Fusion With DNA-Binding Domain TRIZ Cases

Mutated SpCas9 nucleases recognize novel PAM sequences, resolving the trade-off between targeting range and sequence specificity.

Loop mutations in the hA3Bctd domain tune deaminase binding strength to narrow the editing window and reduce genome-wide off-target effects.

Multiple insertion sites enable targeted integration of exogenous nucleic acid sequences into predetermined genomic locations.

A nucleotide construct encodes a peptide with a targeting domain that binds to hypomethylated chromatin in cancer cells.

Increasing net charge via amino acid substitutions boosts transposition efficiency, resolving low delivery rates into immune system cells.

Zinc finger nucleases target paralogous EPSPS genes with high precision, resolving low efficiency in conventional plant genome editing.

Repeatable directed endonucleases cleave DNA at an offset position to preserve the recognition sequence, enabling precise genome engineering and data recording.

Zinc finger nucleases inactivate the TRAC gene to boost modification efficiency and overcome limited patient T cell generation capacity.

A single PCR method introduces mutations into plasmid DNA for directed evolution of biomolecules.

Chimeric heterocyclic polyamide compounds selectively bind to TGGAA pentanucleotide repeats in the bean gene.

Dual prime editing with two guide RNAs targets the DMPK gene to correct expanded CTG repeats causing myotonic dystrophy.

TALE-LSD1 fusion proteins resolve the trade-off between mapping precision and functional data loss by enabling targeted chromatin modification.

N- and C-terminal fusion on TALE monomers bypasses dimerization constraints, expanding targeting flexibility beyond thymine-dependent sequences.

Site-specific nucleases guide transgene insertion into the HPRT locus, reducing oncogene activation risks while ensuring durable expression.

Chemical epigenetic modifiers recruit chromatin regulators to specific loci, resolving the precision-toxicity trade-off in gene therapy.

NOX1 promoters drive targeted IL10 expression in high-lipid environments, resolving packaging limits and off-target effects.

Epigenetic modulators downregulate Nav1.7 and Nav1.8 expression to provide non-addictive pain relief, avoiding opioid addiction risks.

Site-specific SFRP1 disrupting agents modulate gene expression to treat alopecia by targeting the SFRP1 control region.

Segmenting targeting and delivery functions resolves the trade-off between base-level precision and large fragment scalability in gene editing.

Merging transposase and targeting domains resolves the trade-off between high transposition efficiency and site-specific precision.

Segmented RSPO surrogates bind RNF43 to potentiate Wnt signaling, avoiding broad tissue distribution and pleiotropic toxicities.

stiCas9 generates cohesive ends to resolve blunt end limitations, enhancing precision in eukaryotic cell modification.

Extracted catalytic cores reduce protein size while point mutations enhance dimerization stability, enabling high indel rates across long spacer regions.

A GEMS construct uses modular nuclease recognition sequences to enable precise gene insertion into safe harbor sites.

Replacing cationic amino acids with uncharged or negative residues in TALEN terminals reduces off-target cleavage while preserving on-target activity.

Targeting the complementary DNA strand expands the editable window beyond PAM restrictions, enabling efficient A-to-G and C-to-T edits on both DNA strands.

A split dCas9 fusion protein system uses intein splicing to rejoin separate expression cassettes into a functional epigenetic editing complex.

CreERT2-p27K genetic constructs enable real-time tracking of quiescent cellular populations.

Correcting the IVS1-1 mutation via ZFN-mediated editing eliminates iron overload risks from transfusions.

Fusing a nickase DNA binding protein with Rad51 boosts HDR efficiency and reduces indel formation.

Modified beta-solenoid amyloid fibrils replicate ACE2 receptors to capture virions, improving diagnostic sensitivity against viral mutations.

Fusing heterologous domains to Cas12i2 resolves the trade-off between protein structure complexity and binding specificity for precise genetic editing.

Matching a cyanobacterial Fd/FNR system with host enzymes boosts metabolite production levels in mammalian cells.

Targeting the S100A gene cluster in CHO cells resolves expression instability from random integration, ensuring homogeneous therapeutic protein yields.

A self-inactivating CRISPR nuclease system directs guide RNA to terminate editing activity after target mutation.

Fusion polypeptides combine cytidine deaminase domains with CRISPR-Cas binding modules to perform targeted C-to-T base editing.

A nucleic acid base converting enzyme linked to a sequence-recognizing module converts targeted DNA nucleotides without cleaving strands.

Segmented protein assembly directs effectors to specific genome loci through non-covalent linkage, resolving steric hindrance and viral delivery constraints.

Direct injection of zinc-finger nuclease mRNA bypasses difficult embryonic stem cell culture to achieve efficient targeted genome editing in rats.

Altering recognition loop residues restricts cytosine substrate availability, reducing off-target mutations while maintaining precise on-target editing.

Segmented zinc finger domains target expanded CAG repeats to repress mutant Htt alleles, preserving wild-type function while reducing neurodegeneration.

Bulk genome editing with CRISPR/Cas9 creates accurate melanoma models by resolving the trade-off between genetic uniformity and model reliability.

Engineered TAL-Tet1 fusion proteins catalyze hydroxylation of methylated cytosines to achieve targeted DNA demethylation.

Modified TALEN scaffolds overcome design constraints by accepting any starting nucleotide and flexible spacer lengths, improving genome editing efficiency.

Engineered TAL effectors modulate HPPD gene expression, enabling higher herbicide doses without crop damage.

Replacing Zinc Finger Nucleases with TALEN systems overcomes specificity limits, enabling efficient FUT8 knockout cell lines.

Star Repeat Variable Diresidues accommodate methylated cytosine, restoring binding efficiency on modified DNA targets.

VP16-CREB fusion protein boosts transgene expression and growth density in CHO cells, eliminating gene amplification instability.