Human HSP27 ELISA kit
- Known as:
- Human HSP27 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- LF-EK50641
- Product Quantity:
- 1
- Category:
- Elisa Kits
- Supplier:
- Abfron
- 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
- Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis and induces systemic physiological changes. This study aimed to identify stress-associated serum biomarker candidates in chronically stressed beagle dogs and to evaluate the anti-stress effects of var. (Maxim.) Kitam. extract (CZE). Beagle dogs were subjected to movement restriction-induced chronic stress for 42 days, with or without repeated oral administration of CZE. Serum cortisol and corticosterone concentrations were measured using ELISA, and hematological and serum biochemical parameters were analyzed. Serum samples collected at day 0 and day 42 of the 84-day chronic stress model were subjected to LC-MS/MS-based proteomic analysis. Chronic stress increased serum cortisol and corticosterone concentrations and induced alterations in hematological and serum biochemical parameters, whereas CZE administration tended to attenuate or stabilize these stress-associated changes. Proteomic analysis identified 380 serum proteins, of which 348 quantified proteins were subjected to differential expression analysis. The differentially expressed proteins were primarily associated with immune response, inflammatory response, extracellular matrix organization, angiogenesis, neurogenesis, and secretion. TIMP1, TREM2, RAB8A, KRT9, PPBP, THBS1, and HSPB1 were identified as candidate stress-associated serum biomarkers. These findings indicate that chronic stress induces endocrine, hematological, biochemical, and serum proteomic alterations in beagle dogs. Changes in proteins related to immune-inflammatory regulation and extracellular matrix organization suggest that prolonged stress may affect systemic immune responses and tissue remodeling. CZE may contribute to the maintenance of physiological homeostasis under chronic stress conditions and may have potential as a functional anti-stress material, while the identified serum proteins may provide a basis for the development of biomarkers for chronic stress. - Source: PubMed
Publication date: 2026/08/26
Yang Ye JinKim Min JungKim Hee HoHeo Ji WoongChun Ju LanShin Eui-CheolKim Kyeong SooKim Hyun-WookJeong Eun JuLee DongbinPark Kwang Il - Advanced CRC patients frequently accompanied by hepatic metastasis (HM). Malignant epithelial cells, as the core in metastasis, have not been fully investigated. This study investigates the role of malignant epithelial cells in CRC HM and its underlying mechanisms. - Source: PubMed
Publication date: 2026/09/12
Zhu WenlongDong AoHu RongbingZhou SileiYao JialiMa BinghuaDing JinZhang Yanjie - 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