GRP78 Antibody (OASE00341)
- Known as:
- GRP78 Antibody (OASE00341)
- Catalog number:
- oase00341
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GRP78 Antibody (OASE00341)
Related genes to: GRP78 Antibody (OASE00341)
- Gene:
- HSPA5 NIH gene
- Name:
- heat shock protein family A (Hsp70) member 5
- Previous symbol:
- GRP78
- Synonyms:
- BiP
- Chromosome:
- 9q33.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-26
- Date modifiied:
- 2015-11-19
Related products to: GRP78 Antibody (OASE00341)
Related articles to: GRP78 Antibody (OASE00341)
- Endoplasmic reticulum stress (ERS) is an important pathophysiological mechanism involved in the development and progression of sepsis-related myocardial injury (SRMI). This study aims to investigate the protective effect of the ERS inhibitor 4‑phenylbutyric acid (4PBA) against myocardial injury in lipopolysaccharide (LPS)‑induced SRMI. - Source: PubMed
Xiong WeiDai JinweiXu WenyeJin RuiChen YitingZhang LinaQian Zhaoxin - Fluvoxamine maleate (FM) is a selective serotonin reuptake inhibitor (SSRI) that has attracted increased attention owing to its strong agonistic activity at the sigma 1 receptor (σ1R). This review consolidates the current understanding of its processes highlighting σ1R-mediated chaperone activity in the endoplasmic reticulum (ER), which alleviates protein misfolding, ER stress, and neuroinflammation in mental and neurological illnesses. Fluvoxamine demonstrates one of the highest affinities for σ1R among SSRIs, exceeding those of sertraline and fluoxetine, via dissociating σ1R from BiP chaperones to improve protein refolding and cellular resilience. Preclinical experiments illustrate its inhibition of unfolded protein response indicators, reinstatement of glutamatergic transmission, and stimulation of parvalbumin interneurons, resulting in antipsychotic-like effects in schizophrenia and neuroprotection against ketamine-induced impairments. In addition to serotonin reuptake inhibition, fluvoxamine influences inflammation, apoptosis, and extracellular matrix dynamics. Supplementary activities include advantages against tardive dyskinesia and cognitive improvement in depression by mitigating stress induced neuronal atrophy. Repurposing initiatives underscore fluvoxamine's potential beyond obsessive compulsive disorder (OCD) and depression. σ1R agonism is fundamental to its effectiveness in disorders caused by ER stress, such as schizophrenia and tardive dyskinesia, and in neuropsychiatric sequelae associated with protracted COVID. Clinical translation encounters obstacles in dose optimization and σ1R selectivity; yet, current studies highlight its multimodal efficacy in neurodegeneration, fibrosis, and psychopharmacology. - Source: PubMed
Publication date: 2026/08/27
Sharma ChiragSharma SheenamChaudhary RishabhKumar SatishBansal SeemaNair AnroopGupta Sumeet - Oxidative stress is a central pathological mechanism in neurodegenerative diseases (NDDs), contributing to mitochondrial dysfunction, impaired proteostasis, and progressive neuronal loss. The sigma-1 receptor (S1R) is an endoplasmic reticulum (ER)-resident chaperone that coordinates cellular stress responses and has emerged as a promising therapeutic target for neuroprotection. In this study, we investigated the neuroprotective properties and mechanisms of the structurally related N-benzylamides, N-benzylcinnamide (NBCA) and N-benzylbenzamide (NBBA) using complementary in vitro, in vivo and in silico approaches. Neuroprotective activity was initially evaluated using glutamate-induced oxidative injury in HT22 hippocampal neurones and HO-induced oxidative stress in SH-SY5Y neuroblastoma cells. Both compounds significantly attenuated oxidative injury, although NBCA consistently showed greater efficacy and was therefore selected for detailed mechanistic investigation. NBCA reduced intracellular reactive oxygen species (ROS) production and lipid peroxidation while restoring endogenous antioxidant enzyme activities, mitochondrial membrane potential, ATP production, and cholinergic homeostasis. Immunofluorescence analysis showed that NBCA modulated nuclear factor erythroid 2-related factor 2 (NRF2) and S1R immunoreactivity after oxidative stress. NBCA also promoted neurite outgrowth in wild-type (WT) Neuro-2a cells, whereas these effects were absent in S1R knockout cells, supporting the involvement of S1R-associated signalling. Molecular docking predicted favourable interactions between NBCA and the stress-response proteins S1R, BiP and TMEM97, suggesting modulation of interconnected cellular stress-response networks. In Caenorhabditis elegans, NBCA improved resistance to oxidative stress, preserved learning and memory, delayed amyloid-β-induced paralysis, and reduced amyloid deposition in transgenic Alzheimer's disease (AD) models. Collectively, these findings demonstrate that NBCA exerts neuroprotective effects across multiple experimental models by preserving redox homeostasis, mitochondrial function, and neuronal integrity. The convergence of pharmacological, genetic, imaging, computational, and whole-organism evidence supports the involvement of S1R-associated signalling in NBCA's biological activity. Together, these findings demonstrate that modulation of S1R-associated cellular stress-response networks is a promising strategy for preserving neuronal function during oxidative stress and neurodegeneration and identify NBCA as a valuable lead compound for future mechanistic and therapeutic investigation. - Source: PubMed
Mamangam SubarajaDhanabalan Anantha KrishnanVerma KanikaPrasanth Mani IyerBrimson SirikalayaBrimson James Michael - Diabetic kidney disease (DKD) causes high mortality and imposes a substantial healthcare burden, representing a major global public health challenge. The natural flavonoid diosmetin (DIO) shows promising therapeutic effects in DKD; however, its molecular mechanisms remain unclear. This study is aimed at clarifying the specific mechanisms and molecular targets through which DIO exerts its effects in DKD. - Source: PubMed
Zhang TianyuZhao NaLiu TongjinGao YameiDi ZhiyueGao YueJi YananLv ShuquanXie QingyingMa JianCui Huantian - Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent liver disease associated with insulin resistance and hepatic lipid accumulation. Polyphenols have attracted considerable attention for their hepatoprotective and lipid-lowering activities. Our previous studies characterized a bound polyphenol extracted from the inner shell of foxtail millet (BPIS) and identified its major active components. In the present study, we investigated the molecular mechanisms underlying its biological activity using HepG2 cells and . BPIS activated AMPK signaling, normalized intracellular glutathione (GSH) levels, and upregulated SLC7A11 and GPX4, suggesting modulation of ferroptosis-related pathways and improved cellular redox homeostasis. BPIS also alleviated endoplasmic reticulum stress by increasing GRP78 expression, inhibiting DRAK2, and regulating the ERK pathway, thereby improving the regulation of key lipid-metabolism-related signaling pathways, including SREBP1c, SCD1, CD36, FASN, and CPT1A. Consistent with these findings, BPIS reduced glucose- and free fatty acid-induced lipid accumulation and improved lipid-related phenotypes in . Overall, BPIS attenuated hepatic steatosis through modulation of ferroptosis-related markers, endoplasmic reticulum stress, and lipid metabolism. These findings provide new mechanistic insights into the biological activities of BPIS and support its potential application as a nutraceutical ingredient for the prevention and management of MASLD. - Source: PubMed
Publication date: 2026/08/31
Ghani IsrarQiao QinqinLi SongtaoLiu YuanshengLi Zhuoyu