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Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene. [5] LAG3, which was discovered in 1990 [6] and was designated CD223 (cluster of differentiation 223) after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000, [7] is a cell surface molecule with diverse biological effects on T cell function but overall has an immune ...
In molecular biology, the transcriptional activator LAG-3 is a transcriptional activator protein. The C. elegans Notch pathway, involved in the control of growth, differentiation and patterning in animal development, relies on either of the receptors GLP-1 or LIN-12. [1]
Frédéric Triebel (born 20 November 1954) is a French immunologist who is best known for his 1990 discovery of the LAG3 immune control mechanism. Triebel worked through the 1990s in a collaboration between Institut Gustave Roussy and Merck Serono to establish LAG-3's mechanism of action in T cells and dendritic cells.
GSK2831781 originated from a chimeric monoclonal antibody to LAG-3 developed in 2008 by the French biotechnology company Immutep. That company had been built around drugs targeting LAG-3 and was associated with Frédéric Triebel, an immunologist generally regarded as a leading authority on LAG-3.
LAG3 acts as a negative regulator of T cell activation and function and can also be expressed on NK cells and other T cells, than T h 3. Because of its structural similarity to CD4, LAG3 can bind MHC class II molecules .
Immutep Ltd (formerly Prima Biomed) is a biotechnology company working primarily in the field of cancer immunotherapy using the LAG3 immune control mechanism. The company was originally built on CVac, a therapeutic cancer vaccine. In late 2014 the privately held French immunotherapy company Immutep SA was purchased by Prima Biotech.
This monoclonal antibody –related article is a stub. You can help Wikipedia by expanding it.
CARDs were originally characterized based on their involvement in the regulation of caspase activation and apoptosis. [2] The basic six-helix structure of the domain appears to be conserved as far back as the ced-3 and ced-4 genes in C. elegans, the organism in which several components of the apoptotic machinery were first characterized.
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