Biology:CD96

From HandWiki
Short description: Protein-coding gene in the species Homo sapiens


A representation of the 3D structure of the protein myoglobin showing turquoise α-helices.
Generic protein structure example

CD96 (Cluster of Differentiation 96) or Tactile (T cell activation, increased late expression) is a protein that in humans is encoded by the CD96 gene.[1] CD96 is a receptor protein which is expressed on T cells and NK cells and shares sequence similarity with CD226 (also known as DNAM-1).[2] The protein encoded by this gene belongs to the immunoglobulin superfamily. It is a type I membrane protein. The protein may play a role in the adhesion of activated T and NK cells to their target cells during the late phase of the immune response. It may also function in antigen presentation[citation needed]. Alternative splicing occurs at this locus and two transcript variants encoding distinct isoforms have been identified. CD96 is a transmembrane glycoprotein that has three extracellular immunoglobulin-like domains and is expressed by all resting human and mouse NK cells. CD96 main ligand is CD155. CD 96 has approximately 20% homology with CD226 and competed for binding to CD155 with CD226.[3]

Function

The protein encoded by this gene belongs to the immunoglobulin superfamily. It is a type I membrane protein. The protein may play a role in the adhesive interactions of activated T and NK cells during the late phase of the immune response. It may also function in antigen presentation. Alternative splicing generates multiple transcript variants encoding distinct isoforms. [provided by RefSeq, Jan 2016].

References

  1. "Entrez Gene: CD96 molecule". https://www.ncbi.nlm.nih.gov/gene/10225. 
  2. "The role of NK cell recognition of nectin and nectin-like proteins in tumor immunosurveillance". Seminars in Cancer Biology 16 (5): 359–366. October 2006. doi:10.1016/j.semcancer.2006.07.002. PMID 16904340. 
  3. "Balancing natural killer cell activation through paired receptors". Nature Reviews. Immunology 15 (4): 243–254. April 2015. doi:10.1038/nri3799. PMID 25743219. 

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.