EIF2S1 Antibody (N-term)
- Known as:
- EIF2S1 Antibody (N-terminus)
- Catalog number:
- AP13469a-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- EIF2S1 Antibody (N-term)
Related genes to: EIF2S1 Antibody (N-term)
- Gene:
- EIF2S1 NIH gene
- Name:
- eukaryotic translation initiation factor 2 subunit alpha
- Previous symbol:
- EIF2
- Synonyms:
- EIF-2alpha, EIF2A
- Chromosome:
- 14q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-03-04
- Date modifiied:
- 2016-10-05
Related products to: EIF2S1 Antibody (N-term)
Related articles to: EIF2S1 Antibody (N-term)
- Osteoarthritis (OA) is a heterogeneous joint disease characterized by cartilage degeneration. The interplay between extracellular matrix (ECM) remodeling, endoplasmic reticulum (ER) stress, and inflammatory signaling in OA pathogenesis remains incompletely understood. This study aimed to identify robust diagnostic biomarkers and explore the mechanistic convergence of key genes in OA cartilage through an integrated transcriptomic framework. - Source: PubMed
Publication date: 2026/06/15
Lv XueyaYu YangFan JiawenGuo LianjiangZhu XiangLi Xingye - Platelets, a crucial source of liquid biopsy samples, play a significant role in the progression of various malignancies, including non-small cell lung cancer (NSCLC). However, specific biomarkers for early-stage NSCLC have not yet been identified. In this study, we employed bioinformatics approaches to identify differentially expressed genes (DEGs) in tumor-educated platelets (TEPs) from NSCLC. Subsequently, we validated these genes using specimens from patients with early-stage lung cancer, highlighting their potential as biomarkers for NSCLC. - Source: PubMed
Publication date: 2026/06/08
Xu ZhenLi WenxinYu YuenengWu HuifangZhang Lin - Glioblastoma multiforme is one of the common central nervous system tumors characterized by a low survival rate and a high risk of recurrence. This study aimed to investigate the cell viability and ER stress in the T98G glioma cell line after the application of Biochanin A, an isoflavone. - Source: PubMed
Publication date: 2026/05/19
Demir EzelAvcu Elif MerveErdem BerilSaglar Ozer Emel - Glioma is a malignant central nervous system tumor that poses a threat to patient survival. Eukaryotic translation initiation factor 2 subunit alpha (EIF2S1) is closely associated with the progression of multiple human cancers. This study aimed to investigate the effects of EIF2S1 on glioma cells and the underlying molecular mechanisms. We analyzed EIF2S1 expression in glioma tissues and cell lines. Small interfering RNA (siRNA) targeting EIF2S1 was constructed and transfected into glioma cell lines to silence EIF2S1 expression. We then evaluated cell proliferation, apoptosis, and metastatic capacity. Western blotting (WB) was used to determine the effect of EIF2S1 knockdown on the phosphorylation levels of PI3K and AKT. Finally, glioma cells were co-treated with the PI3K activator 740 Y-P to verify whether the PI3K/AKT pathway mediates the function of EIF2S1 in glioma cells. EIF2S1 was significantly up-regulated in glioma. Knockdown of EIF2S1 markedly inhibited glioma cell proliferation, promoted apoptosis, and suppressed metastatic potential. Western blot analysis indicated that EIF2S1 silencing significantly reduced the phosphorylation levels of PI3K and AKT. Moreover, 740 Y-P significantly reversed the inhibitory effect of si-EIF2S1 on glioma cells. Our in vitro findings suggeste that EIF2S1 contributes the malignant progression of glioma cells by regulating the PI3K/AKT pathway, providing a theoretical basis for future exploring EIF2S1 as a potentical therapeutic target for glioma. - Source: PubMed
Publication date: 2026/05/29
Li GangWang MinWei NaQiu Zheng - 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