| First Author | Li W | Year | 2012 |
| Journal | J Biol Chem | Volume | 287 |
| Issue | 4 | Pages | 2500-8 |
| PubMed ID | 22084235 | Mgi Jnum | J:181388 |
| Mgi Id | MGI:5311261 | Doi | 10.1074/jbc.M111.303123 |
| Citation | Li W, et al. (2012) Core fucosylation of mu heavy chains regulates assembly and intracellular signaling of precursor B cell receptors. J Biol Chem 287(4):2500-8 |
| abstractText | alpha1,6-Fucosyltransferase (Fut8) knock-out (Fut8(-/-)) mice showed an abnormality in pre-B cell generation. Membrane assembly of pre-BCR is a crucial checkpoint for pre-B cell differentiation and proliferation in both humans and mice. The assembly of pre-BCR on the cell surface was substantially blocked in the Fut8-knockdown pre-B cell line, 70Z/3-KD cells, and then completely restored by re-introduction of the Fut8 gene to 70Z/3-KD (70Z/3-KD-re) cells. Moreover, loss of alpha1,6-fucosylation (also called core fucosylation) of muHC was associated with the suppression of the interaction between muHC and lambda5. In contrast to Fut8(+/+) CD19(+)CD43(-) cells, the subpopulation expressing the muHC.lambda5 complex in the Fut8(-/-) CD19(+)CD43(-) cell fraction was decreased. The pre-BCR-mediated tyrosine phosphorylation of CD79a and activation of Btk were attenuated in Fut8-KD cells, and restored in 70Z/3-KD-re cells. The frequency of CD19(low)CD43(-) cells (pre-B cell enriched fraction) was also reduced in Fut8(-/-) bone marrow cells, and then the levels of IgM, IgG, and IgA of 12-week-old Fut8(-/-) mice sera were significantly lower than those of Fut8(+/+) mice. Our results suggest that the core fucosylation of muHC mediates the assembly of pre-BCR to regulate pre-BCR intracellular signaling and pre-B cell proliferation. |
