Human HSP27 ELISA kit
- Known as:
- Human HSP27 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- lf-ek50641
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Human HSP27 ELISA kit
Related genes to: Human HSP27 ELISA kit
- Gene:
- HSPB1 NIH gene
- Name:
- heat shock protein family B (small) member 1
- Previous symbol:
- -
- Synonyms:
- HSP27, HSP28, Hs.76067, Hsp25, CMT2F
- Chromosome:
- 7q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-09
- Date modifiied:
- 2019-04-23
Related products to: Human HSP27 ELISA kit
Related articles to: Human HSP27 ELISA kit
- Canine malignant melanoma is an aggressive neoplasm with limited remedial options. Therefore, the development of novel antineoplastic agents is urgently needed. This study investigated the medicinal potential and molecular mechanisms of Roxb. essential oil (CEO) against canine melanoma. Phytochemical profiling via GC-MS identified 22 compounds, with monoterpenoids (90.99%) predominating, specifically sabinene (53.25%) and terpinen-4-ol (17.99%). CEO exhibited potent, concentration-dependent cytotoxicity across four canine melanoma cell lines, with a mean IC₅₀ of approximately 0.006% v/v. Quantitative proteomic mapping of CEO-treated M5 cells identified a total of 222 differentially expressed proteins associated with systemic cellular collapse. Key mechanisms included significant genotoxic stress (upregulation of H2AX and histone variants), endoplasmic reticulum stress (suppression of CALR and HSPB1), and the activation of a coordinated necroptosis/mitophagy axis (modulation of Drp1, VDAC, and p62). Protein-protein interaction network analysis further identified SLC2A1 as a central metabolic hub with high-confidence connectivity to conventional chemotherapies, suggesting that CEO-induced metabolic disruption converges onto core pathways targeted by 5-fluorouracil and imatinib. These findings suggest that CEO induces complex cell death signatures through coordinated nuclear and organelle stress. Ultimately, it should be considered as a promising candidate for future translational research and functional validation. - Source: PubMed
Publication date: 2026/08/26
Chongrattanameteekul PeerawitKe Chiao-HsuLin Chen-SiChuammitri PhongsakornMatchimakul PitchayaLumsangkul ChompunutOkonogi SiripornMektrirat Raktham - This study employed a bidirectional 2-step, two-sample Mendelian randomization approach to investigate the causal relationships between ferroptosis-related genes and juvenile idiopathic arthritis (JIA) and to explore the mediating role of immune cells. Ferroptosis genes were identified from the deCODE database and matched with protein quantitative trait locus data as exposures to evaluate their causal effects on JIA, while immune cell traits were similarly assessed. For genes showing positive Mendelian randomization results, further analyses were conducted to determine whether immune cells mediated the effects on JIA, with mediation analysis performed only in the presence of causal associations. Data were sourced from the GWAS, FerrDb, and other public repositories. Nine ferroptosis-related genes were found to have causal links with JIA: HSPB1, DECR1, LIFR, and CTSB increased JIA risk, whereas PIEZO1, DPP4, BID, and others were protective. Forty immune cell traits were also causally associated with JIA. Mediation analysis revealed that several immune cells, including CD127- CD8+ T cells, partially mediated the genetic effects, with mediation proportions reaching up to 18.6%. Collectively, these results point to a ferroptosis-immune-JIA axis, suggesting that ferroptosis-related genes contribute to JIA pathogenesis through immune cell mediation and offering new mechanistic insights and potential therapeutic targets. - Source: PubMed
Yang Chun-WuPan Xiu-HuaWang Ji-Gan - Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer; however, its prognosis remains poor, and the underlying molecular mechanisms have yet to be fully elucidated. In this study, a prognostic model was constructed based on manganese metabolism-related genes, which effectively stratifies patients with LUAD with different prognoses and drug sensitivity. Mendelian randomization analysis identified glutathione peroxidase 3 (GPX3) as a key prognostic gene, which was downregulated in LUAD and significantly correlated with favorable outcomes. Functionally, GPX3 was found to inhibit LUAD cell proliferation, invasion, and metastasis while promoting apoptosis. Mechanistically, GPX3 binds to heat shock protein β-1 (HSPB1), induces its ubiquitination, and facilitates its degradation, thereby activating the Hippo signaling pathway and suppressing malignant phenotypes in LUAD cells. In summary, this study not only established a robust prognostic model based on manganese metabolism-related genes but also uncovered the critical regulatory role of the GPX3/HSPB1/yes-associated protein (YAP) axis in LUAD progression, underscoring the therapeutic potential of targeting GPX3. - Source: PubMed
Publication date: 2026/09/02
Wu SixuanHuang HePan JunfanZheng YaqinPan QihongChen SihuiZhang JingLi YuehuaXu Yiquan - We aimed to characterize associations between plasma proteins and indices of left ventricular (LV) diastolic function in two population-based studies. Eighty-six cardiovascular-related plasma proteins measured by proximity extension assay (PEA) and echocardiography were assessed in the population-based studies PIVUS (n = 1,016; all aged 70) and POEM (n = 502; all aged 50). PIVUS served as the discovery cohort, and the Benjamini-Hochberg procedure was applied to control the false-discovery rate (FDR) < 0.05. POEM was used as the replication cohort. The protein panel was related to diastolic echocardiographic parameters. A larger protein panel of 1,322 proteins was examined only in POEM. Seven of 86 proteins showed replicated associations to the E/A ratio: CD40 ligand (CD40LG), proto-oncogene tyrosine-protein kinase Src (SRC), heat shock protein beta-1 (HSPB1), epidermal growth factor (EGF), TNF superfamily member 14 (TNFSF14), vascular endothelial growth factor D (VEGFD), and endothelial cell-specific molecule 1 (ESM1). Using the larger protein panel in POEM, 81 proteins showed significant associations with the E/A ratio, and five showed significant associations with LA diameter. Pathways linked to LV diastolic filling pattern were signal transduction, metabolic, disease and immune system pathways, enhancing the understanding of LV diastolic function and offering potential for future drug development. - Source: PubMed
Publication date: 2026/09/02
Eerola EliasLind LarsMalinovschi Andrei - Endothelial cell (EC) mechanosensing is essential for vascular homeostasis and atherosclerosis development, though the influence of blood flow patterns on EC signaling is not fully understood. Discoidin domain receptor 1 (DDR1), a tyrosine kinase receptor, acts as a mechanosensor linking shear force to endothelial responses. Atheroprotective laminar shear flow induces rapid, transient DDR1 activation and condensation through liquid-liquid phase separation without harmful effects, while atherogenic shear causes delayed, sustained condensation, leading to Yes-associated protein (YAP) activation and downstream pathological signaling. We show that heat shock protein 27 (HSP27) regulates shear-dependent DDR1 condensation and phase transition. Specifically, the interaction between DDR1 and HSP27, mediated by their respective domains, is crucial for DDR1 condensate disassembly. Atherogenic shear, unlike atheroprotective shear, triggers prolonged DDR1-mediated HSP27 phosphorylation, promoting DDR1 gel transition and activating YAP signaling. The DDR1-HSP27 axis is key in endothelial YAP activation and atherogenesis in vivo. Targeting this pathway may offer therapeutic potential for preventing endothelial dysfunction and atherosclerosis. - Source: PubMed
Publication date: 2026/08/14
Zhao DiLiu JiayuLiu YueqiLiang ZhenhuiGui KeYao WeijuanPeng QinWang XiaohongZhou Jing