Ask about this productRelated genes to: PDIA4 antibody
- Gene:
- PDIA4 NIH gene
- Name:
- protein disulfide isomerase family A member 4
- Previous symbol:
- -
- Synonyms:
- ERP70, ERP72
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-03-02
- Date modifiied:
- 2016-10-05
Related products to: PDIA4 antibody
Related articles to: PDIA4 antibody
- Extracellular matrix remodeling, cellular stress responses, and blood-brain/blood-tumor barrier-related alterations are important processes involved in brain tumor biology. This exploratory cross-sectional pilot study evaluated circulating circulating protein disulfide isomerase A4 (PDIA4), matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and claudin-2 (CLDN2) concentrations in vitamin D-deficient patients with different brain tumor entities and aimed to provide preliminary effect-size estimates for future studies. A total of 62 vitamin D-deficient participants were included, comprising patients with glioblastoma (GBM; = 15), brain metastases ( = 20), and meningioma ( = 8) and surgical controls with degenerative spine disease ( = 19). Serum biomarker concentrations were measured using enzyme-linked immunosorbent assays. Global between-group effect sizes were estimated using η, while exploratory pairwise comparisons and associations with tumor size were assessed using non-parametric methods. Effect-size estimates were prioritized, with -values reported to provide complementary inferential context. The largest global between-group effect-sizes were observed for CLDN2 (η = 0.35) and MMP-2 (η = 0.22), whereas the estimated effects were small for MMP-9 (η = 0.05) and negligible for PDIA4 (η = 0.00). Exploratory pairwise comparisons indicated lower serum MMP-2 concentrations in patients with GBM than in surgical controls and lower CLDN2 concentrations in patients with GBM and brain metastases than in controls. Positive exploratory associations were observed between tumor size and PDIA4 concentration in the GBM group (Spearman's rho = 0.56; 95% CI: 0.02-0.90) and between tumor size and MMP-2 concentration in patients with brain metastases (rho = 0.46; 95% CI: 0.01-0.90). These preliminary effect-size estimates, together with the exploratory correlations with tumor size, may inform biomarker selection and sample-size planning in future prospective studies. The findings should not be interpreted as robust diagnostic or prognostic evidence and require validation in larger, independent, and well-controlled cohorts. - Source: PubMed
Publication date: 2026/08/10
Gromadzki BartłomiejWiciński MichałSiedlecki ZygmuntPorzych RafałPisarski Igor - A strong crosstalk exists between endoplasmic reticulum (ER) stress and synovitis. Beyond their canonical role in protein folding, ER stress chaperones may promote inflammation, cell survival, and fibroblast activation under pathological conditions. This study aimed at localizing and quantifying 11 ER stress proteins (BiP, HYOU1, MANF, PDIA4, GANAB, HSP90B1, TXNDC5, DNAJB11, LMAN1, ERP29, CALR) in human inflamed synovial membranes and at investigating their expression in fibroblast-like synoviocytes (FLS) under ER stress, pro-inflammatory, or pro-fibrotic stimuli. By immunohistochemistry, on a first cohort of formalin-fixed paraffin-embedded (FFPE) biopsies obtained from patients with osteoarthritis (OA), chronic pyrophosphate arthropathy (CPPA), and rheumatoid arthritis (RA), these ER chaperones were primarily localized to the lining in low-grade inflammation (Tak <4) and expanded to the sublining under high inflammatory conditions (Tak ≥4), with a widespread distribution in RA. Imaging mass cytometry, applied to a second cohort of FFPE tissue samples collected from patients diagnosed with OA and RA, revealed the co-expression of ER stress proteins with CD55⁺ FLS in the lining and their progressive infiltration into the sublining along with CD34⁺CD31 FLS during inflammation. These observations were confirmed by immunofluorescence on a larger cohort of OA patients. As inflammation progresses, there is a loss of co-expression with CD55 in the lining, accompanied by a gradual shift towards co-expression with CD34 in the sublining. In vitro, ER stress proteins, particularly BiP, HYOU1, MANF, PDIA4, HSP90B1, LMAN1, CALR, and DNAJB11 are overexpressed in human OA FLS following ER stress, pro-inflammatory or pro-fibrotic stimulation, with BiP, PDIA4, HSP90B1, ERP29, and CALR also being secreted. PDIA4 emerged as a central player: its depletion significantly impaired FLS proliferation and migration, highlighting a direct role in driving synovitis. This study provides the first spatial and functional characterization of ER chaperones in human arthritic synovium, linking ER stress to fibroblast plasticity, inflammation, and fibrosis. - Source: PubMed
Publication date: 2026/08/12
Gendebien ZoéPoulet ChristopheDeroyer CélinePaulissen GenevièveSalpetier PaulineHego AlexandreLefèvre GaëtanCobraiville GaëlNeuville SophiePlener ZeldaDaniel ChristopheThirion ThierrySokolova TatianaDurez PatrickHemon PatriceDelarue YunaMarec NadègeBianchi ElettraDelvenne PhilippeRibbens Cliode Seny Dominique - Oxidative stress and inflammation, and the accumulation of unfolded proteins are primary causes in the pathophysiology of peripheral artery disease (PAD), which develops in the presence of type 2 diabetes mellitus (T2DM), characterized by hyperglycemia and insulin resistance. It has been reported that the interaction between endoplasmic reticulum (ER) stress protein, protein disulfide isomerase (PDIA4), and receptor for advanced glycation end products (RAGE) make significant contributions to these processes. Our study aimed to investigate variations in the -2 rs35652124 and -2 rs6721961 polymorphic regions in PAD and examine the relationship between these variations and RAGE and PDIA4 protein levels. - Source: PubMed
Publication date: 2026/07/07
Kara Hatice ZühreYanar FatihPunar ŞeymaAbacı NeslihanEkmekçi Sema SırmaBaşar YılmazSalmayenli NihalÖzkök Elif - Breast cancer remains a leading cause of cancer-related mortality in women, and current prognostic models are suboptimal. The transcriptomic role of programmed cell death (PCD) in breast cancer progression is not fully understood. Here, we integrated single-cell RNA sequencing data from breast tumors with nine bulk transcriptomic cohorts to systematically analyze 19 PCD modalities. Using a machine learning framework incorporating 14 algorithms, we constructed a prognostic signature, with a ridge regression-based PCD riskscore showing optimal performance and being further integrated into a clinical nomogram. Functional roles of key genes were validated through and experiments. We identified a prognostic signature comprising 26 core PCD genes, which effectively stratified patients into distinct risk groups and robustly predicted overall survival. Single-cell analyses revealed that a high PCD risk core was associated with an immunosuppressive tumor microenvironment and reduced immune checkpoint expression, whereas low-risk patients showed greater sensitivity to targeted therapies. Among the signature genes, was consistently overexpressed in 50 paired breast cancer tissues, and its knockdown markedly inhibited tumor growth and malignant phenotypes. This study establishes a novel PCD-based prognostic signature for breast cancer and identifies as a functionally important oncogene. - Source: PubMed
Publication date: 2026/07/25
Jiang JixuanWang YiwenHuang YujuYan WeiwenLi ShuweiWang Ruoxi - Cervical cancer continues to pose a considerable challenge to global health, necessitating innovative approaches for improved diagnostics and personalized treatment strategies. Prior investigations have suggested that plasma proteins may play a role in the pathogenesis of cervical cancer; however, these studies do not confirm a causal relationship. To address this gap, conducted a large-scale Mendelian randomization (MR) study of the plasma proteome. - Source: PubMed
Publication date: 2026/07/01
Zhao Yan-HongRuan Qing-FenNing Jing-HuaZhang XinQu RunZou JingLiang YiZhang Cheng-GuiZhang Yu-Zhe