c-Jun N-terminal kinase/c-Jun inhibits fibroblast proliferation by negatively regulating the levels of stathmin/oncoprotein 18
Yvonne YC Yeap, Ivan HW Ng, Bahareh Badrian, Tuong-Vi Nguyen, Yan Y Yip, Amardeep S Dhillon, Steven E Mutsaers, John Silke, Marie A Bogoyevitch, Dominic CH Ng
BIOCHEMICAL JOURNAL | PORTLAND PRESS LTD | Published : 2010
The JNKs (c-Jun N-terminal kinases) are stress-activated serine/threonine kinases that can regulate both cell death and cell proliferation. We have developed a cell system to control JNK re-expression at physiological levels in JNK1/2-null MEFs (murine embryonic fibroblasts). JNK re-expression restored basal and stress-activated phosphorylation of the c-Jun transcription factor and attenuated cellular proliferation with increased cells in G1/S-phase of the cell cycle. To explore JNK actions to regulate cell proliferation, we evaluated a role for the cytosolic protein, STMN (stathmin)/Op18 (oncoprotein 18). STMN, up-regulated in a range of cancer types, plays a crucial role in the control of ..View full abstract
Awarded by National Health and Medical Research Council
This work was supported by the National Health and Medical Research Council [grant numbers 628335 (to D.C.N.), 466804 (to M.A.B.), 433013,541901,541902 (all to IS)]. D.C.N. is supported by a joint-funded National Heart Foundation and National Health and Medical Research Council (NHMRC) Fellowship.