GRP78 Antibody - C-terminal region (ARP30176_P050)
- Known as:
- GRP78 Antibody - C-terminal region (ARP30176_P050)
- Catalog number:
- arp30176_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GRP78 Antibody - C-terminal region (ARP30176_P050)
Related genes to: GRP78 Antibody - C-terminal region (ARP30176_P050)
- 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 - C-terminal region (ARP30176_P050)
Related articles to: GRP78 Antibody - C-terminal region (ARP30176_P050)
- Tauroursodeoxycholic acid (TUDCA) has been shown to improve endothelial dysfunction in type 2 diabetes mellitus (T2DM). However, its role in attenuating endothelial insulin resistance in diabetes is not well understood. - Source: PubMed
Publication date: 2026/04/16
Mustapha SagirAzemi Ahmad KhusairiRasool Aida Hanum GhulamMokhtar Siti Safiah - Yeast models are widely used to study molecular chaperones from diverse organisms, including plants, because of their well-characterized genetics and the conservation of the protein-folding machinery among eukaryotes. Cross-species complementation studies in yeast have yielded valuable insights into conserved biochemical activity and molecular functions that manage protein folding, assembly, and repair during stress. This study evaluated the functional capacity of three potato isoforms (, , and ) to complement the deletion () strain under a range of environmental and ER stress conditions. All three partially restored colony growth under normal conditions, demonstrating that they are functional orthologs of yeast and can support core ER housekeeping functions. Under severe stress, however, the isoforms diverged: most effectively complemented the strain during heat- and chemically induced ER stress, whereas and provided weaker protection. Unfolded protein response (UPR) activation, monitored via mRNA splicing, further highlighted isoform-specific differences in how the StBiPs support IRE1-HAC1 signaling under ER stress and oxidative stress. A conserved cysteine in the nucleotide-binding domain, previously implicated in Kar2 redox control, was also critical for StBiP3-mediated protection in yeast, although the same mutation led to different consequences in plant tissues. Together, these findings provide evidence of subfunctionalization among potato BiP isoforms, with StBiP3 emerging as a stress-specialized chaperone that is a promising target for improving ER stress resilience in solanaceous crops. - Source: PubMed
Publication date: 2026/03/28
Adhikari BinitaGordon Donna MVerchot Jeanmarie - Senecavirus A (SVA), also known as Seneca Valley virus (SVV), is an important small RNA virus that causes swine vesicular disease, posing a significant threat to the global swine industry. To date, the molecular mechanism of SVA replication remains poorly understood. Heat shock proteins (HSPs) are a family of molecular chaperone proteins that are widely present in organisms. More and more studies have shown that HSPs are associated with viral infections. Here, we screened HSPs and found that overexpression of HSPA5 significantly inhibited SVA replication, while knockout of HSPA5 promoted SVA proliferation. Further analysis showed that HSPA5 started to inhibit SVA proliferation at the stage of viral replication, and by screening SVA-encoded proteins, we found that HSPA5 degraded and interacted with the viral protein VP2 through the autophagy pathway. Mechanistically, HSPA5 participates in the degradation of VP2 proteins by activating autophagy mediated by the PERK-eIF2α pathway. In addition, the NBD region of HSPA5 is critical for VP2 degradation, and the Thr180 residue of VP2 has been identified as a key target for HSPA5 to inhibit the VP2 protein. The VP2 mutant virus rT180N showed resistance to the antiviral activity of HSPA5 compared with wild-type SVA and repair virus rT180N(R). In conclusion, these findings indicate that HSPA5 is an effective antiviral factor that suppresses SVA infection and contributes to a better understanding of the antiviral mechanism of HSPA5 and virus-host interactions. - Source: PubMed
Publication date: 2026/04/13
Li LiangBi RuiminLi JieChang MeifangZhao JintingWang XuanWei LiChang XinyueCheng YanYin ZongjunWang JunZhou YingchunBo ZongyiShen HaixiaoYan JunfangLiu XuelanSun Pei - Progranulin (PGRN) exerts neuroprotective effects. However, the roles of PGRN in cerebral ischemia/reperfusion (I/R) injury have not been reported. - Source: PubMed
Publication date: 2026/04/10
Su GuilongLi BinruLu WanxingHuang ZhengxiangNong WeidongLuo Chun - Chronic short sleep (CSS) is an emerging public health issue that frequently begins in adolescence and is common among healthcare professionals and others engaged in shift work. Epidemiological studies associate CSS and sleep disruption with metabolic disorders, cardiovascular disease, cognitive decline, and heightened Alzheimer's disease risk. Building on our prior findings that sleep deprivation perturbs proteostasis and activates endoplasmic reticulum (ER) stress pathways, we investigated the long-term consequences of CSS in young adult wild-type mice over the course of one year. Mice exposed to CSS displayed impaired cognition in hippocampal dependent tasks by 28 weeks of age, indicating emerging memory deficits. At the molecular level, CSS disrupted hippocampal proteostasis-particularly protein folding processes-and triggered ER stress and activation of the unfolded protein response (UPR). Importantly, disrupted proteostasis preceded the behavioral decline, with diminution of the key chaperone and UPR regulator BiP occurring at 20-22 weeks of age. CSS also increased markers of cellular stress and neuroinflammation while reducing the expression of proteins associated with memory function. Age also seemed to be a cellular stressor, causing a longitudinal increase in UPR, ISR, and neuroinflammation markers. Together, these results indicate that both chronic short sleep and age compromise proteostasis and promote neuroinflammation, contributing to progressive cognitive dysfunction. - Source: PubMed
Publication date: 2026/03/30
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