Hsp40 (Hdj2) Recombinant Human Protein
- Known as:
- Hsp40 (Hdj2) Recombinant Human Protein
- Catalog number:
- ASASPP-405F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Hsp40 (Hdj2) Recombinant Human Protein
Related genes to: Hsp40 (Hdj2) Recombinant Human Protein
- Gene:
- DNAJB1 NIH gene
- Name:
- DnaJ heat shock protein family (Hsp40) member B1
- Previous symbol:
- HSPF1
- Synonyms:
- Hsp40, Sis1, RSPH16B
- Chromosome:
- 19p13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-02
- Date modifiied:
- 2015-11-19
Related products to: Hsp40 (Hdj2) Recombinant Human Protein
Related articles to: Hsp40 (Hdj2) Recombinant Human Protein
- Type 2 diabetes mellitus (T2DM) and sarcopenia demonstrate a significant comorbidity, particularly in the elderly, yet the molecular mechanisms linking them, especially through oxidative stress, remain incompletely understood. This study aimed to identify oxidative stress-related hub genes involved in T2DM-associated sarcopenia (T2DS) by integrating single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data with machine learning. We analyzed scRNA-seq datasets (GSE244515, GSE268953) to characterize cellular heterogeneity and bulk RNA-seq datasets (GSE202295, GSE226151) for differential expression. Cell type annotation revealed key involvement of neuromuscular junctions and myofibers. Functional enrichment analyses highlighted pathways like the proteasome, TNF signaling, and ubiquitin-mediated proteolysis. From an initial set of oxidative stress-related genes, a comprehensive machine learning framework comprising 127 algorithm combinations was employed. The Lasso+Stepglm[both] model identified 12 candidate genes. Subsequent Protein-Protein Interaction (PPI) network analysis refined this to seven core hub genes: TNFRSF1B, PSMA2, UBE2D1, UBE2N, HSP90AA1, RAD23A, and DNAJB1. These genes are functionally interconnected, primarily implicating TNFRSF1B-mediated inflammatory signaling that activates the ubiquitin-proteasome system, leading to enhanced protein degradation-a key pathway in muscle atrophy. ROC curve analysis confirmed the strong diagnostic value of these hub genes across training, test, and external validation sets. Our findings systematically reveal novel oxidative stress-related hub genes and mechanisms in T2DS, providing potential biomarkers and therapeutic targets for this debilitating condition. - Source: PubMed
Publication date: 2026/07/07
Zhu GuangwenZou KaiLiang YiXie LitingChen Qiu - Fibrolamellar carcinoma (FLC) is a rare liver malignancy affecting adolescents. FLCs harbor a DNAJB1-PRKACA gene fusion that combines heat shock protein DNAJB1 with the catalytic subunit of protein kinase A. Surgery with systemic therapy provides 5-year survivals of 30-50%, but advanced disease remains largely incurable. Three-dimensional explants from 41 FLC patients were interrogated for drug sensitivity, resistance, and synergy against cytotoxics, targeted agents, and signal transduction inhibitors. Sterile specimens from histologically confirmed FLC patients were analyzed by Ex Vivo Analysis of Programmed Cell Death (EVA/PCD™) in a CLIA-licensed laboratory. Following mechanical and enzymatic disaggregation, explants underwent 72 h drug exposure. LC values were derived from five-point dose-response curves and compared with a database of over 10,000 human tumor analyses. Synergy was assessed by combination index. In parallel, targeted metabolomic profiling was performed in five FLC patients using tandem MS/MS. Forty-one samples were analyzed. Of 24 drugs selected, tumor-cell yields were adequate for testing in 18 (75%). Single-agent activity favored vorinostat, followed by phenformin and 6-diazo-5-oxo-L-norleucine. Combinations favored gemcitabine plus oxaliplatin (GEMOX) and 5-FU plus interferon. Metabolomic analysis identified distinct signature consistent with mitochondrial dysfunction and altered polyamine metabolism. The present findings are exploratory, and hypothesis-generating and should not be interpreted as evidence of clinical efficacy. Prospective clinical validation and mechanistic studies will be required to further define the therapeutic relevance of these observations in fibrolamellar carcinoma. - Source: PubMed
Publication date: 2026/05/27
Schneider Sabina AD'Amora PauloEvans Steven SKent PaulStockwell TomBakaya Vikrant SBernard Paula JFrancisco Federico RTorres LuisaHenry JohnSilva Ismael D C GNagourney Robert A - Stress granules are conserved biomolecular condensates that form under stress and rapidly disassemble during recovery. Stress granules have been linked to pathological protein aggregation and their impaired disassembly reduces cell viability, yet the mechanisms governing their clearance and protein aggregation remain unclear. We find that human HSP70 and a subset of J-domain proteins (JDPs) localize to stress granules and that chemical or genetic inhibition of these chaperones markedly slows granule disassembly. Conversely, overexpressing these JDPs, particularly DNAJB1, accelerates disassembly without altering assembly. In vitro, HSP70 and DNAJB1 partition into G3BP1 condensates and reduce their size in an ATP-dependent manner. In cells expressing amyotrophic lateral sclerosis (ALS)-linked mutant FUS, DNAJB1 depletion further impairs stress granule clearance and promotes pre-amyloid accumulation, while depleting a non-stress granule JDP has no effect. Our findings demonstrate that specific JDP chaperones enhance stress granule disassembly and help limit aberrant protein aggregation. - Source: PubMed
Publication date: 2026/06/08
Mastromarco Giovanni JEarnshaw RebeccaMoore GaelenXu X Y SherwinSadek Nour HCui FionaLo NatalieLee Hyun O - Spinocerebellar ataxia type 3 (SCA3), the most common inherited ataxia, lacks effective therapies. Current microRNA (miRNA) approaches directly targeting ataxin-3 (ATXN3) mRNA risk reducing essential wild-type ATXN3, a key regulator of proteostasis and various signaling pathways. Consequently, developing neuron-targeted, noninvasive miRNA delivery strategies that employ alternative mechanisms is critical for SCA3. In this study, we engineered rabies virus glycoprotein (RVG)-modified exosomes to deliver miR-370 inhibitors to the brains of SCA3 mice, thereby upregulating the molecular chaperone DnaJ homolog subfamily B member 1 (DNAJB1) to promote clearance of mutant ATXN3. Systemic administration of RVG-exosomes carrying miR-370 inhibitors led to increased DNAJB1 expression, reduced mutant ATXN3 aggregation, improved neuronal survival, and restored motor coordination in SCA3 mice. Furthermore, combining miR-370 inhibitors with miR-25-a miRNA that directly targets ATXN3 mRNA-synergistically enhanced the reduction of pathogenic ATXN3 and provided greater neuroprotection compared to either therapy alone. These findings support the use of RVG-exosome-mediated miR-370 inhibition as a noninvasive strategy to improve proteostasis in SCA3 and demonstrate its potential in combination with ATXN3 mRNA-targeting miRNAs, offering a promising therapeutic paradigm for SCA3 and similar neurodegenerative disorders. - Source: PubMed
Zhang ZiyiGao ShuguangQin LixiaHe Miao - Intraductal oncocytic papillary neoplasms (IOPNs) are rare tumors that develop from biliary and pancreatic ductal epithelium and progress to lethal cancers. Human IOPNs and IOPN-associated carcinomas are known to harbor the gene fusion, however the role of the oncogenic fusion in carcinogenesis is poorly understood. We developed a Cre-inducible mouse model of human DNAJB1-PRKACA expression and substantiated that the fusion gene is a bona fide driver of IOPN-associated biliary and pancreatic carcinoma. By analyzing the unique histopathologic and transcriptional changes that occur at each stage of tumor development, we found that these murine tumors closely mimic human driven tumors. Furthermore, we identified that many of the salient features of invasive carcinoma are established at the pre-invasive stage, including evidence of tumor cell metabolic dysregulation, immunosuppressive tumor stroma and expression of genes strongly associated with invasive driven cancer in humans. Finally, we found that , a characteristic regulated super-enhancer associated gene, serves as a robust biomarker of malignant transformation from IOPN to invasive carcinoma. - Source: PubMed
Publication date: 2026/05/27
Carney Patrick RNukaya ManabuCarter Jason AVeltri Anthony JMatkowskyj Kristina AStram AustinRubinstein C DustinVeith Alex CPillarisetty Venu GBradfield Christopher ARonnekleiv-Kelly Sean M