| First Author | Wang D | Year | 2000 |
| Journal | Immunity | Volume | 13 |
| Issue | 1 | Pages | 25-35 |
| PubMed ID | 10933392 | Mgi Jnum | J:63679 |
| Mgi Id | MGI:1861367 | Doi | 10.1016/s1074-7613(00)00005-4 |
| Citation | Wang D, et al. (2000) Phospholipase Cgamma2 is essential in the functions of B cell and several Fc receptors. Immunity 13(1):25-35 |
| abstractText | Many receptors activate phospholipase Cgamma1 or -gamma2. To assess the role of PLCgamma2, we derived enzyme-deficient mice. The mice are viable but have decreased mature B cells, a block in pro-B cell differentiation, and B1 B cell deficiency. IgM receptor-induced Ca2+ flux and proliferation to B cell mitogens are absent. IgM, IgG2a, and IgG3 levels are reduced, and T cell-independent antibody production is absent. The similarity to Btk- or Blnk-deficient mice demonstrates that PLCgamma2 is downstream in Btk/Blnk signaling. FcRgamma signaling is also defective, resulting in a loss of collagen-induced platelet aggregation, mast cell FcepsilonR function, and NK cell FcgammaRIII and 2B4 function. The results define a signal transduction pathway broadly utilized by immunoglobulin superfamily receptors. |
