GADD45G Antibody (OAAF03022)
- Known as:
- GADD45G Antibody (OAAF03022)
- Catalog number:
- oaaf03022
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- GADD45G Antibody (OAAF03022)
Related genes to: GADD45G Antibody (OAAF03022)
- Gene:
- GADD45G NIH gene
- Name:
- growth arrest and DNA damage inducible gamma
- Previous symbol:
- -
- Synonyms:
- DDIT2, GADD45gamma, GRP17, CR6
- Chromosome:
- 9q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-06
- Date modifiied:
- 2016-10-05
Related products to: GADD45G Antibody (OAAF03022)
Related articles to: GADD45G Antibody (OAAF03022)
- Heat stress compromises dairy cow productivity and metabolic health through impaired nutrient partitioning and oxidative stress. Cobalamin is an essential cofactor for methylmalonyl-CoA mutase, the key enzyme regulating ruminal propionate production and hepatic gluconeogenic metabolism. However, the underlying molecular mechanisms, particularly the hepatic transcriptional responses to cobalamin under heat stress conditions, remain unclear. This study evaluated the effects of coated cobalamin (CCA) supplementation on lactation performance, nutrient digestibility, rumen fermentation, blood metabolites, and hepatic transcriptome in heat-stressed Holstein cows. - Source: PubMed
Publication date: 2026/09/03
Liu YongjiaGuo ZitaiCao NaDiao ZhichengMa LuYang YongxinZhang YuBu Dengpan - Senescence-related molecular nodes linking hepatic stress with immune dysregulation in metabolic dysfunction-associated steatotic liver disease (MASLD) remain poorly defined. This study aimed to identify and experimentally validate a senescence-related gene (SRG) signature associated with immune dysregulation in MASLD. Four transcriptomic datasets (127 controls, 127 MASLD) were integrated as the discovery cohort. Candidate SRGs were identified through differential expression analysis, weighted gene co-expression network analysis, and three machine learning algorithms. Immune infiltration was assessed using CIBERSORT, and a three-gene signature was evaluated in internal and external cohorts. Potential GADD45G-associated compounds were predicted by molecular docking. Experimental validation was performed in high-fat diet (HFD)-induced obese mice and palmitic acid (PA)-stimulated bone marrow-derived macrophages (BMDMs). Single-cell RNA sequencing analysis of GSE300744 was further performed to evaluate GADD45G distribution in hepatic cell populations. SOCS1, SOCS2, and GADD45G were identified as core SRGs. Their expression was reduced in MASLD liver tissues and correlated with histological features and immune alterations. The three-gene signature showed favorable classification performance in validation cohorts. In HFD mice, GADD45G expression was decreased at both mRNA and protein levels, with reduced immunoreactivity in F4/80-positive hepatic macrophages. Single-cell analysis further supported macrophage-associated expression of Gadd45g. In PA-stimulated BMDMs, reduced GADD45G protein expression was partially restored by camptothecin and myristicin treatment. Overall, SOCS1, SOCS2, and GADD45G represent a candidate senescence-related immune signature associated with MASLD. The macrophage-associated reduction in GADD45G and its modulation in vitro provide preliminary evidence for a potential role of GADD45G in MASLD-associated immune dysregulation. - Source: PubMed
Publication date: 2026/08/07
Tang WenjingWang WeixiaZhang ShuyangZhou XinHe LinfengZeng Tianshu - Reproductive inefficiency remains a major contributor to heifer culling and reduced herd longevity in beef systems. This study examined the molecular basis of fertility by analyzing granulosa cells and follicular fluid from Angus-Simmental crossbred heifers classified as fertile or subfertile. - Source: PubMed
Publication date: 2026/07/29
Banerjee PriyankaPhillips RachelHolliman Anna GRodning Soren PDiniz Wellison J SDyce Paul W - Realgar (AsS) has shown antitumor activity, but its pharmaceutical application is limited by poor aqueous solubility, low bioavailability, and systemic toxicity. In this study, we developed AS1411-functionalized albumin nanoparticles (AsS@ BSA-AS1411 NPs) for targeted delivery of realgar to triple-negative breast cancer (TNBC). Bulk AsS was converted into nanosized clusters and encapsulated in a bovine serum albumin (BSA) matrix, followed by surface conjugation with the nucleolin-targeting aptamer AS1411. The resulting nanoparticles showed suitable physicochemical properties and good colloidal stability in physiologically relevant media, together with enhanced cellular internalization in 4T1 cells. Compared with non-targeted nanoparticles, AS1411 modification significantly increased cytotoxicity and reduced the migratory ability of 4T1 cells. Mechanistic studies showed that treatment with AsS@BSA-AS1411 NPs was associated with upregulation of GADD45G and downregulation of mTOR, suggesting a stress-related antiproliferative effect. fluorescence imaging demonstrated increased tumor accumulation of AS1411-functionalized NPs. In 4T1 tumor-bearing mice, systemic administration of AsS@BSA-AS1411 NPs produced greater tumor growth inhibition than non-targeted controls, accompanied by increased apoptosis and reduced proliferative activity in tumor tissues. In addition, the formulation showed good tolerability, with no evident systemic toxicity or hemolytic activity. These findings indicate that AS1411-functionalized albumin NPs are a promising delivery system for improving the antitumor efficacy and safety profile of realgar in TNBC. - Source: PubMed
Publication date: 2026/07/29
Dong LipingRan WenzhuoLi YanqiongYang LixiaZhou Xi - CXCL13 T cells and LAMP3 dendritic cells (DCs) are pivotal players in orchestrating anti-tumor immune responses, particularly within tumor tertiary lymphoid structures (TLS). However, their heterogeneity, differentiation trajectories, and clinical relevance in bladder cancer remain incompletely defined. This study integrated single-cell RNA sequencing (scRNA-seq) data (16 bladder cancer patients, 113,905 post-quality-control cells) and spatial transcriptomics to characterize CXCL13 T cell/LAMP3 DC subsets, their differentiation pathways (via Velocyto trajectory analysis), and intercellular crosstalk (via receptor-ligand mapping). A risk model (DTscore) was constructed using marker genes of these cells and validated in the IMvigor210 (atezolizumab-treated bladder cancer) and TCGA-BLCA cohorts. scRNA-seq clustering identified 10 immune and 3 nonimmune cell types, with T cells stratified into 8 subpopulations (including CD4CXCL13 T cells and CD8CXCL13 T cells) and DCs into 9 subgroups (including LAMP3 DCs). Receptor-ligand mapping and spatial transcriptomics confirmed functional crosstalk between CXCL13 T cells and LAMP3 DCs via key pairs (e.g., CCR7-CCL19, CXCR5-CXCL13, PDCD1-CD274) within TLS. The DTscore was developed using 8 marker genes (TSHZ2, ALOX5AP, GADD45G, TXN, CHN1, CCL19, CXCL13, ICA1) and exhibited robust prognostic and predictive performance: In the IMvigor210 cohort, high DTscore correlated with significantly poorer overall survival (OS) and a 3.27-fold lower immunotherapy response rate (11% vs. 36%, p = 4.23e-07); multivariate Cox regression confirmed DTscore as an independent OS predictor (hazard ratio = 1.97, p < 0.001). DTscore retained prognostic value in TCGA-BLCA (OS: p = 0.003; disease-specific survival: p < 0.001) and effectively predicted atezolizumab response even in the "immune desert" phenotype (p = 0.04). Combining DTscore with tumor mutational burden/tumor neoantigen burden yielded an AUC of 0.8122 for response prediction. Additionally, high DTscore was associated with higher OS hazard ratios in patients with wild-type TTN, RB1, EP300, or FGFR3 (all p < 0.01), while FGFR3 mutations correlated with lower immune checkpoint/CXCL13 expression. This study delineates the heterogeneity and interactions of CXCL13 T cell/LAMP3 DC subsets in bladder cancer TLS and validates DTscore as a robust tool for predicting OS and immunotherapy response, offering a potential guide for personalized bladder cancer treatment. - Source: PubMed
Publication date: 2026/08/05
Zhou LinZhu JinchaoLiu YushanXu Bin