PFDN1 Antibody
- Known as:
- PFDN1 Antibody
- Catalog number:
- XW-8018
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PFDN1 Antibody
Related genes to: PFDN1 Antibody
- Gene:
- PFDN1 NIH gene
- Name:
- prefoldin subunit 1
- Previous symbol:
- -
- Synonyms:
- PFD1
- Chromosome:
- 5q31.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-06
- Date modifiied:
- 2016-10-05
Related products to: PFDN1 Antibody
Related articles to: PFDN1 Antibody
- Early detection of cancer is essential for effective treatment. However, current prostate cancer screening methods lack sufficient sensitivity and specificity, leading to overdiagnosis and unnecessary treatment. There is also an unmet need to distinguish clinically significant from insignificant prostate cancer. To identify complementary biomarkers for improved screening and diagnosis, we performed transcriptional profiling of cancer-associated transcripts in circulating extracellular vesicles (EVs) isolated from peripheral blood of patients with suspected prostate cancer prior to biopsy and healthy donors. Expression data for 2549 mRNAs were obtained from 28 men. CAPN5 expression was significantly lower, whereas BIRC2, CASP3, CD63, FMO5, IRF6, PFDN1, PRDX6, PSMD2, RIT1, S100A2, THBS1, and XRCC2 were significantly elevated in EVs from patients with significant prostate cancer (n = 14) compared with cancer-free individuals and patients with insignificant disease (n = 14). Candidate biomarkers were subsequently evaluated by in silico validation using the The Cancer Genome Atlas (TCGA) prostate adenocarcinoma dataset and the GEO dataset GSE70768 containing benign and malignant prostate tissues. This analysis identified CASP3, XRCC2, and RIT1 transcripts in circulating EVs as promising biomarkers for the early detection of significant prostate cancer. - Source: PubMed
Publication date: 2026/03/26
Werner StefanTennstedt PierrePose Randi CMüller ChristianBesler KatharinaSchneegans SvenjaAlawi MalikRoesch Marie CPeine SvenBonci DesireeBudna-Tukan JoannaLianidou EviAlix-Panabières CatherineTilki DeryaPantel Klaus - Aortic stenosis (AS) is a prevalent valvular heart disease that is increasing due to aging population and longer life expectancy. While most individuals have a tricuspid aortic valve (TAV), some are congenitally born with a bicuspid aortic valve (BAV). The mechanisms underlying AS pathogenesis remain unclear, limiting advancements in clinical treatment and biomedical research. This study aimed to identify differentially expressed protein (DEPs) in aortic valve interstitial cells (VICs) from AS patients with TAV and BAV using quantitative proteomic analysis. - Source: PubMed
Publication date: 2025/09/01
Song NaaleumYu JiyoungJi EunhyeYoon JinChoi Kyoung-HeeYu Jeong EunKim BokyungKim JihyeonKim MinjoongLee SahminKim KyunggonAikawa Elena - Prefoldin1 (PFDN1), a molecular chaperone, is essential for stabilizing cytoskeletal proteins like actin and tubulin, supporting cellular processes such as survival, migration, and cell cycling. Recent evidence suggests that PFDN1 also influences key cancer-related signaling pathways. However, the complete mechanisms involved and the downstream genes implicated in such action remain relatively undiscovered. This study investigated the effects of PFDN1 silencing on cellular processes and gene expression in triple-negative breast cancer (TNBC) cells, focusing on its potential as a therapeutic target. MDA-MB-231 cells, a TNBC model, were transfected with PFDN1-targeting siRNA to knock down PFDN1 expression. The effects of PFDN1 silencing were assessed through various assays, including phase contrast and scanning electron microscopy (SEM) for morphological changes, colony formation and wound healing assays for proliferation and migration, and flow cytometry for cell cycle and apoptosis analysis. Gene expression changes were evaluated using a qRT-PCR array targeting 84 genes involved in cancer progression. PFDN1 silencing resulted in a 54.8% reduction in PFDN1 protein levels (p < 0.0001). Morphological analysis revealed cytoplasmic shrinkage, chromatin condensation, roughened membranes, and microvilli loss, consistent with apoptotic changes. Colony formation assays showed a 10.33% reduction in colony number and size (p < 0.05) in PFDN1-silenced cells. Migration was significantly impaired, with reduced wound closure observed in wound healing assays (p < 0.01). Flow cytometry revealed a G2/M phase arrest (p < 0.05) and increased early apoptotic populations (20.93% vs. 5.42% in controls, p < 0.01). Gene expression analysis showed downregulation of genes associated with angiogenesis (KDR, TEK), EMT (FOXC2, SNAI1), and hypoxia signaling (CA9, EPO), while proapoptotic genes, such as FASLG, were upregulated. This study highlights the critical role of PFDN1 in TNBC progression, demonstrating that its silencing disrupts survival, migration, cell cycling, and apoptosis pathways. PFDN1 knockdown also significantly alters the expression of key cancer-related genes, further impairing angiogenesis, EMT, and hypoxia adaptation. These findings suggest that targeting PFDN1 could be a promising therapeutic strategy for TNBC, warranting further investigation in preclinical models. - Source: PubMed
Publication date: 2025/03/10
Alokda Abdulrahman MSoffar Ahmed AbdelmagiedYousef Amany IIbrahim Fawziya A REl-Sewedy TarekElmetwalli Alaa - Previous studies have demonstrated widespread brain neurodegeneration in Alzheimer's disease (AD). However, the neurobiological and pathogenic substrates underlying this structural atrophy across the AD spectrum remain largely understood. - Source: PubMed
Publication date: 2024/11/01
Lu YingqiZhang XiaodongHu LiyuCheng QinxiuZhang ZheweiZhang HaoranXie ZhuoranGao YihengCao DezhiChen ShangjieXu Jinping - Although mounting evidence supports that aberrant DNA methylation occurs in the hearts of patients with atrial fibrillation (AF), noninvasive epigenetic characterization of AF has not yet been defined. - Source: PubMed
Publication date: 2023/11/22
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