Ask about this productRelated genes to: DOK2 antibody
- Gene:
- DOK2 NIH gene
- Name:
- docking protein 2
- Previous symbol:
- -
- Synonyms:
- p56dok-2, Dok-2
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-05
- Date modifiied:
- 2015-11-10
Related products to: DOK2 antibody
Related articles to: DOK2 antibody
- Prostate cancer (PCa) is a heterogeneous disease characterised by a highly complex cellular ecosystem within its tumour microenvironment (TME). However, the crosstalk patterns between tumour and immune cells remain poorly understood. - Source: PubMed
Publication date: 2026/02/23
Mei ZongweiChen ChenZhou JilongJiang Qing - Lung squamous cell carcinoma (LUSC) is the second most prevalent type of lung cancer worldwide. Despite its global health burden, the molecular mechanisms driving LUSC remain poorly characterized, posing considerable challenges for the development of targeted preventive therapies. Here, by integrating human plasma proteomes ( = 54,219) with GWAS summary data for LUSC (7426 cases and 55,627 controls), we performed genome-wide Mendelian randomization (MR) and colocalization analyses to identify potential druggable targets associated with LUSC risk. After applying Bonferroni correction, sensitivity analyses, and reverse causation detection, we identified 12 potential druggable proteins significantly associated with LUSC risk. Five of these proteins (DOK2, FKBPL, NCF2, PDIA3, and TCL1A) showed strong evidence of colocalization. Furthermore, protein-protein interaction (PPI) networks and druggability assessments were used to refine therapeutic target selection. Additionally, mediation analyses were performed to elucidate the mediating effects of modifiable risk factors on the relationship between plasma proteins and LUSC risk, and we identified 14 modifiable risk factors that could mitigate LUSC risk through targeted interventions. More importantly, we stratified the 12 proteins into four tiers based on colocalization, differential expression, PPI networks, and druggability potential. Notably, DOK2 emerged as a Tier 1 target, while FKBPL, NCF2, AXL, and PDIA3 were classified as Tier 2 targets, representing promising candidates for further drug development. Overall, we identified 12 proteins with druggable potential associated with LUSC risk and demonstrated how modifiable risk factors mediate these associations. These findings advance our understanding of LUSC etiology and provide a foundation for developing targeted therapeutic strategies while emphasizing the importance of addressing modifiable risk factors in both prevention and treatment efforts. - Source: PubMed
Publication date: 2025/11/21
Zhang YutongZhao YiranFan LingliLi XiaoyanLi Yuanyuan - Recent studies have determined a close association between host microbiota and breast cancer initiation, growth and therapeutic outcomes. We previously uncovered how enterotoxigenic Bacteroides fragilis (ETBF), a gut microbe present in malignant breast tissue, aids breast cancer development and metastatic progression via activating multiple oncogenic pathways and modulating breast tumor microenvironment. Brief exposure to ETBF-secreted toxin, BFT (Bacteroides fragilis toxin), imparts long-term oncogenic, pro-stemness and pro-metastasis memory in breast cancer cells indicating the involvement of epigenetic alterations hence, we aimed to investigate the potential involvement of epigenetics in biological impact of ETBF in breast cancer. - Source: PubMed
Publication date: 2025/09/26
Verma DeepakNandi DeeptashreeParida SheetalSaxena ArchishaSharma Dipali - Atopic dermatitis (AD) and autoimmune diseases exhibit epidemiological comorbidity, yet the shared genetic architecture remains incompletely understood. We investigated the genetic overlap between AD and three autoimmune disorders including inflammatory bowel disease (IBD), rheumatoid arthritis (RA), and vitiligo, leveraging genome-wide association data. Despite modest evidence for global genetic correlations, we found 113 independent pleiotropic loci shared among AD and autoimmune diseases, with 11 displaying a concordant effect across all 3 pairwise comparisons. Gene-set and tissue enrichment analyses evidenced the inflammatory background of pleiotropic associations. Multi-trait colocalization analysis prioritized 22 loci, linking the tissue-specific expression of , , , , , , and pleiotropic genes with AD risk. Mendelian randomization revealed no causal effect of genetic liability to AD on autoimmune diseases. Nevertheless, genetic liability to IBD increased AD risk, while vitiligo exhibited a protective effect post outlier correction. Our findings provide mechanistic insights into the multimorbidity of atopic dermatitis (AD) and autoimmune diseases, offering additional evidence for the pleiotropic genetic architecture of AD that contributes to systemic immune dysregulation across multiple organ systems. - Source: PubMed
Publication date: 2025/09/18
Lazanas PanagiotisAntonatos CharalabosTsoumani Konstantina TSgourou ArgyroVasilopoulos Yiannis - Autoantibodies such as antinuclear antibodies (ANAs) and anti-smooth muscle antibodies (ASMAs), which are detected in many cases of autoimmune hepatitis (AIH), are not disease-specific; thus, they have limited value in disease diagnosis. In this study, we aimed to identify disease-specific autoantibodies related to AIH diagnosis or pathogenesis. - Source: PubMed
Publication date: 2025/09/22
Abe KazumichiWada JunHayashi ManabuSugaya TatsuroAbe NaotoTakahata YosukeFujita MasashiTakahashi AtsushiKanno YukikoKuroda MasahitoSaito KeietsuNozawa YoshihiroMigita KiyoshiYatsuhashi HiroshiOhira Hiromasa