Selective cytotoxicity, or the ability to selectively remove certain cell types from a population, is a vital technology that is often applied to various therapeutic applications.
Stanford scientists have developed a new, better binder for the tumor-associated macrophage marker CD206. This binder can be conjugated to a variety of payloads, including an anti-immune checkpoint protein antibody for more selective immune checkpoint blockade.
Researchers at Stanford have developed an inducible and programmable CRISPR-mediated transcript organization (CRISPR-TO) method for repositioning RNAs to various desired subcellular compartments.
Researchers at Stanford have developed methods to link antigenic or immunomodulatory molecules to bacterial surface proteins of commensal bacteria that result in a high immune response when applied to an epithelial surface of a mammal.
A team of Stanford researchers has developed humanized and chimeric mouse anti-human CD99 monoclonal antibodies with demonstrated activity against AML (acute myeloid leukemia) cells in vitro and in vivo.
Introduction: Blood cell transfusion plays a vital role in modern medicineāsupporting surgery, obstetrics, trauma care, and cancer chemotherapy. In the US alone, more than 12 million red-cell units are consumed annually.
Stanford Medicine's Ji Research Group has developed a simple, quantitative method for detecting and characterizing gene fusions that uses DNA rather than RNA as analyte.
Non-alcoholic steatohepatitis (NASH) is the most common liver disease, leading to cirrhosis and hepatocellular carcinoma (HCC). HCC is one of the most common cancers and has a dismal prognosis as currently available medical treatment only improves survival by a few months.
Stanford scientists have created a de novo protein design platform that designs binding proteins that specifically target antigens in the major histocompatibility complex (MHC).
Researchers at Stanford have identified a novel class of ribonucleic acid (RNA)-reactive groups that effectively modify the RNA by placing heteroaryl and aryl groups at the 2'-hydroxyl (OH) positions.
Researchers at Stanford University have discovered a first-in-class covalent inhibitor that binds to activated Fis1 and prevents mitochondrial fission and dysfunction.