Polymorphism Uses TRIZ Cases

Guide RNAs target heterozygous APOA1 SNPs to knock out the mutant allele while preserving functional apoA-1 expression and limiting amyloid fibrils.

Customized guide RNA directs CRISPR/Cas to the MYD88 L265P mutation, killing B-cell lymphoma cells while sparing healthy cells.

CRISPR guide RNAs selectively disable the mutant ELANE allele to treat SCN or CyN while preserving functional protein expression.

Selective RNA-targeting agents suppress toxic cytoplasmic G4R1 while preserving nuclear G4R1, reducing off-target cellular effects.

Chemically modified antisense oligonucleotides improve SNP-level target specificity while preserving effective nucleic acid modulation.

Selective siRNA silences the PLN R14del mutant transcript while preserving wild-type expression to improve cardiac function and lower arrhythmia risk.

Sequence-specific guide RNAs use heterozygous SNPs to disable the mutant APOA1 allele while preserving functional protein expression.

Complementary ASOs bind SETBP1 nucleic acid sequences to inhibit expression and lower protein levels in associated diseases.

CRISPR targeting of mutant ELANE alleles addresses SCN and CyN while preserving the wild-type allele and reducing reliance on G-CSF therapy.

This case uses RNA editing oligonucleotides and endogenous ADAR to correct USH2A stop-codon mutations without delivering the full gene.

Controlled oligonucleotide structures with specific sugar modifications resolve stability complexity trade-offs to improve therapeutic delivery.

Sleeping Beauty transposase integrates GBA1 into pluripotent stem cell genomes, restoring GCase activity for consistent dopamine neuron differentiation.

Modified TREM compositions increase isoacceptor tRNA abundance to resolve contextually rare codon bottlenecks and improve protein production yields.

RNA aptamers detect specific alpha-synuclein fiber conformers through high-affinity molecular recognition.

A platform using genome-edited iPSC cardiomyocytes with KCNH2 mutations to model interindividual genetic variations.

A guide RNA molecule targets mutant SAMD9 alleles using specific SNP recognition to enable precise genetic knockout.

Segmented antisense oligonucleotides recruit endogenous ADAR enzymes to deamine target adenosines, resolving size constraints that hinder cellular uptake.

RNA interference oligonucleotides reduce mutant HNRNPH2 protein production through targeted mRNA degradation.

Circularizing linear guide RNAs via spacer domains prevents exonuclease degradation, increasing editing efficiency and stability.

Co-targeting HPRT with Cas9 resolves transfection variability and oncogenic risks through iterative HAT selection.

Segmented guide and passenger strands enable precise ADAR-mediated editing of disease-associated single nucleotide polymorphisms.

Small molecule compounds enhance homology-directed repair efficiency while maintaining hematopoietic cell viability during CRISPR editing.

Recombinant adeno-associated viral vectors deliver short hairpin RNA molecules to increase UBE3A expression in neurons.