| First Author | Ashworth T | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 5 | Pages | 2631-5 |
| PubMed ID | 17312101 | Mgi Jnum | J:144122 |
| Mgi Id | MGI:3830144 | Doi | 10.4049/jimmunol.178.5.2631 |
| Citation | Ashworth T, et al. (2007) Cutting Edge: TFII-I controls B cell proliferation via regulating NF-kappaB. J Immunol 178(5):2631-5 |
| abstractText | The multifunctional transcription factor TFII-I physically and functionally interacts with Bruton's tyrosine kinase in murine B cells. However, the downstream functions of TFII-I in B cells are unknown. Toward achieving this goal, we established stable posttranscriptional silencing of TFII-I in WEHI-231 immature murine B cells, which undergoes growth arrest and apoptosis either upon anti-IgM or TGF-beta signaling. In this study, we show that TFII-I promotes growth arrest of cells in a signal-dependent manner. Unlike control cells, B cells exhibiting loss of TFII-I function fail to undergo arrest upon signaling due to up-regulation of c-Myc expression and concomitant down-regulation of both p21 and p27. Loss of TFII-I is also associated with simultaneous increase in nuclear c-rel and decrease in p50 homodimer binding. Thus, besides controlling c-myc transcription, TFII-I controls B cell proliferation by regulating both nuclear translocation of c-rel and DNA-binding activity of p50 NF-kappaB. |
