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
- 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 - Parkinson's disease (PD) is a neurodegenerative disease characterized by progressive loss of dopaminergic neurons. Studies have shown that mesenchymal stem cells (MSCs) have prominent neuroprotective potential to improve PD. Previous study found that dental pulp‑derived MSCs, including stem cells from human exfoliated deciduous teeth (SHED), significantly ameliorated PD-related pathology, but the underlying molecular mechanism remains unclear. In this study, HSPB1 and PARK7 were initially identified through transcriptomic analyses of mouse and clinical samples, immunoprecipitation‑mass spectrometry (IP‑pulldown), and protein‑protein interaction (PPI) network analysis. Using an MPTP-induced SH-SY5Y cell model of PD, we found that SHED treatment alleviated oxidative stress, restored mitochondrial membrane potential, and inhibited apoptosis, accompanied by significant upregulation of HSPB1 and PARK7. Using siRNA interference, we confirmed that both HSPB1 and PARK7 are involved in the improvement of PD by SHED. Rescue experiments showed that HSPB1 overexpression partially restored the neuroprotective effects impaired by PARK7 knockdown, whereas PARK7 overexpression failed to compensate for HSPB1 deficiency, suggesting a functional dependence between PARK7 and HSPB1 in SHED-mediated neuroprotection. This study demonstrates that SHED improves PD pathological progression through the PARK7/HSPB1-related mechanism and indicates that HSPB1 may serve as a potential therapeutic target for PD. - Source: PubMed
Publication date: 2026/08/14
Yu YiqiChen HongyuZheng JingleiLiu ShutingWang XiaoXing CencanDu Hongwu - Retinoblastoma (RB) is one of the most common primary intraocular malignancies in children. Its pathogenesis involves multiple signaling pathways that remain incompletely understood, and effective treatment strategies are still limited. This study aims to identify ferroptosis-related biomarkers and explore their roles in immune infiltration and therapeutic response in RB using bioinformatics approaches. - Source: PubMed
Publication date: 2026/07/28
Fu XingxinGong ChengzhenZhang JunWu MingxingLi XuhuiDai XueshanXu Yan