c_Jun (Phospho_Ser243) Antibody
- Known as:
- c_Jun (Phospho_Ser243) Antibody
- Catalog number:
- E011025-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- c_Jun (Phospho_Ser243) Antibody
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Related articles to: c_Jun (Phospho_Ser243) Antibody
- Drug-induced liver injury is the most common cause of acute liver failure in Western countries, but the choice of effective antidotes is restricted in most conditions. Glycine-N-acyltransferase (GLYAT) catalyzes the conjugation of glycine to acyl-CoA, serving as a crucial phase II metabolic enzyme for hepatic detoxification. However, few studies have clarified the role of GLYAT in drug-induced liver injury. Our study showed that hepatic glycine level and Glyat expression were reduced upon APAP exposure, but restored within 12 h, similar to the change of hepatic glutathione (GSH). This dynamic expression pattern may be regulated by liver-enriched transcription factors such as HNF4A identified through promoter analysis. Glyat knockout in female mice reduced circulating alanine transaminase (ALT), aspartate transaminase (AST), hepatic reactive oxygen species (ROS) and phosphorylated c-Jun N-terminal kinase (JNK) / extracellular regulated protein kinases (ERK) levels. Conversely, overexpression of Glyat by injection of adeno-associated virus 8 (AAV8) in female mice displayed exacerbated phenotypes, including elevated serum transaminases, increased oxidative stress, enhanced mitogen-activated protein kinase (MAPK) signaling and aggravated hepatocellular necrosis. However, neither Glyat deletion nor overexpression in male mice had effects on APAP toxicity. These protective effects were associated with increased hepatic glycine and GSH levels, as well as attenuated oxidative stress and inflammatory responses. In addition, glycine supplementation had similar hepatoprotective effects to Glyat deficiency in female mice. Taken together, these findings identify GLYAT as a potential therapeutic target and suggest that glycine supplementation may serve as an adjuvant therapy for APAP-induced liver damage, particularly in females. - Source: PubMed
Publication date: 2026/05/19
Zhao JunLiu QinhuiXie LuyueWang CuitongXiong YiminLiang XinqiSun YingXu YingSong HaiyingXu MingzhuJing XiandanXu YiningLi YanpingMo LiPang JuanHe Jinhan - The UN Sustainable Development Goals highlight the relevance of climate change for global health. At the same time, the academic community-including health-related disciplines such as psychology and behavioural medicine-contributes substantially to greenhouse gas emissions, particularly through work-related travel. To inform discussions on the environmental impact of academic conferences, this study estimates the CO-equivalent (COeq) emissions resulting from attendance at major international psychology conferences. The number of in-person and online attendees at major international psychological conferences was identified by web search and email inquiries. Conference inclusion criteria: International, psychology/behavioural medicine, 1,000 + attendees, years 2023-2025. Total and per capita COeq were estimated separately for in-person and online attendance using emission factors derived from 22 studies on in-person conferences and 10 on online conferences. Attendance at an international in-person conference resulted in an estimated 1.26 t COeq per participant, with approximately 94% attributable to travel, compared to 0.02 t COeq for online attendance-corresponding to a reduction rate of about 98%. Across the 21 included major international psychology conferences, total emissions were estimated at approximately 63,481 t of COeq. These estimates illustrate the scale of greenhouse gas emissions associated with conference-related travel in academia. By quantifying emissions from major international psychology conferences-while excluding numerous smaller and regional meetings-this study provides empirical reference points to inform ongoing discussions about conference formats and travel practices among individual scientists, institutional departments and scientific organisations. - Source: PubMed
Warner Lisa MGreen James ATeran-Escobar Claudia - Long-term use of tenofovir disoproxil fumarate (TDF) is associated with renal tubular dysfunction and bone mineral loss. In virologically suppressed people living with HIV (PLWH), optimizing antiretroviral therapy requires maintaining viral suppression while minimizing cumulative drug-related toxicity. We therefore evaluated the efficacy and safety of switching to dolutegravir/lamivudine (DTG/3TC) in Chinese PLWH with TDF-related renal or bone toxicity. - Source: PubMed
Publication date: 2026/05/20
Wang ZhenyanLiu LiChen JunWang JiangrongShen YinzhongQi TangkaiTang YangSong WeiSun JianjunXu ShuibaoYang JunyangChen YoumingShao YuemingZhang Renfang - Non-alcoholic fatty liver disease (NAFLD) is a common metabolic disease with high heterogeneity and currently lacks approved targeted therapies. Identifying druggable genes with diagnostic relevance and potential translational value may facilitate further research into precision medicine approaches for NAFLD. This study integrated transcriptome data from three independent GEO datasets (GSE33814, GSE63067, and GSE89632) and used sva and limma to correct for batch effects. Differentially expressed genes (DEGs), druggable genes obtained from DGIdb, and genes from WGCNA modules significantly associated with NAFLD were intersected to identify candidate genes. Candidate genes were systematically evaluated using functional enrichment analysis (GO, KEGG, GSEA), immune infiltration analysis (CIBERSORT), receiver operating characteristic (ROC) analysis, and co-expression networks. Finally, the expression of key genes was verified by immunohistochemistry (IHC) and immunofluorescence (IF). A total of nine key candidate drug targets were identified: FABP4, ADAMTS1, FOS, GPR88, IL1RL1, CD52, JUN, SERPINE1, and THBS1. These genes are primarily involved in metabolism, inflammatory response, extracellular matrix remodeling, and immune regulation. ROC analysis showed that FOS and JUN had high diagnostic accuracy. Furthermore, IHC and IF results demonstrated that CD52 was significantly upregulated in NAFLD tissues, suggesting its potential relevance as a candidate target for further investigation. This study systematically identified key druggable genes for NAFLD through bioinformatics analysis and partially validated selected candidates experimentally. In particular, CD52 was upregulated in NAFLD tissues, suggesting a potential association with NAFLD-related pathological alterations. These findings provide new insights into the molecular pathogenesis of NAFLD and may provide a basis for future target validation studies. - Source: PubMed
Publication date: 2026/05/20
Zhang XiangqianSu HanyangZhou QuanZhou Yuling - Treatment selection in breast cancer is guided by risk assessment using molecular subtypes and clinicopathological characteristics. However, current approaches lack the precision required for optimal clinical decision-making. To address this, we use data from 8161 patients to develop and evaluate an AI test integrating digital pathology with clinical data. The AI test provides a robust method for predicting disease-free interval (C-index: 0.71 [0.68-0.75], HR: 3.63 [3.02-4.37, p < 0.001]). In a direct comparison, the AI test displays numerically higher discrimination (C-index: 0.67 [0.61-0.74]) than the standard-of-care 21-gene assay (C-index: 0.61 [0.49-0.73]). Across molecular subtypes, the AI test demonstrates robust prognostic performance, including in triple negative breast cancer (C-index: 0.71 [0.62-0.81], HR: 3.81 [2.35-6.17, p=0.02]), where no guideline-recommended assays currently exist. These findings highlight the potential of AI-based pathology tests as a promising tool for improved risk stratification across all major subtypes, with implications for clinical decision-making. - Source: PubMed
Publication date: 2026/05/20
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