Ask about this productRelated genes to: EIF2S1 antibody
- 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
Related articles to: EIF2S1 antibody
- 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
Ahmmed ReazAntu Umme SamiaNoor TasfiaFaysal Md FahimAkter Mst TahminaNesa MeherunMollah Md Nurul Haque - Influenza A virus (IAV) remains a major global threat, highlighting the need for host-targeted antiviral strategies. While some probiotics offer prophylactic protection, their therapeutic potential post-infection is poorly understood. Here, we investigated human-derived ZG2488 for its antiviral potential against IAV. Strikingly, a more pronounced reduction in viral titer was observed when live bacteria were administered therapeutically post-infection, compared to preventive pretreatment. Transcriptomic analysis suggested that the therapeutic effect of viable bacteria was associated with a modulated host response, including the downregulation of specific host factors implicated in viral replication (e.g., , , ) and a delayed interferon-beta (IFNB1) induction. In contrast, preventive effects appeared to be mediated by heat-stable components. These findings highlight a viability-dependent mode of action for ZG2488 and contribute to the growing evidence that certain probiotics may exert antiviral effects through targeted host modulation rather than solely through broad immune activation. - Source: PubMed
Publication date: 2026/03/05
Chen MengshanChen YuluCao ZhijieRen ZhihongYue KunYang JingPu JiLuo WenboXu Jianguo - Bone marrow mesenchymal stem cells (BMSCs) play crucial roles in bone tissue regeneration and repair due to their self-renewal ability and multidifferentiation potential. Additionally, miRNAs play crucial roles in controlling osteogenic differentiation. The purpose of this study was to investigate the impact of miR-20b-5p on the osteogenic differentiation of BMSCs under inflammatory conditions. Human BMSCs were treated with 1 µg/mL lipopolysaccharide (LPS) for 24 h to establish an in vitro inflammatory model simulating inflammation in bone injury. The levels of miR-20b-5p, proteins, and inflammatory cytokines were detected via RT-qPCR, Western blotting, and ELISA, and osteogenic differentiation of the BMSCs was evaluated via ALP and alizarin red staining. Consistent with previous findings, LPS downregulated osteogenic markers (RUNX2, OCN, OPN) and upregulated inflammatory cytokines (TNF-α, IL-6, and IL-1β) in BMSCs. Furthermore, the levels of miR-20b-5p were decreased, and the levels of endoplasmic reticulum stress-related proteins (p-EIF2S1, ATF4, CHOP, and GRP78) were increased in LPS-induced BMSCs. However, overexpression of miR-20b-5p weakened the effect of LPS and promoted osteogenic differentiation. Mechanistically, miR-20b-5p overexpression alleviated ER stress caused by LPS-induced inflammation by decreasing EIF2S1 levels, thereby promoting the osteogenic differentiation of BMSCs. Our research indicates that increasing miR-20b-5p expression could be an innovative approach to promote osteogenic differentiation of BMSCs. - Source: PubMed
Pan ZhipengZhao QingsenLi PiaoDing MeiwenLi YaGao LiangminXiong YunxiangTang KaihuaGong ChunyanYao Liqing