C1orf106 Protein Stability Modulation for Intestinal Barrier Integrity
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Solution Overview
Problem
Current treatments for inflammatory bowel diseases (IBD) and intestinal disorders are ineffective due to the complex interaction of factors involving the intestinal mucosa, immune system, and microbial milieu, with unclear mechanisms contributing to impaired epithelial barrier integrity.
Innovation Solution
Modulating the expression and stability of the C1orf106 protein using a CRISPR gene editing system to enhance intestinal epithelial cell integrity, migration, proliferation, and function, thereby reducing inflammation and susceptibility to diseases like IBD.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If current treatments for inflammatory bowel diseases are used, then existing therapeutic approaches are applied, but they are ineffective due to unclear mechanisms and complex interactions
Solution Approach 1:
The patent extracts and focuses on a specific target gene (C1orf106) from the complex intestinal system, isolating one key molecular mechanism to study and treat IBD. By using CRISPR/Cas9 gene editing to specifically modify C1orf106, the invention simplifies the complex multi-factorial problem into a targeted molecular intervention, making the treatment mechanism clear and actionable despite the overall complexity of the intestinal system
Solution Approach 2:
The invention changes the molecular parameter of C1orf106 expression levels and protein stability through CRISPR-mediated gene editing. By introducing specific genetic modifications that increase C1orf106 protein stability and expression, the patent directly alters this key parameter to improve epithelial barrier function and reduce inflammation, providing a reliable treatment mechanism despite the complex system interactions
2Stability of the object's composition
If the stability of C1orf106 protein is increased to improve intestinal epithelium integrity, then barrier function is enhanced, but this requires precise molecular targeting and gene editing
Solution Approach 1:
The patent uses CRISPR/Cas9 as an intermediary tool to achieve precise targeting of the C1orf106 gene. This molecular machinery acts as a mediator that guides the editing process to the exact location in the genome, overcoming the difficulty of precise detection and measurement by providing a built-in targeting mechanism through guide RNA that directs Cas9 to the specific C1orf106 locus
Solution Approach 2:
The invention incorporates feedback mechanisms through validation assays that detect and measure the stability and expression levels of C1orf106 protein after gene editing. By establishing methods to monitor C1orf106 protein stability and epithelial barrier function, the patent creates a feedback loop that confirms the precision of gene targeting and the effectiveness of the intervention, allowing for measurement and verification of the molecular changes
3Object-affected harmful factors
If C1orf106 protein stability is modulated to prevent inflammatory disease, then disease incidence decreases, but this requires novel therapeutic agents and approaches
Solution Approach 1:
The patent applies preliminary action by using CRISPR/Cas9 gene editing to pre-establish stable C1orf106 expression and protein stability in intestinal epithelial cells before disease development. By proactively modifying the genome to ensure proper C1orf106 function, the invention prevents inflammatory disease incidence rather than treating established disease, eliminating the need for complex therapeutic agents by addressing the root cause preventively
Solution Approach 2:
The invention creates a model system that copies and replicates the C1orf106 gene function in controlled settings, allowing for the development and testing of therapeutic approaches. By establishing cell lines and animal models with modified C1orf106, the patent enables the creation of standardized therapeutic protocols and agents that can be manufactured and tested systematically, improving ease of manufacture compared to developing entirely novel therapies
Data Source
AI summary
Embodiments disclosed herein provide methods for modulating intestinal epithelial cell integrity, migration, proliferation, differentiation, maintenance and/or function in which the expression of Cp1orf106 or its protein product are modulated such that the stability of the protein is altered. In certain example embodiments, increasing the stability or preventing a decrease in the stability of Cp1orf106 protein increases the overall integrity of the intestinal epithelium, thereby resulting in a decreased incidence of inflammatory disease. Increased integrity or stability of the epithelium may prevent invasion of migratory cells such as cancer cells.