GroEL pAb
- Known as:
- GroEL pAb
- Catalog number:
- ASASPS-875E
- Product Quantity:
- 100 µL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- GroEL pAb
Related genes to: GroEL pAb
- Gene:
- HSPD1 NIH gene
- Name:
- heat shock protein family D (Hsp60) member 1
- Previous symbol:
- SPG13
- Synonyms:
- GroEL, HSP60
- Chromosome:
- 2q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-19
- Date modifiied:
- 2015-11-19
Related products to: GroEL pAb
Related articles to: GroEL pAb
- Early detection of gastric cancer (GC) and reliable risk stratification for metachronous gastric lesions (MGLs) remain societal and clinical challenges, particularly in intermediate risk populations. Non-invasive approaches such as saliva-based biomarkers could complement current strategies. The aim of this study was to identify and validate a tissue-based gene expression signature for early gastric lesions, explore its potential for MGL prediction, and assess its detectability in saliva. - Source: PubMed
Lopes CatarinaBrandão AndreiaVavoulis DimitrisPaulino SofiaCosta Joãode Sá Inês MarquesArcher SaraKüttner-Magalhães RicardoMarcos-Pinto RicardoLibânio DiogoDinis-Ribeiro MárioPereira Carina - Prostate cancer is the predominant malignancy in males, with bone metastasis representing a defining characteristic of its progression. Bone tissue involvement significantly deteriorates patient quality of life and incurs substantial healthcare expenditure. Emerging evidence suggests a potential link between cuproptosis and tumor biology, thereby identifying cuproptosis-related genes (CRGs) as promising biomarkers for bone metastatic prostate cancer (BMPC). Consequently, this bioinformatics study aimed to identify specific biomarkers and establish a robust diagnostic model. - Source: PubMed
Publication date: 2026/04/22
Li JuanYao ShaoqinLuo JunhuaLi TaiyongZhang Jie - Doxorubicin (DOX), is an indispensable first-line chemotherapeutic. Despite this first-line indication, clinical use of DOX is limited by severe, off-target, and often irreversible cardiotoxicity. DOX induces cytotoxicity in rapidly dividing cancer cells via inhibition of Topoisomerase IIα. However, the underlying mechanisms by which DOX causes cell death in non-replicative, terminally differentiated cardiomyocytes remain poorly understood. Emerging evidence suggests that mitochondrial uptake of DOX is contributory to cardiotoxicity. Whether mitochondrial stress pathways, including the mitochondrial unfolded protein response (UPR), are activated and critical for mediating DOX cardiotoxicity is poorly understood. Moreover, whether phosphorylation of eukaryotic translation initiation factor 2α (eIF2α), a mediator of the Integrated Stress Response, regulates potential UPR signaling during DOX treatment is also unknown. Here, using human AC-16 cardiac cells, we examined the role of eIF2α phosphorylation during DOX treatment. Our data suggest that DOX triggers a transient increase in eIF2α phosphorylation, followed by a progressive decline. Further, knockdown of eIF2α decreased key transcriptional regulators of UPR signaling such as C/EBP Homologous Protein and ATF5, blunted the induction of UPR genes (AFG3L2, CLPP, HSPA9, HSPD1, LONP1, SPG7), and aggravated DOX induced cytotoxicity. Together, these findings identify eIF2α as a critical upstream regulator of UPR signaling, and suggest that activation of the UPR may confer cardio-protection against DOX-induced mitochondrial stress in human cardiac cells. - Source: PubMed
Publication date: 2026/05/20
O'Dwyer Kienan PBauer Perry EPal SubhankhiBrundage KathleenVenkatesh Sundararajan - The mitochondrial unfolded protein response (UPR) maintains proteostasis, but its dysregulation dictates cell fate. This study aimed to elucidate the signaling mechanism by which triptolide (TP), a bioactive component of Tripterygium wilfordii Hook. f., triggers hepatocellular Lipoapoptosis, focusing on HSP60-mediated UPR overactivation. - Source: PubMed
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Yu ZhichaoHu LanDing JingLi XiangZhang QiZhang QiaoyuChen ShuoyuZhang PeiZhang JiaqiJiang BaopingZhou XuepingZhou Lingling - Mitophagy plays a critical role in the pathology of Parkinson's disease (PD) via mitochondrial quality control, making it a promising therapeutic target. However, the precise mechanistic role of mitophagy in PD pathogenesis and progression remains unclear. - Source: PubMed
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