Figure 1. Superior Signal-to-Noise Ratio. Comparison of ChIP-seq peak calling quality. CD Genomics' optimized protocol (bottom) yields sharp, distinct peaks with minimal background compared to standard methods.
Figure 2. De Novo Motif Discovery. Identification of enriched DNA binding motifs within ChIP-seq peaks, confirming the specificity of the transcription factor binding.
Figure 3. Integrative Multi-Omics Analysis. Correlation of transcription factor binding sites (ChIP-seq peaks) with target gene expression levels (RNA-seq), revealing direct regulatory mechanisms.
The research team suspected that the protein NELFE drives liver cancer progression via Liquid-Liquid Phase Separation (LLPS). However, they lacked the high-resolution structural evidence to prove how these phase-separated condensates interact with the genome to regulate specific oncogenes. They needed a partner to map the precise genomic binding sites and chromatin state changes.
To address this complex question, CD Genomics designed a comprehensive Epigenomic Multi-Omics strategy for the client:
- ChIP-Seq Execution: We performed high-sensitivity ChIP-seq using anti-NELFE antibodies to identify genome-wide binding peaks, ensuring high signal-to-noise ratios even in complex cancer cell lines.
- ATAC-Seq Integration: We conducted ATAC-seq to assess chromatin openness.
- Bioinformatics Support: Our analysis team performed an Integrative Analysis, overlaying the ChIP-seq signals with ATAC-seq tracks to visualize how NELFE binding directly remodels chromatin architecture at promoter regions.
Figure 1. CD Genomics Data Output. Integrated genome browser view showing the correlation between NELFE binding (ChIP-seq, Top) and Open Chromatin (ATAC-seq, Bottom). The distinct peaks produced by our pipeline confirmed that NELFE recruits chromatin remodelers to activate oncogenes.
The data generated by CD Genomics provided the "smoking gun."
- Precise Localization: Our ChIP-seq analysis pinpointed NELFE binding specifically at the promoters of key oncogenes (e.g., MYC, CCND1).
- Mechanism Revealed: By correlating our ChIP-seq data with the client's ATAC-seq data, we demonstrated that NELFE binding sites perfectly overlap with regions of increased chromatin accessibility. This proved that NELFE condensates physically "open up" chromatin to drive gene transcription.
With these high-quality, publication-ready figures, the client successfully published their findings in Cell Death & Disease (Nature Portfolio). This case exemplifies how CD Genomics empowers researchers to connect novel physical mechanisms (phase separation) with genetic outcomes.
