Ask about this productRelated genes to: HSP90B1 Blocking Peptide
- Gene:
- HSP90B1 NIH gene
- Name:
- heat shock protein 90 beta family member 1
- Previous symbol:
- TRA1
- Synonyms:
- GP96, GRP94
- Chromosome:
- 12q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-03
- Date modifiied:
- 2016-10-11
Related products to: HSP90B1 Blocking Peptide
Related articles to: HSP90B1 Blocking Peptide
- (pea aphid) is a major pest of Fabaceae (legume) crops, causing direct feeding damage and transmitting plant diseases. Conventional control relies on broad-spectrum insecticides and natural enemies, both of which can harm non-target organisms and ecosystems. RNA interference (RNAi) offers a promising, species-specific alternative by silencing essential genes double-stranded RNA (dsRNA). This study targeted two heat shock protein Genes-Heat Shock 70 kDa Protein 1-Like () and Heat Shock Protein 90 kDa beta (Grp94) Member 1 ()-key players in protein folding, quality control, and stress response within the Unfolded Protein Response () pathway. These chaperones stabilize proteins, assist in folding newly synthesized polypeptides, and target misfolded proteins for degradation. Silencing these genes was hypothesized to cause accumulation of misfolded proteins, triggering Endoplasmic Reticulum (ER) stress, overload, and ultimately apoptosis, leading to aphid mortality. Total RNA was extracted from adult pea aphids, reverse-transcribed to cDNA, and used to synthesize gene-specific dsRNAs for and . These dsRNAs were encapsulated in Branched-Amphiphilic Peptide Capsules (BAPCs) and delivered orally at concentrations of 10 ng/μL and 100 ng/μL artificial diet feeding. Survival was monitored every 6 hours for 48 hours on dsRNA diet, followed by transfer to healthy faba bean leaves. Preliminary studies indicated positive correlations between gene knockdown and elevated mortality. Results demonstrated significantly reduced survival in treated groups compared to controls at both concentrations (Kaplan-Meier survival analysis, log-rank p<0.001), supporting the induction of apoptosis. This approach highlights the potential of -targeted RNAi for eco-friendly, targeted pest control. - Source: PubMed
Publication date: 2026/01/06
Davies GriffinBalthazor James - The developmental pace and sex ratio of preimplantation embryos have major implications for pregnancy outcome and herd replacement. We asked whether selecting embryos that develop faster preferentially captures distinct molecular and metabolic states and inadvertently affects the sex ratio in bovine in vitro produced (IVP) blastocysts. Hatching-stage blastocysts (pool of blastocysts undergoing and having completed the hatching process) developed on Day 7 and Day 8 of in vitro culture (IVC) were analyzed by RNA-sequencing, alongside assessments of lipid content, mitochondrial activity, and reactive oxygen species (ROS). Sexing was performed via Y-chromosome multiplex PCR, and candidate genes were quantified by qPCR in individually sexed hatching-stage embryos. RNA-sequencing identified 192 differentially expressed genes. Notably, significantly higher expression of pregnancy recognition factors (IFNT2, IFNT3) and the trophoblast marker TKDP1, along with glycolytic, lipid transport genes was observed on Day 8. In contrast, hatching-stage blastocysts from Day 7 displayed upregulation of oxidative phosphorylation genes. Mitochondrial activity and ROS levels were comparable between groups, but Day 7 embryos contained significantly more lipids. Interestingly, sexing analysis revealed a significant male bias among these blastocysts on Day 7 (66.7%) and Day 8 (58.5%). Candidate gene expression analysis revealed sexually dimorphic regulation of UQCRC2 and developmental day-dependent regulation of ENO1, UQCRC2, HSP90B1, and APOA1. Collectively, these findings indicate that hatching-stage blastocysts developed on Day 7 and Day 8 of IVC represent distinct physiological states and demonstrate that selecting embryos for rapid development can inadvertently skew sex ratios and molecular profiles in bovine IVP embryos. - Source: PubMed
Publication date: 2026/04/24
Baddela Vijay SimhaFersterer TheresPöhland Ralfde Andrade Melo-Sterza FabianaLudwig Carolin L MBecker DoreenKühn ChristaVanselow Jens - Heat shock protein Gp96 (also known as Grp94 or endoplasmin) is the endoplasmic reticulum (ER)-resident paralog of the Hsp90 family and a central regulator of ER proteostasis and immune receptor biogenesis in mammalian cells. By controlling the folding, quality control, and trafficking of a restricted yet functionally critical set of client proteins, including Toll-like receptors, integrins, and immunoglobulins, Gp96 plays an essential role in innate immunity and inflammatory signaling. In the context of malaria, accumulating evidence suggests that host-derived Gp96 is involved in immune activation and disease severity, notably through its extracellular release under conditions of cellular stress, where it functions as a danger-associated molecular pattern (DAMP). Elevated circulating Gp96 levels have been associated with severe malaria phenotypes, supporting its potential value as a biomarker of host stress and immune dysregulation. In parallel, expresses its own ER-resident Hsp90 homolog, PfGp96, which retains the conserved domain architecture of Hsp90 while exhibiting parasite-specific adaptations, including divergence in ER retention motifs. However, the biological functions, client repertoire, and essentiality of PfGp96 remain poorly defined, and direct evidence supporting its validation as a drug target is currently limited. This review critically synthesizes current knowledge on Gp96 and PfGp96, emphasizing experimentally validated functions, host-parasite interface dynamics, and unresolved knowledge gaps. We discuss the opportunities and challenges of targeting Gp96-related pathways for biomarker development and therapeutic intervention in malaria, while outlining key priorities for future functional and translational research. - Source: PubMed
Publication date: 2026/03/26
Djoumoi DjibabaDiouara Abou Abdallah MalickDiop MamadouNguer Cheikh MomarMbengue BabacarThiam Fatou - The transcriptomic effects of hybridization and triploidization were investigated in diploid and triploid rainbow trout, diploid brook trout, as well as triploid hybrids of rainbow trout and brook trout. The examined fish were reared under identical conditions for about two and a half years after hatching. Expression of ten genes involved in cellular respiration (, ), mitochondrial functioning (, ), ribosome biogenesis (, ), proteasome-mediated protein turnover (, ), and protein chaperoning (, ) was studied in liver and muscle tissues. Most of the analyzed genes (, , , , , , and ) displayed comparable expression levels in the liver tissue across the examined triploid hybrids and diploid parental species, with stabilization of genes that were both positively and negatively compensated in the triploid rainbow trout. In turn, significant upregulation of , , and genes, together with downregulation of gene, was observed in the triploid rainbow trout liver and muscle, respectively. On the other hand, triploid hybrids showed marked transcriptional upregulation of genes primarily associated with energy metabolism and protein synthesis (, , , and ) relative to all the fish groups examined. Although protein-synthesis- and energy-related genes were upregulated in the muscles of triploid hybrids, the recorded growth performance data did not indicate clear evidence of growth heterosis (MPH = -14.3% for body weight; MPH = -0.4% for body length), suggesting that potential benefits of increased heterozygosity in this cross may not be fully reflected in enhanced growth. Three- to four-fold downregulation of the heat shock protein () gene was also observed in both tissues of triploid hybrids compared with purebred diploid and triploid trout, which may reflect potential maladaptive genomic effects commonly observed in distant salmonid crosses, suggesting altered stress-response regulation in the examined triploid hybrids. - Source: PubMed
Publication date: 2026/03/17
Kuciński MarcinRożyński RafałOcalewicz Konrad - Cellular senescence remodels the microenvironment via SASP, and immune inflammation promotes carcinogenesis through DNA damage and immune remodeling; the “senescence-inflammation” vicious cycle formed by these two processes is a core driver of cancer development and progression, yet its mechanism in prostate cancer progression remains unclear. The regulatory mechanisms of “senescence-inflammation” related genes in prostate cancer were revealed, targeted drugs were predicted, and new insights were provided for the clinical treatment of prostate cancer. In this study, gene expression profile data of prostate cancer were obtained from the Gene Expression Omnibus (GEO). Differentially expressed genes were screened out through bioinformatics analysis and verified by experiments; GO and KEGG analyses were used to explore the prostate cancer-specific biological processes and signaling pathways involved, immune infiltration characteristics were revealed by combining immune infiltration tools with single-cell technology, and finally, drugs with therapeutic potential were predicted through core gene target analysis. Prostate cancer-related differentially expressed genes were found to number 203. Notable hub genes included ACTB, RPLP0, TOP2A, TXN, HSP90B1, TAGLN, RPSA, and ANXA2. According to enrichment analysis, apoptosis, cellular senescence, inflammation, and the initiation of immunological responses are the main factors contributing to the development of bladder cancer. The immunological processes of prostate cancer are significantly influenced by memory B cells, CD8 T cells, follicular helper T cells, M1 macrophages, monocytes, and NK cells, as confirmed by immune infiltration and single-cell data. Furthermore, hub genes were found to be significantly expressed in a variety of immune cells by single-cell studies; monocytes and macrophages in particular exhibited high levels of ACTB, RPLP0, RPSA, and ANXA2. We next used Western blotting, PCR, and immunohistochemistry to evaluate these genes’ expression in clinical samples. Lastly, Miconazole, Fostamatinib, Quercetin, Resveratrol, and Regorafenib were shown to be possible important drugs or ingredients for the treatment of prostate cancer by our drug-target interaction prediction analysis. We clarified the mechanism by which immune-inflammatory and aging-related genes contribute to the pathogenesis of prostate cancer. We identified and validated four core genes, namely TXN, TOP2A, ANXA2, and HSP90B1, and predicted potential therapeutic agents, specifically resveratrol and regorafenib. These findings provide a theoretical basis for research on the molecular mechanisms of prostate cancer and its clinical treatment. - Source: PubMed
Publication date: 2026/03/07
Wang YingLiu QinYi MeiLiu YanHe Ji'ang'shuZhang Han Chao