Enterprise AI Analysis
CDK13 drives clear cell renal carcinoma through METTL16-mediated m6A modification of ACLY mRNA
Core Finding: CDK13 acts as a master regulator of lipid dysregulation in clear cell renal cell carcinoma (ccRCC). Mechanism: It promotes de novo lipogenesis via a phosphorylation-dependent RNA N6-methyladenosine (m6A) modification axis. Clinical Relevance: CDK13 overexpression correlates with advanced tumor stage, poor prognosis, and aberrant lipid accumulation in ccRCC patients. Therapeutic Implication: Targeting the CDK13-METTL16-ACLY pathway holds promise for precision therapies against ccRCC.
Executive Impact: Key Metrics
Understanding the quantifiable impact of CDK13's role in ccRCC lipid metabolism for strategic decision-making.
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ROC AUC for CDK13 as ccRCC diagnostic biomarker
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Correlation between CDK13 and METTL16 expression
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Correlation between METTL16 and ACLY mRNA
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Correlation between YTHDC2 and ACLY mRNA
Deep Analysis & Enterprise Applications
Select a topic to dive deeper, then explore the specific findings from the research, rebuilt as interactive, enterprise-focused modules.
CDK13 orchestrates lipid metabolic reprogramming
CDK13 promotes de novo lipogenesis by directly phosphorylating METTL16 at Ser329, enhancing its catalytic activity to install m6A modifications on ACLY mRNA.
CDK13 as a prognostic biomarker and therapeutic target
Elevated CDK13 correlates with advanced tumor stages, poor prognosis, and aberrant lipid accumulation in ccRCC. Disrupting the CDK13-METTL16-ACLY axis suppresses tumor growth and metastasis in vitro and in vivo.
Critical Discovery Spotlight
Ser329 Key phosphorylation site on METTL16 by CDK13Enterprise Process Flow
CDK13 Activation
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METTL16 Phosphorylation (Ser329)
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m6A Modification of ACLY mRNA
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YTHDC2 Recognition
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ACLY mRNA Stabilization
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Increased Acetyl-CoA Production
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Enhanced Lipogenesis & ccRCC Progression
| Approach | Impact on Lipogenesis | Impact on Tumor Growth |
|---|---|---|
| CDK13 Inhibition (1NM-PP1) |
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| METTL16 Depletion |
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| Combination Therapy |
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Clinical Relevance & Future Directions
The CDK13-METTL16-ACLY axis is a novel target for precision therapies in ccRCC. Understanding the structural interactions for inhibitor design, crosstalk with other ccRCC pathways, and developing specific METTL16 modulators are key next steps. ACLY expression and m6A patterns in liquid biopsies could also serve as non-invasive diagnostic and monitoring biomarkers.
Calculate Your Potential ROI with AI
Estimate the impact of advanced AI integration on your operational efficiency and cost savings, inspired by the metabolic reprogramming insights.
Estimated Annual Savings
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Annual Hours Reclaimed
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Your AI Implementation Roadmap
A structured approach to integrating transformative AI solutions, mirroring the precision of molecular targeting.
Phase 01: Discovery & Strategy
In-depth analysis of your current metabolic (operational) processes, identifying key bottlenecks and high-impact areas for AI intervention.
Phase 02: Solution Design & Prototyping
Develop tailored AI models (e.g., for targeted drug discovery or personalized treatment plans) and create prototypes for rapid validation.
Phase 03: Full-Scale Deployment
Seamless integration of validated AI solutions into your enterprise infrastructure, ensuring robust performance and scalability.
Phase 04: Optimization & Monitoring
Continuous monitoring of AI model performance, iterative refinement, and adaptation to evolving clinical or operational needs.
Ready to Transform Your Enterprise?
Just as CDK13 orchestrates metabolic pathways, we can help orchestrate your AI strategy for unparalleled efficiency and innovation. Book a free consultation to explore how these insights apply to your organization.
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