Deregulation of Translational Control of the 65-kDa Regulatory Subunit (PR65α) of Protein Phosphatase 2A Leads to Multinucleated Cells (*)
Deregulation of Translational Control of the 65-kDa Regulatory Subunit (PR65α) of Protein Phosphatase 2A Leads to Multinucleated Cells (*)
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蛋白磷酸酶 2A 65-kDa 调节亚基 (PR65α) 翻译控制的失调导致多核细胞 (*)
DOI:
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发表时间:
1995
影响因子:
4.8
通讯作者:
B. Hemmings
中科院分区:
文献类型:
--
作者:
S. Wera;Anne Fernandez;N. Lamb;P. Turowski;M. Hemmings;R. E. Mayer;B. Hemmings
Efficient translation of the mRNA encoding the 65-kDa regulatory subunit (PR65α) of protein phosphatase 2A (PP2A) is prevented by an out of frame upstream AUG and a stable stem-loop structure (ΔG = −55.9 kcal/mol) in the 5′-untranslated region (5′-UTR). Deletion of the 5′-UTR allows efficient translation of the PR65α message in vitro and overexpression in COS-1 cells. Insertion of the 5′-UTR into the β-galactosidase leader sequence dramatically inhibits translation of the β-galactosidase message in vitro and in vivo, confirming that this sequence functions as a potent translation regulatory sequence. Cells transfected or microinjected with a PR65α expression vector lacking the 5′-UTR, express high levels of PR65α, accumulating in both nucleus and cytoplasm. PR65α overexpressing rat embryo fibroblasts (REF-52 cells) become multinucleated. These data and previous results (Mayer-Jaekel, R. E., Ohkura, H., Gomes, R., Sunkel, C. E., Baumgartner, S., Hemmings, B. A., and Glover, D. M.(1993) Cell 72, 621-633) suggest that PP2A participates in the regulation of both mitosis and cytokinesis.
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DOI:
10.1073/pnas.83.24.9373
发表时间:
1986-12-01
影响因子:
11.1
作者:
FREIER, SM;KIERZEK, R;TURNER, DH
通讯作者:
TURNER, DH
DOI:
10.1073/pnas.84.14.4880
发表时间:
1987-07-01
影响因子:
11.1
作者:
GREEN, DD;YANG, SI;MUMBY, MC
通讯作者:
MUMBY, MC
影响因子:
2.9
作者:
S. Zołnierowicz;C. Csortos;J. Bondor;A. Verin;M. Mumby;A. DePaoli-Roach
通讯作者:
S. Zołnierowicz;C. Csortos;J. Bondor;A. Verin;M. Mumby;A. DePaoli-Roach
影响因子:
56.9
作者:
LIN, TA;KONG, XM;LAWRENCE, JC
通讯作者:
LAWRENCE, JC
影响因子:
5.3
作者:
KOZAK, M
通讯作者:
KOZAK, M