Rabbit anti Human DAP12

DAP12 is a transmembrane adaptor protein that is non-covalently associated with several cell surface receptors on natural killer (NK), myeloid, and presumably neuronal cells (1,2). DAP12 contains an ITAM domain that preferentially recruits the protein tyrosine kinase Syk to initiate signal transduction (3). Deficiency of DAP12 results in reduced antigen presentation function by myeloid cells and defects in function of certain NK cell receptors in mice (4,5), as well as presenile dementia and bone cysts in Humans (6).

This product is intended FOR RESEARCH USE ONLY, and FOR TESTS IN VITRO, not for use in diagnostic or therapeutic procedures involving Humans or animals.

1. Lanier, L.L. , Bakker, A.B. 'The ITAM-bearing transmembrane adaptor DAP12 in lymphoid and myeloid cell function.' Immunol. Today 2000, 21:611-614_x000D_ 2. Campbell, K.S. , Colonna, M. 'DAP12: a key accessory protein for relaying signals by natural killer cell receptors.' Intl J Biochem Cell Biol 1999, 31:631-636_x000D_ 3. McVicar, D.W., et al. 'DAP12-mediated signal transduction in natural killer cells. A dominant role for the Syk protein-tyrosine kinase.' J Biol Chem 1998, 273:32934-32942_x000D_ 4. Bakker, A.B., et al. 'DAP12-deficient mice fail to develop autoimmunity due to impaired antigen priming.' Immunity 2000, 13:345-353_x000D_ 5. Tomasello E., et al. 'Combined natural killer cell and dendritic cell functional deficiency in KARAP/DAP12 loss of function mutant mice.' Immunity 2000, 13:355-363_x000D_ 6. Paloneva, J., et al. 'Loss-of-function mutations in TYROBP (DAP12) result in presenile dementia with bone cysts.' Nature Genetics 2000, 25:357-361_x000D_ 7. Zou, Wei. et al., 'DAP12 Couples c-Fms Activation to the Osteoclast Cytoskeleton by Recruitment of Syk'. Molecular Cell, Aug 8, 2008, Vol 31 (3) 422-431._x000D_ 8. Campbell K.S. er al. 'NKp44 Triggers NK Cell Activation through DAP12 Association That Is Not Influenced by a Putative Cytoplasmic Inhibitory Sequence'. Journal of Immunology, 2004 Vol 172 (2) 899-906; DOI: https://doi.org/10.4049/jimmunol.172.2.899