Stanford researchers have developed an innovative platform that enables transplantation of human forebrain assembloids into the rodent brain, supporting advanced neuronal maturation and functional neural activity readouts.
PirB (PIR-B) knockout mice are genetically modified mice in which the gene encoding the PirB receptor (paired immunoglobulin-like receptor B) has been disrupted or "knocked out." PirB is a member of the immunoglobulin superfamily and plays a role in regulating immune responses
Stanford researchers have patented a system for precise genetic modification of human embryonic stem cells (ECSs) and induced pluripotent stem cells (iPSCs).
Mice heterozygous for the targeted allele are viable and fertile. This polyubiquitin B (Ubb) mutation is characterized by a GFP-puror fusion protein "knock-in" allele that also abolishes endogenous gene function.
Peptidase carboxypeptidase A3 (Cpa3; originally named mast cell carboxypeptidase A14) is highly expressed in mast cells, but is also expressed in basophils and can be expressed in some populations of T-cell progenitors and thymic T cells and in certain hematopoietic progenitor
Researchers at Stanford University have developed a method which integrates cell barcoding and high-throughput sequencing to quantify tumor growth in genetically engineered mouse models of human cancer (called 'Tuba-seq” for Tumor barcoding coupled with seq
Cell culture is a central technique used for a plethora of research applications including in the modeling of complex diseases, creating transgenic animals, gene therapy, cell therapy, regenerating lost tissue, and organ biogenesis.
Stanford researchers have made a genetic mouse model to mimic the human LOXHD1 p.R1090Q mutation as a means to further investigate, understand and combat human Age-Related Hearing Loss (ARHL).
Adeno-associated virus (AAV) vectored products are currently leading candidates for gene therapy applications with multiple approved products and many more in clinical trials.
Our researcher has developed a mouse model of 16p11.2 deletion syndrome. A copy number variation on human chromosome 16p11.2 is among the most common genetic variations found in autism spectrum disorders.