CD19

CD19 molecule
Identifiers
Symbols CD19; B4; CVID3; MGC12802
External IDs OMIM107265 MGI88319 HomoloGene1341 GeneCards: CD19 Gene
RNA expression pattern
More reference expression data
Orthologs
Species Human Mouse
Entrez 930 12478
Ensembl ENSG00000177455 ENSMUSG00000030724
UniProt P15391 Q3TA95
RefSeq (mRNA) NM_001178098.1 NM_009844.2
RefSeq (protein) NP_001171569.1 NP_033974.2
Location (UCSC) Chr 16:
28.94 – 28.95 Mb
Chr 7:
133.55 – 133.56 Mb
PubMed search [1] [2]

B-lymphocyte antigen CD19 also known as CD19 (Cluster of Differentiation 19), is a protein that in humans is encoded by the CD19 gene.[1][2]

Contents

Function

Lymphocytes proliferate and differentiate in response to various concentrations of different antigens. The ability of the B cell to respond in a specific, yet sensitive manner to the various antigens is achieved with the use of low-affinity antigen receptors. This gene encodes a cell surface molecule that assembles with the antigen receptor of B lymphocytes in order to decrease the threshold for antigen receptor-dependent stimulation.[1]

CD19 is expressed on follicular dendritic cells and B cells. In fact, it is present on B cells from earliest recognizable B-lineage cells during development to B-cell blasts but is lost on maturation to plasma cells. It primarily acts as a B cell co-receptor in conjunction with CD21 and CD81. Upon activation, the cytoplasmic tail of CD19 becomes phosphorylated, which leads to binding by Src-family kinases and recruitment of PI-3 kinase.

As on T cells, several surface molecules form the antigen receptor and form a complex on B lymphocytes. The (almost) B cell-specific CD19 phosphoglycoprotein is one of these molecules. The others are CD21 and CD81. These surface immunoglobulin (sIg)-associated molecules facilitate signal transduction. On living B cells, anti-immunoglobulin antibody mimicking exogenous antigen causes CD19 to bind to sIg and internalize with it. The reverse process has not been demonstrated, suggesting that formation of this receptor complex is antigen-induced. This molecular association has been confirmed by chemical studies. Mutations in CD19 are associated with severe immunodeficiency syndromes characterized by diminished antibody production.[3][4]

Interactions

CD19 has been shown to interact with:

References

  1. ^ a b "Entrez Gene: CD19 CD19 molecule". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=930. 
  2. ^ Tedder TF, Isaacs CM (July 1989). "Isolation of cDNAs encoding the CD19 antigen of human and mouse B lymphocytes. A new member of the immunoglobulin superfamily". J. Immunol. 143 (2): 712–7. PMID 2472450. 
  3. ^ Pesando JM, Bouchard LS, McMaster BE (December 1989). "CD19 is functionally and physically associated with surface immunoglobulin". J. Exp. Med. 170 (6): 2159–64. doi:10.1084/jem.170.6.2159. PMC 2189531. PMID 2479707. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=2189531. 
  4. ^ van Zelm MC, Reisli I, van der Burg M, Castaño D, van Noesel CJ, van Tol MJ, Woellner C, Grimbacher B, Patiño PJ, van Dongen JJ, Franco JL (May 2006). "An antibody-deficiency syndrome due to mutations in the CD19 gene". N. Engl. J. Med. 354 (18): 1901–12. doi:10.1056/NEJMoa051568. PMID 16672701. 
  5. ^ a b Bradbury LE, Kansas GS, Levy S, Evans RL, Tedder TF (November 1992). "The CD19/CD21 signal transducing complex of human B lymphocytes includes the target of antiproliferative antibody-1 and Leu-13 molecules". J. Immunol. 149 (9): 2841–50. PMID 1383329. 
  6. ^ a b Horváth G, Serru V, Clay D, Billard M, Boucheix C, Rubinstein E (November 1998). "CD19 is linked to the integrin-associated tetraspans CD9, CD81, and CD82". J. Biol. Chem. 273 (46): 30537–43. doi:10.1074/jbc.273.46.30537. PMID 9804823. 
  7. ^ a b Imai T, Kakizaki M, Nishimura M, Yoshie O (August 1995). "Molecular analyses of the association of CD4 with two members of the transmembrane 4 superfamily, CD81 and CD82". J. Immunol. 155 (3): 1229–39. PMID 7636191. 
  8. ^ Doody GM, Billadeau DD, Clayton E, Hutchings A, Berland R, McAdam S, Leibson PJ, Turner M (November 2000). "Vav-2 controls NFAT-dependent transcription in B- but not T-lymphocytes". EMBO J. 19 (22): 6173–84. doi:10.1093/emboj/19.22.6173. PMC 305817. PMID 11080163. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=305817. 

Further reading

External links

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