| First Author | Zou X | Year | 2000 |
| Journal | Mol Cell Biol | Volume | 20 |
| Issue | 2 | Pages | 628-33 |
| PubMed ID | 10611241 | Mgi Jnum | J:59574 |
| Mgi Id | MGI:1351810 | Doi | 10.1128/mcb.20.2.628-633.2000 |
| Citation | Zou X, et al. (2000) p53 deficiency increases transformation by v-Abl and rescues the ability of a C-terminally truncated v-Abl mutant To induce pre-B lymphoma In vivo. Mol Cell Biol 20(2):628-33 |
| abstractText | Abelson murine leukemia virus (A-MuLV) is an acute transforming retrovirus that preferentially transforms early B-lineage cells both in vivo and in vitro. Its transforming protein, v-Abl, is a tyrosine kinase related to v-Src but containing an extended C-terminal domain. Many mutations affecting the C-terminal portion of the molecule block the pre-B-transforming activity of v-Abl without affecting the fibroblast-transforming ability. In this study we have determined the abilities of both wild-type and C-terminally truncated (p90) forms of v-Abl to transform cells from p53(-/-) mice. Lack of p53 increases the susceptibility of bone marrow cells to transformation by v-Abl by a factor of more than 7 but does not alter v-Abl's preference for B220(+) IgM(-) pre-B cells. p53-deficient mice have earlier tumor onset, more rapid tumor progression, and decreased survival time following A-MuLV infection, but all of the tumors are pre-B lymphomas. Thus, p53-dependent pathways inhibit v-Abl transformation but play no role in conferring preferential transformation of pre-B cells. Surprisingly, the C-terminally truncated form of v-Abl (p90) transforms pre-B cells very efficiently in mice lacking p53, thus demonstrating that the C terminus of v-Abl does not determine preB tropism but is necessary to overcome p53-dependent inhibition of transformation. |
