First Author | Nishina H | Year | 1998 |
Journal | J Immunol | Volume | 161 |
Issue | 7 | Pages | 3416-20 |
PubMed ID | 9759859 | Mgi Jnum | J:77941 |
Mgi Id | MGI:2182968 | Doi | 10.4049/jimmunol.161.7.3416 |
Citation | Nishina H, et al. (1998) Impaired TCR-mediated apoptosis and Bcl-XL expression in T cells lacking the stress kinase activator SEK1/MKK4. J Immunol 161(7):3416-20 |
abstractText | The dual specificity kinase SEK1 (MKK4) is a direct activator of stress-activated protein kinases (SAPK/JNK) in response to environmental stresses or mitogenic factors. We show in Sek1(-/-)Rag(-/-) chimeric mice that a Sek1 null mutation augments the susceptibility of peripheral T cells to TCR/CD3 religation-induced apoptosis. Sek1(-/-) T cells failed to induce expression of the death suppressor Bcl-XL in response to Ag receptor activation. The Sek1 mutation did not alter the induction of apoptosis in response to etoposide, cisplatinum, Adriamycin, and gamma-irradiation. Moreover, we show that CD3epsilon activation alone leads to SEK1 activation in Sek1(+/+) T cells. These results suggest that SEK1 transduces cellular survival signals during T cell stimulation. |