Ask about this productRelated genes to: GroES protein
- Gene:
- HSPE1 NIH gene
- Name:
- heat shock protein family E (Hsp10) member 1
- Previous symbol:
- -
- Synonyms:
- CPN10, GroES, HSP10, EPF
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-16
- Date modifiied:
- 2015-11-19
Related products to: GroES protein
Related articles to: GroES protein
- - Source: PubMed
Publication date: 2026/04/10
Li XueyangLiu YihengHe Hongtao - Heat dissipation relies on an intact cardiovascular system to dilate cutaneous blood vessels and increase cardiac output. However, the heart becomes a vulnerable organ and is susceptible to cardiac arrhythmias, functional failure, and focal myocardial necrosis in a hyperthermic state. In particular, individuals with cardiovascular dysfunction are at a much higher risk of exertional heat stroke (EHS). This study aimed to investigate and validate the cell signaling pathways and key genes associated with EHS. The findings are intended to elucidate the mechanisms underlying cardiac injury and to provide a theoretical basis for the early identification of biomarkers for cardiac injury in EHS. A total of 310 differentially expressed genes (DEGs) were identified across all cell types between the two groups using the SeuratFindMarkers function with the logfc. threshold = 0.25, adjusted P value = 0.05 (Bonferroni correction), and min. pct = 0.1. Of these, 18 genes with substantial variability were chosen for further verification. Finally, RT-qPCR and immunohistochemistry tests verified that Hspa8 and Hspe1 were further up-regulated, while Id1, Ndufa4, and Cd36 were down-regulated. These screened hypervariable genes play different roles in heat stress-induced mitochondrial and myocardial mechanical damage, protein misfolding, and may serve as potential biomarkers in the mechanism of cardiac injury or play an important role in the functional pathway described above. - Source: PubMed
Publication date: 2026/02/11
Luo ZhenghanLi ZhiTang ChengliangZhang JinhaiChen LeruFu QianyunZhang QiYan HanYang ZhanWang ChunhuiZheng Feng - Pancreatic ductal adenocarcinoma (PDAC) remains one of the deadliest human malignancies, with limited therapeutic options and a lack of druggable vulnerabilities beyond a narrow set of oncogenic drivers. To identify cancer dependencies that are both essential in vivo and drug-tractable, we performed an unbiased genome-wide CRISPR loss-of-function screen under in vivo tumor-selective pressure. This approach revealed the mitochondrial co-chaperone HSPE1 (Hsp10) as a previously unrecognized, tumor-promoting dependency in PDAC. Genetic depletion of HSPE1 markedly impaired tumor growth, survival, and tumor-initiating capacity across multiple PDAC models in vitro and in vivo, including patient-derived xenografts. Mechanistically, HSPE1 functioned as a central survival node by engaging two parallel and targetable mitochondrial pathways. First, HSPE1 cooperated with its canonical partner HSPD1 to regulate cell-cycle progression, and apoptosis. Second, HSPE1 was functionally associated with mitochondrial dynamics, correlating with altered regulation of the OPA1/OMA1 axis, revealing an HSPD1-independent mechanism linking mitochondrial stress adaptation to cancer cell fitness. This dual signaling architecture exposes a previously unappreciated mitochondrial vulnerability selectively exploited by PDAC cells. Importantly, both HSPE1-regulated pathways were amenable to therapeutic targeting in vivo. Pharmacological inhibition of the HSPD1/HSPE1 complex or the OPA1/OMA1 pathway significantly suppressed tumor growth, while combined targeting produced robust synergistic antitumor activity in both cell line–derived and patient-derived PDAC models. Moreover, this combination strategy provides a modest yet consistent incremental benefit to standard-of-care chemotherapies, underscoring its translational relevance. Together, these findings establish HSPE1 as a bona fide cancer dependency uncovered through in vivo functional genomics, uncover a dual mitochondrial vulnerability, and provide a rational framework for combination therapy design. More broadly, this work highlights the power of in vivo CRISPR screening to directly inform therapeutic strategies and identifies mitochondrial stress adaptation as a promising and generalizable target in cancer. - Source: PubMed
Publication date: 2026/02/05
Boudreault JulienRahimirad ShimaWang NiYan GangLima Leslie ChaltelPoulet SophieDai MeiouAli SuhadLebrun Jean-Jacques - Psoriasis is a chronic skin disease influenced by genetic susceptibility and environmental factors. Ochratoxin A (OTA) is a ubiquitous foodborne mycotoxin known for its immunotoxicity, however, its specific role in psoriasis pathogenesis remains underexplored. This study implemented an integrated systems biology framework that combined network toxicology, machine learning, and molecular dynamics to elucidate the mechanisms of OTA-induced psoriasis. By intersecting OTA-associated targets with psoriasis-related genes, we identified 242 potential targets that were significantly enriched in the IL-17 and TNF signaling pathways. We utilized a weighted gene co-expression network analysis combined with nine machine learning algorithms to identify five hub genes based on their high feature importance and diagnostic robustness: ,,,, and , with an area under the curve of 0.988 in the training set and 1.00 in the external validation. These hub genes positively correlated with activated dendritic cells and eosinophils, suggesting that they mediate a pro-inflammatory microenvironment. Molecular docking and dynamics simulations demonstrated stable binding affinities (up to − 8.8 kcal/mol) between OTA and the corresponding proteins. Our findings establish a mechanistic link whereby OTA directly interacts with key regulatory proteins to drive immune dysregulation, providing novel biomarkers and a theoretical basis for managing OTA-induced psoriasis. - Source: PubMed
Publication date: 2026/01/28
Hu JianTang MingZheng Quan-YouLiang Shen-JuXu Gui-LianZhang Ke-Qin - Mitochondrial metabolism plays a critical role in tumor growth and progression. However, its specific influence on osteosarcoma prognosis remains unclear. - Source: PubMed
Publication date: 2026/01/08
Pan ShuxianHu WenfangXie PeiZhang ZhongyuMa JiakangWang Chenyang