Ask about this productRelated genes to: DNAJC10 antibody
- Gene:
- DNAJC10 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member C10
- Previous symbol:
- -
- Synonyms:
- ERdj5, PDIA19
- Chromosome:
- 2q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-20
- Date modifiied:
- 2015-11-19
Related products to: DNAJC10 antibody
Related articles to: DNAJC10 antibody
- Recent studies suggested that genetic mutations in the DNAJC family might elevate the risk of Parkinson's disease (PD). Nevertheless, the role of some DNAJC genes in PD remains controversial, and previous studies lacked downstream research. In this study, we aim to explore the relationship between DNAJC family genes and PD in a European cohort through a comprehensive method. - Source: PubMed
Publication date: 2026/04/09
Yang DehaoXu JingxuanZhu YushengLu YangguangYao RuotongYe ZihanYu BohuaiChen JiaxuanZhang TingxuanLiu BowenHuang SuwenChen Guangyong - Following their domestication, chickens were translocated around the world to novel environments. Through a combination of natural and artificial selection, chickens adapted to these local conditions, creating significant genetic diversity across populations worldwide. Studying this diversity in the context of local environmental conditions may offer insights into mechanisms of adaptation to environmental stressors. In this study, we analyzed genomic data from the Chicken Genomic Diversity Consortium, applying multiple statistical approaches, including fixation index (F), nucleotide diversity (π), Tajima’s D, and runs of homozygosity (ROH), to identify selective sweeps among indigenous chickens from Afghanistan, China, Indonesia, Iran and Pakistan, compared with White Leghorn chickens. We identified sweeps in 14 genes related to heat tolerance, associated with relevant gene ontology (GO) terms and located within ROH regions. These genes, such as , , , , , , , , , , , , , , and play crucial roles in calcium signaling pathways, thermal sensation, and the plasticity of neurodevelopmental processes. These findings illustrate the significant role of selection in shaping genomic differentiation across chicken populations and provide insights into the genetic basis of adaptation to environmental stressors. - Source: PubMed
Publication date: 2026/04/07
Hosseinzadeh SevdaRafat Seyed AbbasJavanmard ArashHasanpur KarimBardou PhilippeCharles MathieuKlopp ChristopheSmith Adrian LFiddaman Steven R - Chinese hamster ovary (CHO) cells are widely utilised in the biopharmaceutical industry to produce therapeutic proteins. Understanding the mechanisms of endoplasmic reticulum (ER) stress and its interplay with protein degradation pathways remains pivotal for improving production efficiency and product quality. In this study, we investigated the proteomic responses of CHO-K1 (non-producer), CHO DP-12 (IgG-producer), and NISTCHO (IgG-producer) cell lines under ER stress induced by a combination of the proteasome inhibitor MG132 and the glycosylation inhibitor tunicamycin. Viability, cell growth, and IgG titre were measured after 24 h, 48 h, and 72 h of treatment and the 48 h timepoint was used for the comparative analysis of the proteomic data across the three cell lines. Proteasome inhibition with MG132 intensified ER stress and altered ER-associated protein degradation (ERAD). Combined tunicamycin + MG132 treatment was associated with cell line-specific proteomic changes: NISTCHO upregulated ER translocation and glycoprotein quality control proteins (SSR4, SEC24C, UGGT1), CHO DP-12 activated redox/disulfide regulators (DNAJC10, CAPN1), while CHO-K1 showed broad proteome shifts, suggesting differences in baseline stress handling. These findings provide mechanistic insights into ER stress and protein quality control in CHO cells, offering a foundation for strategies to enhance cell line robustness and optimise biopharmaceutical production. - Source: PubMed
Publication date: 2026/02/10
Sideri Christiana-KondyloRyan DavidHenry MichaelEfeoglu EsenMeleady Paula - Filaminopathies, caused by pathogenic FLNC variants, are rare neuromuscular disorders characterized by protein aggregation, z-disk pathology and lead to progressive muscle weakness and/or cardiomyopathies. - Source: PubMed
Publication date: 2026/02/12
Daya Nassam MSchänzer AnneHentschel AndreasKienitz Marie-CecileSellung DominikSuedkamp NicolinaKrause KarstenKinold Jaqueline CVolke LeonSchreiner AnjaSchlierbach HannaNelke ChristopherKleefeld FelixGuettsches Anne-KatrinZaehres HolmRuck TobiasMavrommatis LamprosRoos AndreasVorgerd Matthias - Glioblastoma (GBM) is characterized by the highly infiltrative growth of cancer cells into the surrounding brain parenchyma. DnaJ Heat Shock Protein Family (Hsp40) Member C10 (DNAJC10, also known as ERDJ5 and PDIA19), involved in endoplasmic reticulum-associated degradation (ERAD), has been identified as a tumor suppressor in several cancers. However, its precise role and underlying mechanism in GBM remain unclear. We found that DNAJC10 expression is downregulated in GBM patients and correlated with poor survival outcomes. Overexpression of DNAJC10 reduced GBM cell migration and invasion in vitro, while its knockdown promotes these processes. Moreover, DNAJC10 overexpression inhibits infiltrative growth of GBM cells, suppresses tumor propagation and prolongs survival in xenografted mice. Mechanistically, DNAJC10 regulates multiple molecules and pathways involved in cell motility, including the epidermal growth factor receptor (EGFR) pathway. Importantly, DNAJC10 overexpression decreases EGFR transcription by inhibiting spliced X-box binding protein 1 (XBP-1s). DNAJC10 regulates XBP-1s splicing through the inositol-requiring enzyme 1α (IRE1α) branch of the unfolded protein response (UPR). XBP-1s binds the EGFR promoter and enhances recruitment of SET7/9 methyltransferase, H3K4me3, and H3K4me1. Pharmacological inhibition of histone methylation attenuates XBP-1s-induced EGFR transcription, indicating XBP-1s promotes EGFR expression via recruiting SET7/9 for H3K4 methylation. XBP-1s overexpression reverses DNAJC10-mediated EGFR downregulation. Collectively, DNAJC10 suppresses EGFR transcription by inhibiting the UPR IRE1α-XBP-1s axis, reducing SET7/9 recruitment and H3K4 methylation at the EGFR promoter. Targeting DNAJC10 or XBP-1s could be a potential approach for inhibiting GBM infiltration and may represent a novel avenue for GBM treatment. - Source: PubMed
Publication date: 2025/10/24
Zhao ErdiYu YueGao YingliLi TengHao ShiyuChen MeiyangXu MingArjun SinkemaniYang ChunyanYin YancunLi Minjing