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Mapping RNA Regulatory Networks with Subcellular Precision
Creative Biolabs uses our advanced CLIP-Seq (Cross-Linking and Immunoprecipitation Sequencing) technology to provide insights into RNA-binding interactions across the transcriptome. By harnessing our proprietary crosslinking techniques, high-fidelity immunoprecipitation, and AI-powered bioinformatics, we deliver confident and precise binding maps tailored exclusively for preclinical applications in transcriptomics, disease biology, and target identification.
Technology Overview: The CLIP-Seq Advantage
CLIP-Seq captures physiological RNA-protein interactions through UV-induced covalent crosslinking, followed by target-specific immunoprecipitation and deep sequencing. This approach overcomes the limitations of traditional methods by:
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True in vivo binding: UV crosslinking "freezes" transient interactions within live cells, preserving authentic binding sites.
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Single-nucleotide resolution: Advanced pipelines pinpoint binding motifs with base-level accuracy.
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Reduced false positives: Rigorous RNase digestion eliminates non-bound RNA fragments, enhancing signal-to-noise ratios.
Featured Services
Comprehensive CLIP-Seq Workflow
We deliver modular research solutions spanning experimental design to biological interpretation:
Fig.1 CLIP-Seq Service Workflow.
Advanced Bioinformatics
Our customizable analytical framework provides scalable computational insights:
Analysis Tier
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Core Deliverables
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Genome-Wide Binding Map
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Genome-wide binding site identification; motif discovery
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Functional Annotation
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Binding site enrichment analysis (3'UTR/noncoding regions); pathway associations
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Multi-RBP Networks
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Cooperative/competitive RBP interaction modeling
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Disease Context
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Integration with public disease-relevant databases
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Related RNA-Protein Interaction Services
RIP-Seq Based Analysis
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Native Complex Profiling: Identification of physiological RBP interactions without crosslinking artifacts
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Transcriptome-Wide Screening: Genome-scale mapping of steady-state RNA-protein associations
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RBP Network Discovery: Foundational analysis for regulatory mechanism hypotheses
ChIRP Based Analysis
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lncRNA-Centric Mapping: Targeted interrogation of noncoding RNA interactomes
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Chromatin Proximity Insights: Integration of RNA-chromatin tethering effects
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Multicomplex Isolation: Capture of nested ribonucleoprotein assemblies
RAP Based Analysis
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Endogenous Complex Capture: In vivo preservation of native RNA-protein topologies
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Comprehensive Interactomes: System-wide identification of direct/indirect interactors
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Functional Module Discovery: Deconvolution of cooperative regulatory units
mRNA Interactome Capture
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Translatome Profiling: Global snapshot of mRNA-bound proteomes
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RBP Activity Benchmarking: Basal interaction network establishment
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Translational Machinery Analysis: Ribosome-associated factor characterization
Emerging Research Applications for CLIP-Seq
1. miRNA Target Deconvolution
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Multi-omics integration redefines validation paradigms
Converging experimental perturbation data (e.g., miRNA knockout/overexpression) with computational predictions has uncovered clinically relevant regulatory hubs. In oncology, integrated approaches recently revealed miR-30a-mediated cell cycle control through CDC7-DBF4 targeting, with target expression correlating with patient survival outcomes.
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Single-cell resolution unlocks cellular heterogeneity
Recent advancements in single-cell pri-miRNA mapping in plants uncovered cell-type specific regulatory networks (e.g., miR858a repressing MYB transcription factors in vascular cell pri-miRNAs), opening up new avenues for tissue-specific mechanism studies.
2. Splicing Machinery Dynamics
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Splice factors as immuno-oncology targets
Recent genome-wide CRISPR screening revealed the splice factor PTPN2 as a negative regulator of antitumor immunity, implicating the splicing machinery in the modulation of tumor microenvironment cross-talk.
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3D genome-splicing interplay
Spatial chromatin organization coordinates with splice factor recruitment (e.g., SF3B1 at TAD boundaries), where disruption of architectural proteins alters exon selection patterns in neural development models.
3. RNA-Centric Disease Mechanisms
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Nuclear morphology as mechanistic biomarker
Aberrant TDP-43/FUS aggregation induces quantifiable nuclear envelope alterations in neurodegeneration models, detectable via AI-enhanced imaging approaches.
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Multi-scale regulatory hierarchies
Recent studies reveal that certain RBPs maintain local chromatin stability despite global structural disruption, suggesting layered regulatory mechanisms.
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Targeting cancer stemness vulnerabilities
RBP-RNA interactions (e.g., LIN28/IGF2BP-MYC axis) sustain tumor-initiating cell properties, with disruption showing synergistic effects with conventional therapies.
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Metabolic reprogramming interfaces
RNA-binding proteins increasingly emerge as post-transcriptional regulators of cancer metabolism, influencing therapeutic response pathways.
4. CRISPR-Guided RBP Perturbation
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Physiological context screening
Organoid-AAV hybrid platforms now enable RBP functional screening in near-physiological environments, revealing regeneration-associated chromatin remodelers.
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Multi-modal perturbation phenotyping
Simultaneous genomic architecture and transcriptome profiling following gene perturbation identifies novel 3D genome regulators (e.g., CHD7 deletion reducing compartment interactions).
Partner with Creative Biolabs
Why Choose Us?
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End-to-End Expertise:10+ years in RNA-protein interaction studies, from optimized protocols to publication-ready data visualization
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Technology Leadership:Pioneers in implementing high-resolution interaction capture methodologies with continuous innovation
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Preclinical Integrity:100% research-focused services—strictly for mechanistic exploration, zero therapeutic claims
Initiate Your Project
Share your target RBP, biological model, and research objectives with our specialists to receive a tailored proposal, including experimental design recommendations and analytical strategy. Contact our team to schedule a technical consultation and accelerate your research.
FAQs
Q1: How does CLIP-Seq differ from RIP-Seq?
A: CLIP-Seq's UV crosslinking step captures transient interactions with base precision, while RIP-Seq lacks crosslinking and has higher background noise.
Q2: Can CLIP-Seq analyze non-polyadenylated RNAs?
A: Yes. Our protocols capture lncRNAs, circRNAs, and pre-rRNAs.
Q3: What input materials are required?
A: Standard: 5–10 million cells per condition. Low-input protocols available (≥500,000 cells).
Q4: Is bioinformatics support included?
A: Yes. Our pipeline covers peak calling, motif discovery, and multi-omics integration. Custom analyses available.
Featured mRNA ProductsReferences
References
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Zhang, Zijun, and Yi Xing. "CLIP-seq analysis of multi-mapped reads discovers novel functional RNA regulatory sites in the human transcriptome." Nucleic acids research 45.16 (2017): 9260-9271. Distributed under Open Access license CC BY-NC 4.0, without modification. https://doi.org/10.1093/nar/gkx646
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Li, Yang Eric, et al. "Identification of high-confidence RNA regulatory elements by combinatorial classification of RNA–protein binding sites." Genome biology 18 (2017): 1-16. Distributed under Open Access license CC BY 4.0, without modification. https://doi.org/10.1186/s13059-017-1298-8
All products and services are For Research Use Only and CANNOT be used in the treatment or diagnosis of disease.