Engineered CRISPR-associated Tn7 transposases enable precise nucleic acid insertion and editing through guide RNA targeting.
Fusing a neuropilin-binding peptide with scFv antibodies widens endothelial gaps, overcoming low permeability in solid tumor tissues.
Codon optimization of NmeCas9 polynucleotides increases liver editing efficiency while reducing immunogenic cytokine elevation.
Chimeric polypeptides degrade peptidoglycan in the periplasmic space, reducing populations of antibiotic-resistant Gram-negative bacteria.
Lipopeptide anchor stabilizes large protein payloads on cell membranes, eliminating lysis and purification complexity.
Coupling cell-penetrating peptides to thymidine phosphorylase degrades toxic thymidine, avoiding high mortality rates from stem cell transplantation.
A kit using photocatalysts to induce covalent bonds between proteins and interactomes within living cells.
Modified peptides mimic adaptor proteins to activate Akt signaling, reducing spleen and thymus weight loss in stress-associated diseases.
Recombinant nucleic acid construct encodes a CD44v6-specific chimeric antigen receptor paired with a checkpoint inhibitory molecule and an immune stimulatory cytokine.
Segmenting activation signals through an MHC intermediary reduces off-target toxicities while maintaining antigen specificity in T cell therapies.
ROR-1 targeted chimeric antigen receptors enhance therapeutic efficacy against hematological cancers resistant to CD19 therapies.
JP1 peptide inhibits astrocyte over-activation, protecting dopamine neurons from excitotoxicity while reducing neuronal death.
Base editing creates durable STAT3 inhibition without repeated dosing, resolving the trade-off between treatment reliability and administration frequency.
Segmenting signaling into distinct modules eliminates autoimmune risks from cross-pairing while enhancing effector functions.
SOX9 inhibitor compounds decrease CSPG expression, resolving the trade-off between scar structural support and axonal regeneration.
Engineered Promab PD-L1-CAR-T cells combine optimized scFv fragments with CD28 and 4-1BB domains to overcome low cytotoxic activity in existing immunotherapies.
Engineered piggyBac-like transposases overcome low expression levels by boosting integration efficiency of large DNA sequences.
A chimeric antigen receptor uses HH1-derived variable regions to bind CD37 on malignant B-cells.
Polyspecific binding molecules bridge T cells and white blood cells to overcome insufficient activation in solid tumor immunotherapy.
Viral vector delivery of recombinant polynucleotides expressing ENPP1 or ENPP3 reduces ectopic calcification by increasing pyrophosphate levels.
Effector polypeptides target the CD95 extracellular domain to block pro-tumorigenic signaling while preserving intracellular survival mechanisms.
Modified hinge region sequences optimize CAR-T cell flexibility to overcome limited tumor infiltration and short survival time in solid tumors.
Engineered peptides derived from retroviral zinc finger domains penetrate membranes to deliver substances efficiently without damaging the cell.
Replacing conventional peptides with the NSP24 signal sequence resolves low secretion efficiency and biological activity trade-offs in filamentous fungi.
Charged tails mediate surface attachment through electrostatic salt bridges, preventing nonspecific adsorption and maintaining biological activity.
Chimeric polypeptides integrate binding and catalytic domains to overcome poor cellulose breakdown efficiency in biofuel production.
Targeting alternative CD19 splice variants overcomes resistance from wild-type evasion in relapsed B-cell malignancies.
A chimeric antigen receptor polypeptide combines heavy and light chain variable regions from distinct antibodies to form a single binding domain.
Fusion protein with a covalently bound targeting peptide enhances virus-like particle specificity for precise cell targeting.
Peptisomes bypass endosomal degradation by using ultrasound to trigger direct intracellular cargo release.
BMP9 and BMP10 polypeptides increase hemoglobin levels without the cardiovascular risks associated with high-dose EPO therapy.
Codon optimization of batroxobin cDNA with mutated alpha-factor secretion signals resolves E. coli expression bottlenecks, achieving 4-13 fold higher yields.
Fusing single-domain antibodies with thermostable kinases resolves cytoplasmic misfolding by promoting correct disulfide bond formation and thermal stability.
Kv2.1 channel-derived peptides disrupt syntaxin binding to inhibit apoptotic potassium currents.
AAV9 vectors deliver natriuretic polypeptide genes to cardiac cells for sustained local peptide expression.
A cell co-localizes beta-2 microglobulin with an intracellular signaling domain to present immunogenic peptides.
Segmented polypeptide conjugates transport mitochondrial modulators across the blood-brain barrier to treat neurological disorders.
Kv2.2-derived peptides block Kv2.1 channel membrane insertion, preventing cytoplasmic ion loss and preserving neuronal viability after ischemic stroke.
Constitutive STAT5/STAT3 activation sustains CAR-T proliferation in cytokine-poor tumor microenvironments.
Pre-treating PBMCs with a MYC fusion polypeptide enhances cell viability and recovery, addressing damage from freeze-thaw cycles.
QTY Fc fusion proteins replace hydrophobic amino acids to create water-soluble decoys that rapidly reduce cytokine levels in cytokine release syndrome.
A kit screens multiple secretion cassettes to identify optimal mRNA targeting elements for eukaryotic cells.
Activated CAR-T extracellular vesicles deliver cytotoxic payloads to solid tumors, bypassing cytokine release syndrome risks.
Replacing conventional signaling domains with Fc alpha receptor intracellular domain overcomes immune resistance in solid tumors.
Specific peptides disrupt the LRRK2 and PP1 protein interaction to enhance neuronal health.
Modifying the hemagglutinin proteolytic loop prevents premature cleavage, resolving folding accuracy issues to boost immunogenicity and yield.
Multivalent antibody fusion proteins overcome viral immune evasion by mimicking spike protein oligomerization patterns.
A fusion peptide links a clot-targeting sequence with microplasminogen to form a nanocage that binds thrombi and initiates localized dissolution.