaling observed in mice that showed improvement in cardiac function compared to mice with HF. Overall, our data suggests that altering extracellular matrix regulation and cytoskeletal signaling pathways may contribute to myocardial recovery. Further studies targeting these pathways are required to identify new HF therapeutic targets. - Source: PubMed
Publication date: 2026/05/15
Shankar Thirupura SMarchetti MarcoSrinivasan HariniVisker Joseph RHamouche RanaJohnson EzraJeong JamesKyriakoulis IoannisLing JingSideris KonstantinosSelzman Craig HHernandez Edgar JTristani-Firouzi MartinTseliou EleniDrakos Stavros GWever-Pinzon Omar