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)
- Leveraging multi-omics to better understand the molecular signatures and pathways underlying Alzheimer's disease (AD) pathogenesis is critical for early diagnosis and disease modifying interventions. We performed peripheral blood transcriptome ( = 669) and epigenome microarray analyses ( = 553) on non-Hispanic white participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) to identify molecular signatures of AD. We identified specific transcripts (e.g., , , ) and co-expression networks that were dysregulated in AD, marked by a strong influence of ε4 genotype, and characterized by a consistent pattern of immune activation, inflammation, and metabolic suppression. Further, these peripheral signatures were linked to central AD pathology (amyloid PET, CSF p-tau181) and neurodegeneration (plasma NfL, regional atrophy), with two genes, and , identified as protective against progression from MCI to AD. Our work emphasizes the importance of genotypes in AD pathophysiology and highlights potential targets for biomarker discovery and personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/08/31
Mitchell Brendan AHausle IsabellaSmith SaraThropp PamelaSirota MarinaTosun Duygu - : Prostate cancer (PCa) remains a prevalent malignancy among men, often complicated by recurrence and unfavorable clinical outcomes. Consequently, precise risk stratification and timely clinical intervention are paramount. Initially, we delineated distinct expression profiles of histone modification regulators via unsupervised clustering, identifying PCa subtypes with divergent survival probabilities and biological phenotypes. Subsequently, we sought to develop a prognostic gene signature, derived from the transcriptomic variations among these regulator-defined subtypes, to predict outcomes in PCa patients following radical prostatectomy (RP). : Clinical and transcriptomic data from PCa cohorts were retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) repositories for comprehensive analysis. Subtypes driven by histone modification regulators were established using unsupervised consensus clustering, followed by in-depth characterization of their molecular features and associated pathways. A risk-scoring model was then developed to evaluate its prognostic efficacy in this patient population. : Stratification based on histone modification regulators yielded four distinct PCa subtypes exhibiting heterogeneous survival outcomes, functional pathways, and genomic mutational landscapes. Following rigorous feature selection, a 21-gene risk signature (HIS_score)-comprising MXD3, CCDC28B, COL11A2, SLC39A5, GPT, DNASE1L2, PIF1, KRTAP5-9, TTLL10, KRTAP5-1, KRTAP5-10, HAGHL, MSLNL, AMH, NKAIN4, CCDC114, SLC9A3, SULT1E1, ALB, SLC6A14, and RPE65-was constructed. Survival analyses demonstrated that patients assigned to the high HIS_score cohort experienced significantly worse clinical outcomes compared to their low-score counterparts. Furthermore, we integrated this signature into a novel clinical nomogram to facilitate individualized prognostic assessments. : Derived from transcriptomic disparities between extreme epigenetic subtypes, the HIS_score and its associated nomogram serve as robust prognostic instruments. These tools effectively encapsulate the downstream transcriptional sequelae of histone modification dysregulation, offering clinicians a valuable framework to accurately predict post-RP outcomes and expedite the formulation of personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/05/28
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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
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