| First Author | Kee BL | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 7 | Pages | 4518-27 |
| PubMed ID | 16177095 | Mgi Jnum | J:118939 |
| Mgi Id | MGI:3700850 | Doi | 10.4049/jimmunol.175.7.4518 |
| Citation | Kee BL (2005) Id3 induces growth arrest and caspase-2-dependent apoptosis in B lymphocyte progenitors. J Immunol 175(7):4518-27 |
| abstractText | The E-protein transcription factors E2A, HEB, and E2-2 play an essential role in the differentiation, proliferation, and survival of B lymphocyte progenitors (BLPs). In this study, we show that the E-protein antagonist Id3 induces apoptosis of both primary and transformed BLPs through a caspase-2-dependent mechanism that does not require p53 and is not inhibited by bcl-2. Id3 expressing B lineage cells show reduced expression of known E-protein target genes as well as multiple genes involved in cell proliferation. We hypothesize that Id3 induces activation of caspase-2 as a consequence of severe or 'catastrophic' growth arrest. In support of this hypothesis, we show that chemical-induced growth arrest is sufficient to activate caspase-2 and induce apoptosis in BLPs. Our data suggest that E-proteins function in the control of differentiation and proliferation and that diminished E-protein activity results in apoptosis as a consequence of growth arrest. |
