Heat Shock Treatment Decreases E2F1-DNA Binding and E2F1 Levels in Human A549 Cells

Verfasser / Beitragende:
[D. Gerullis, L. Rensing, D. Beyersmann]
Ort, Verlag, Jahr:
2003
Enthalten in:
Biological Chemistry, 384/1(2003-01-27), 161-167
Format:
Artikel (online)
ID: 378849530
LEADER caa a22 4500
001 378849530
003 CHVBK
005 20180305123320.0
007 cr unu---uuuuu
008 161128e20030127xx s 000 0 eng
024 7 0 |a 10.1515/BC.2003.017  |2 doi 
035 |a (NATIONALLICENCE)gruyter-10.1515/BC.2003.017 
245 0 0 |a Heat Shock Treatment Decreases E2F1-DNA Binding and E2F1 Levels in Human A549 Cells  |h [Elektronische Daten]  |c [D. Gerullis, L. Rensing, D. Beyersmann] 
520 3 |a The transcription factor E2F1 plays a decisive role in the G1/S and G2/M checkpoint transitions of proliferating cells. Because cells are arrested at these checkpoints after heat shock it was of interest to test heat shock effects on E2F1 activity. In human A549 cells, heat shock (44C, 30 min) caused an immediate reduction of E2F1-DNA binding as determined by electrophoretic mobility shift assay (EMSA). The complex of E2F1-DNA with the retinoblastoma protein (pRB) was also reduced after heat shock. This indicates that the former effect is not caused by a lower phosphory lation and therefore a higher binding capacity of pRB. Western blot analyses showed that the lower E2F1- DNA binding is probably due to a decrease of the E2F1 level (40% of the controls) induced by heat shock. This result was confirmed by an experiment with HeLa cells in which heat shock decreased the level to 60% of the controls. In order to test whether this decrease resulted from inhibition of transcription, RT-PCR measurements were conducted and showed only a slight reduction of the E2F1mRNA (89% of controls). This indicates that the heat shock effect is not predominantly caused by transcriptional inhibition. Six hours after heat shock the E2F1-DNA binding capacity recovered to control levels. These results provide evidence for E2F1 involvement in heat shockinduced cell cycle arrests at the G1/S and G2/M checkpoints, which also may be relevant for hyperthermic cancer therapy. 
540 |a Copyright © 2003 by Walter de Gruyter GmbH & Co. KG 
690 7 |a Biochemistry  |2 nationallicence 
690 7 |a Molecular biology  |2 nationallicence 
690 7 |a Cellular biology  |2 nationallicence 
700 1 |a Gerullis  |D D.  |4 aut 
700 1 |a Rensing  |D L.  |4 aut 
700 1 |a Beyersmann  |D D.  |4 aut 
773 0 |t Biological Chemistry  |d Walter de Gruyter  |g 384/1(2003-01-27), 161-167  |x 1431-6730  |q 384:1<161  |1 2003  |2 384  |o bchm 
856 4 0 |u https://doi.org/10.1515/BC.2003.017  |q text/html  |z Onlinezugriff via DOI 
908 |D 1  |a research article  |2 jats 
950 |B NATIONALLICENCE  |P 856  |E 40  |u https://doi.org/10.1515/BC.2003.017  |q text/html  |z Onlinezugriff via DOI 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Gerullis  |D D.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Rensing  |D L.  |4 aut 
950 |B NATIONALLICENCE  |P 700  |E 1-  |a Beyersmann  |D D.  |4 aut 
950 |B NATIONALLICENCE  |P 773  |E 0-  |t Biological Chemistry  |d Walter de Gruyter  |g 384/1(2003-01-27), 161-167  |x 1431-6730  |q 384:1<161  |1 2003  |2 384  |o bchm 
900 7 |b CC0  |u http://creativecommons.org/publicdomain/zero/1.0  |2 nationallicence 
898 |a BK010053  |b XK010053  |c XK010000 
949 |B NATIONALLICENCE  |F NATIONALLICENCE  |b NL-gruyter