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CLIP-Seq based RNA-Protein Interaction Analysis Service

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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:

  • True in vivo binding: UV crosslinking "freezes" transient interactions within live cells, preserving authentic binding sites.
  • Single-nucleotide resolution: Advanced pipelines pinpoint binding motifs with base-level accuracy.
  • 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. (Creative Biolabs Authorized)Fig.1 CLIP-Seq Service Workflow.

Advanced Bioinformatics

Our customizable analytical framework provides scalable computational insights:

Analysis Tier Core Deliverables
Genome-Wide Binding Map Genome-wide binding site identification; motif discovery
Functional Annotation Binding site enrichment analysis (3'UTR/noncoding regions); pathway associations
Multi-RBP Networks Cooperative/competitive RBP interaction modeling
Disease Context Integration with public disease-relevant databases

Related RNA-Protein Interaction Services

RIP-Seq Based Analysis

  • Native Complex Profiling: Identification of physiological RBP interactions without crosslinking artifacts
  • Transcriptome-Wide Screening: Genome-scale mapping of steady-state RNA-protein associations
  • RBP Network Discovery: Foundational analysis for regulatory mechanism hypotheses

ChIRP Based Analysis

  • lncRNA-Centric Mapping: Targeted interrogation of noncoding RNA interactomes
  • Chromatin Proximity Insights: Integration of RNA-chromatin tethering effects
  • Multicomplex Isolation: Capture of nested ribonucleoprotein assemblies

RAP Based Analysis

  • Endogenous Complex Capture: In vivo preservation of native RNA-protein topologies
  • Comprehensive Interactomes: System-wide identification of direct/indirect interactors
  • Functional Module Discovery: Deconvolution of cooperative regulatory units

mRNA Interactome Capture

  • Translatome Profiling: Global snapshot of mRNA-bound proteomes
  • RBP Activity Benchmarking: Basal interaction network establishment
  • Translational Machinery Analysis: Ribosome-associated factor characterization

Emerging Research Applications for CLIP-Seq

1. miRNA Target Deconvolution

  • 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.
  • 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

  • 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.
  • 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

  • Nuclear morphology as mechanistic biomarker
    Aberrant TDP-43/FUS aggregation induces quantifiable nuclear envelope alterations in neurodegeneration models, detectable via AI-enhanced imaging approaches.
  • Multi-scale regulatory hierarchies
    Recent studies reveal that certain RBPs maintain local chromatin stability despite global structural disruption, suggesting layered regulatory mechanisms.
  • 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.
  • Metabolic reprogramming interfaces
    RNA-binding proteins increasingly emerge as post-transcriptional regulators of cancer metabolism, influencing therapeutic response pathways.

4. CRISPR-Guided RBP Perturbation

  • Physiological context screening
    Organoid-AAV hybrid platforms now enable RBP functional screening in near-physiological environments, revealing regeneration-associated chromatin remodelers.
  • 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?

  • End-to-End Expertise:10+ years in RNA-protein interaction studies, from optimized protocols to publication-ready data visualization
  • Technology Leadership:Pioneers in implementing high-resolution interaction capture methodologies with continuous innovation
  • 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

  1. 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
  2. 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.