MXD3 antibody - N-terminal region (ARP30089_T100)
- Known as:
- MXD3 (anti-) - N-terminal region (ARP30089_T100)
- Catalog number:
- arp30089_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- MXD3 antibody - N-terminal region (ARP30089_T100)
Related genes to: MXD3 antibody - N-terminal region (ARP30089_T100)
- Gene:
- MXD3 NIH gene
- Name:
- MAX dimerization protein 3
- Previous symbol:
- -
- Synonyms:
- MAD3, bHLHc13
- Chromosome:
- 5q35.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-12
- Date modifiied:
- 2015-08-25
Related products to: MXD3 antibody - N-terminal region (ARP30089_T100)
Related articles to: MXD3 antibody - N-terminal region (ARP30089_T100)
- Clear cell renal cell carcinoma (ccRCC) is characterized by high recurrence and metastatic potential, leading to poor clinical outcomes. There is a critical need to identify reliable prognostic biomarkers and therapeutic targets to improve patient stratification and personalized treatment. - Source: PubMed
Publication date: 2026/01/28
Fu CongSun LinZhou TongBi Yanzhi - Risankizumab has demonstrated remarkable efficacy in the treatment of psoriasis; however, its long-term use faces multiple challenges, including high costs, reduced efficacy over time, and potential safety concerns, such as infections and malignancies. Therefore, identifying potential alternative or adjunctive therapies to risankizumab has significant clinical importance. - Source: PubMed
Publication date: 2026/01/14
Ma YupengZhang ShuminChen XinhongZhang XueZhang Denghai - Prediabetes is one of the main health concerns in public health, and various etiological factors contribute to its onset. This study aimed to evaluate genetic associations and gene-macronutrient interaction with prediabetes-related metabolites to understand how genetic variation and dietary intake contribute to dysglycemia. We analyzed a total of 482 self-identified Mexican American participants recruited from Starr County, Texas in 2018-2019. Untargeted metabolomic profiling was performed using LC-MS. Nutrient densities of six macronutrients were derived from a 106-item food frequency questionnaire. Genetic associations for each metabolite were tested using Generalized linear Mixed Model Association Tests (GMMAT). Gene-macronutrient interactions on prediabetes-associated metabolites were assessed with the Mixed Model Association Test for GEne-Environment Interaction (MAGEE). Age, gender, and BMI were included as covariates in all association tests. Among 308 named and 2,471 unnamed metabolites, 17 novel variant-metabolite pairs were discovered, including rs10947898 in associated with diacylglycerol DG32:1(p-value: 8.95E-09). Among 145 named and 687 unnamed metabolites after filtering, gene-macronutrient interaction analyses identified seven named metabolites, including a variant(rs111251222) in that interacted with monounsaturated fat to influence eicosadienoic acid levels (Interaction p-value: 9.88E-09). Prediabetes and nutrient-related metabolites in Mexican Americans showed significant genetic associations and gene-nutrient interactions. - Source: PubMed
Publication date: 2025/12/16
Chung ShinhyeEvans CharlesBurant Charles FChen HanYu BingAguilar DavidBrown Eric LHanis Craig LJun Goo - Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer, often diagnosed at advanced stages due to a lack of reliable early biomarkers. Recent studies suggest that the traditional Chinese medicine (TCM) body constitution, particularly the Yang-Deficiency Constitution (YDC), may influence tumour development by altering the immune microenvironment. However, the mechanistic connection between YDC and ccRCC prognosis remains largely unexplored. - Source: PubMed
Publication date: 2025/11/20
Kho Boon SengZhou ZongyuanLiu RuiSui YihangZhang YingnanYao JiaqiLu HuanhuanZhou GuoweiZhang BoWang Yinyin - Lung squamous cell carcinoma (LUSC) represents a significant challenge in oncology, necessitating the identification of novel prognostic markers and therapeutic targets. This study is aimed at investigating the oncogenic role of MXD3 (MAX Dimerization Protein 3) in LUSC and its implications for patient prognosis. A retrospective cohort of 199 LUSC patients from the 905th Hospital of People's Liberation Army Navy was analyzed to evaluate MXD3 expression levels and their association with clinicopathological characteristics and survival outcomes. Immunohistochemistry (IHC) staining was performed to assess MXD3 expression in LUSC tissue samples. Survival analyses, including the Kaplan-Meier curves and multivariate Cox regression, were conducted to determine the prognostic significance of MXD3 expression and other clinicopathological factors. Additionally, the methylation status of MXD3 was examined using data from the TCGA database to assess its role in regulating MXD3 expression and survival outcomes. MXD3 expression exhibited significant heterogeneity among LUSC patients, with high MXD3 expression correlating with advanced tumor differentiation grade, larger tumor size, and advanced T and N stages. The Kaplan-Meier survival analyses revealed that high MXD3 expression was associated with shorter cancer-specific survival. Multivariate Cox regression identified MXD3 expression level and lymph node involvement (N stage) as independent prognostic factors for cancer-specific survival in LUSC patients. Additionally, analysis of MXD3 methylation revealed significantly lower methylation levels in LUSC tissues, and reduced methylation correlated with poorer survival outcomes. Our findings highlight MXD3 as a promising prognostic biomarker for LUSC, with high MXD3 expression predicting poorer survival outcomes. MXD3 expression level, along with lymph node involvement and methylation status, could serve as independent prognostic indicators for risk stratification and treatment decision-making in LUSC patients. Further research is warranted to elucidate the underlying mechanisms of MXD3-mediated tumorigenesis and its potential as a therapeutic target in LUSC management. - Source: PubMed
Publication date: 2025/05/15
Cao MingzhiZhang NingChen TangbingJiang Hong