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While conventionally known for its function as an inhibitory neurotransmitter, GABA signaling was recently discovered to have a significant role in fate determination of blood stem cells.

Researchers at Stanford University have found that upregulating cathelicidin gene expression can improve the efficacy of a wide variety of treatments as an adjunct therapy.

Researchers at Stanford have developed an IL-7–conjugated lipid nanoparticle (LNP) platform designed to substantially improve mRNA delivery to T cells for direct in vivo T-cell engineering.

Researchers at Stanford have developed a platform to design and screen novel chimeric large serine recombinases (LSRs), enzymes capable of inserting large DNA payloads into precise locations in the genome.

Researchers from Stanford developed chemically modified adeno-associated virus (AAV) capsids that enable selective gene delivery to either exocrine or endocrine pancreatic cells through unnatural amino acid incorporation and peptide conjugation.

Researchers at Stanford have created the first small primate model to study human heart rhythm disorders and also discovered a new way the heart keeps its beat.

Researchers at Stanford have developed genetically encoded STING agonists that enable controlled activation of the STING pathway from within engineered cells.

Stanford researchers have developed a new therapeutic approach to protect neurons and promote axon regeneration by restoring mitochondrial transport within axons, a key process disrupted in many neurodegenerative diseases.

Stanford researchers have developed novel AsCas12a-expressing mouse models for simultaneous editing of multiple genomic loci in vivo with unique targeting capabilities relative to traditional Cas9 models, enabling the rapid creation of complex genotypes in somatic cells and ca

Glaucoma results from the loss of retinal ganglion cells (RGCs), the primary output neurons of the retina that connect to brain areas responsible for vision. Current treatments focus on lowering intraocular pressure but do not prevent blindness in about 25% of patients.

Stanford researchers have found that inhibiting 15-prostaglandin dehydrogenase (15-PGDH), which breaks down prostaglandin E2 (PGE2), can improve cardiac function in diseased and aged hearts.

Stanford scientists have developed a cell-free method for producing high-purity plasmid DNA without the use of bacterial hosts. This approach eliminates contamination risks, reduces production time, and streamlines manufacturing for gene and cell therapies.

Stanford researchers have developed a novel technology using extracellular vesicles (EVs) to selectively suppress immune responses to AAV vectors, enabling safer and more effective gene therapy.

Stanford researchers have developed an innovative, non-invasive therapeutic strategy to treat myocardial fibrosis (MF), a key driver of arrhythmia and heart failure in LMNA-related dilated cardiomyopathy (LMNA-DCM).

Stanford researchers have developed a novel gene therapy vector, AAV-capGL to overcome immune barriers that currently limit the efficacy and safety of adeno-associated virus (AAV)-based gene therapies.