Polypeptide With Localisation/Targeting Motif TRIZ Cases

Overexpressing HK2, PFK, PKM, and GLUT3 in T cells boosts glycolytic flux and ATP production to counteract tumor microenvironment nutrient deprivation.

An EMPD-specific chimeric antigen receptor redirects T cells to target and eliminate IgE-producing B cells.

Silencing INCA1 with inhibitory nucleic acids prevents PD-L1 upregulation, resolving resistance in immunosuppressive glioblastoma microenvironments.

Recombinant MHC class Ib polypeptides induce antigen-specific tolerance against alpha-Synuclein.

Salvage chimeric antigen receptors redirect immune effector cells to relapsed cancer targets.

Engineered antibodies insert functional domains into the elbow region to create independent binding sites.

DIATHIS-1 fusion protein utilizes an uncleaved Pel B leader sequence to drive oligomer formation and enhance molecular stability.

Targeting conserved internal HIV proteins bypasses surface variability, ensuring broad CTL protection against multiple viral strains without frequent updates.

A Cas9-recombinase fusion protein enables precise gene manipulation via guide RNA targeting.

Engineered gamma delta T cells autonomously secrete optimized STAR molecules, resolving side effects and dosing challenges in cancer treatment.

Linear peptides inhibit CK2-mediated phosphorylation, eliminating methionine oxidation and disulfide bonds to resolve chemical instability.

Targeted peptide inhibitors disrupt aggregated p53 mutants, restoring functional protein activity and enabling effective cancer treatment strategies.

Segmented polypeptides induce lipid bilayer fusion via hetero-oligomeric complexes.

Recombinant antigen-presenting cells activate tumor-reactive T cells using patient-specific neoantigens.

Segmented O-antigen polysaccharide conjugates linked to carrier proteins resolve insufficient subserotype coverage in current vaccines.

Engineered immune cells express a mesothelin-specific chimeric antigen receptor alongside interleukin 7 and chemokine ligand 19.

Biological expression of fusion polypeptides with inclusion body targeting replaces chemical synthesis to overcome harsh reagent requirements.

Humanized BCMA-CAR-T cells resolve specificity trade-offs by using engineered scFv domains to kill myeloma targets while sparing healthy tissue.

Mediator peptides block viral entry while preserving ACE2 physiological functions, reducing lung inflammation and fever.

Engineered CD8+ T cells express heterologous T cell receptors to recognize and eliminate antigen-presenting cells displaying self-antigens.

Focused ultrasound triggers localized gene expression in CAR-T cells, confining activation to tumor sites and reducing off-tumor toxicities.

Segmenting mechanical and chemical pathways preserves signaling while reducing vascular permeability.

A bifunctional anti-PD-1/SIRPa molecule activates T cells and promotes cytokine secretion.

Single domain antibodies target CD33-expressing cells to provide novel therapeutic options for acute myeloid leukemia treatment.

APEX2 enzyme targets the mitochondrial matrix to label proteins, eliminating cytoplasmic contamination and ensuring accurate proteomic data.

CAR utilizing CD27 extracellular domain targets CD70 to reduce tumor burden while sparing normal tissues.

A porcine circovirus type-2 subunit vaccine uses fragmented ORF2 peptides fused with PE and KDEL signals to boost immunogenicity.

A TRAIL-ferritin fusion protein forms a nanocage presenting a trimeric structure to enhance binding affinity.

CAR constructs merge antibody binding with costimulatory signaling to sustain T cell persistence against aggressive solid tumors.

A vector construct fuses a fluorophore to the pVIII coat protein via the E. coli Tat secretory pathway for intrinsically fluorescent phage particles.

Segmented CAR T cells target heterogeneous solid tumors, overcoming antigen variation limits.

CAR-NK constructs targeting CD70 eradicate immunosuppressive tumor microenvironment cells.

Segmented CLL1 gene targeting protects noncancerous hematopoietic cells from therapy-induced depletion while enabling system repopulation.

Engineered CAR-T cells target anthrax toxin receptors to destroy pancreatic cancer while sparing healthy tissue.

Inactivating NKG2D ligands on adoptive cells prevents NK-mediated clearance, eliminating lymphodepletion needs and reducing side effects.

Engineered iPSC-derived macrophages overcome solid tumor penetration limits by combining CAR targeting with antibody co-administration.

Allogeneic T cells with a switchable chimeric antigen receptor reduce immune rejection and exhaustion.

Segmenting the spike protein into a purified receptor binding domain reduces manufacturing complexity while maintaining high protective efficacy.

Fusing Csy4 and Cas9 into one protein boosts editing efficiency at low concentrations while reducing unintended genetic modifications.

Truncating CD28 and 4-1BB intracellular domains in a BCMA-CAR improves surface expression while maintaining T cell activation.

Fusing CTLA-4 cytosolic tails to CAR-T cells enhances surface recycling, reducing trogocytosis and preventing tumor antigen loss.

Segmented peptide chains form binding sites via intermolecular interaction, resolving tonic signaling and autoimmune reactions.

Fusing aMTD and solubility tags resolves the yield-permeability trade-off, enabling effective JAK/STAT suppression in pancreatic cancer therapy.

A cell-penetrating peptide derived from Borna Disease Virus targets mitochondria to preserve cellular functions and enhance filamentation.

A bacterial cell expresses intracellular tubular proteins to form a structure that displays polypeptides for vaccine production.

Segmented dTALE proteins resolve genome manipulation precision versus efficiency trade-offs by enabling customized nucleic acid targeting.

Epitope extraction in normal cells preserves protein function while enabling selective cancer cell elimination.

Virus-like particles display M2e antigens with flagellin adjuvants to overcome weak immunogenicity and provide broad influenza protection.

A single-chain polypeptide fusion protein combines a targeting moiety with a non-cytotoxic protease to inhibit neurotransmitter release in nociceptive sensory afferents.