Monoclonal anti-human EIF2S1 antibody (clone AT5E10)
- Known as:
- Monoclonal (anti-) to-H. sapiens EIF2S1 (anti-) (clonality AT5E10)
- Catalog number:
- ATGA0208
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- Monoclonal anti-human EIF2S1 antibody (clone AT5E10)
Related genes to: Monoclonal anti-human EIF2S1 antibody (clone AT5E10)
- 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: Monoclonal anti-human EIF2S1 antibody (clone AT5E10)
Related articles to: Monoclonal anti-human EIF2S1 antibody (clone AT5E10)
- 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 - Polysaccharides derived from medicinal plants have drawn significant attention for their potential anti-tumor properties and favorable safety profiles. In this research, a novel polysaccharide with anti-tumor activity, named URP70-1, was isolated from the roots of Uncaria rhynchophylla. Structural characterization determined URP70-1 to be a novel 8.2 kDa polysaccharide composed of L-arabinose (52.8%), D-galactose (35.4%), and D-xylose (11.8%). Methylation and NMR spectroscopic analyses further elucidated its primary structure, comprising a backbone of →3,5)-L-Araf-(1→, →4)-D-Galp-(1→, and →2,5)-L-Araf-(1 → residues, with side chains containing →3)-L-Araf-(1→, →5)-L-Araf-(1→, →6)-D-Galp-(1→, L-Araf-(1→, D-Xylp-(1→, and D-Galp-(1 → residues. In vivo evaluation using a zebrafish xenograft model demonstrated that URP70-1 significantly inhibited tumor proliferation in a dose-dependent manner, with no observed toxicity. In vitro studies on CT26 colon carcinoma cells confirmed that URP70-1 suppressed cell viability and migration, elevated intracellular ROS levels, and reduced mitochondrial membrane potential, ultimately promoting apoptosis. Mechanistic investigations revealed that URP70-1 entered cells and induced endoplasmic reticulum stress via the GRP78-EIF2S1-CHOP pathway, while concurrently activating the ROS/ERK/p38 signaling axis. This led to mitochondrial dysfunction, an increased Bax/Bcl-2 ratio, cytochrome C release, and activation of the caspase cascade. Collectively, these findings highlight URP70-1 as a structurally novel polysaccharide with potent anti-tumor activity mediated through endoplasmic reticulum stress and mitochondrial apoptosis pathways, providing a foundation for its further development as a potential therapeutic agent against colon cancer. - Source: PubMed
Publication date: 2026/04/10
Wu ZhongnanLi JunhaoXu XiaolongDong GuotongJiao YukunZhang Shaojie - Several studies indicated that type 2 diabetes (T2D) patients have a higher risk on the development and progression of myocardial infarction (MI) than non-diabetic patients. The management of MI with T2D as comorbidity may become much more complicated compare to the management of MI alone due to several factors including conflicting therapies arises from one-drug for one-disease strategy, since some T2D-drugs may conflict with MI and vice-versa. However, so far, no researcher yet rigorously explored key molecular signatures and their mechanisms associated with both diseases for exploring candidate therapies as the common/unique treatment for both diseases during their co-existence. - Source: PubMed
Publication date: 2026/03/27
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