Activation of the Estrogen Receptor Through Phosphorylation by Mitogen-Activated Protein Kinase

✍ Scribed by Kato, S.; Endoh, H.; Masuhiro, Y.; Kitamoto, T.; Uchiyama, S.; Sasaki, H.; Masushige, S.; Gotoh, Y.; Nishida, E.; Kawashima, H.; Metzger, D.; Chambon, P.

• Book ID: 121155472
• Publisher: American Association for the Advancement of Science
• Year: 1995
• Tongue: English
• Weight: 755 KB
• Volume: 270
• Category: Article
• ISSN: 0036-8075
• DOI: 10.1126/science.270.5241.1491

✦ Synopsis

dine dirners must be replicated so that they may generate the ss DNA to activate recA 112). \ ,

We suggest that other eukaryotic checkpoint control proteins may also participate in DNA damage processing. For example, S-phase checkpoint control may require different proteins to process the type of DNA damage that is induced after DNA replication is inhibited. POLE is required for S but not for G2 checkpoint control (7); perhaps this is because POLE is specifically required for ~rocessine after DNA re~lication is disturbed. Differences in processing may explain the perplexing patterns of checkpoint gene requirements among species. For example, rod1 + and RAD17 in fission and budding veasts encode nutative 3'-5' exo--, nucleases and both are required for the GZ checkpoint in their respective cell types (Fig. 4). However, radl + , yet not R'4D17, is also required at the S-phase checkpoint (1 3). Similarly, cdc2+ and CDC28 in fission and budding yeasts encode conserved protein kinases. cdc2+, yet not CDC28, is needed for S-phase checkpoint control (1 4). Perhaps radl + and cdc2+ in fission yeast are required for DNA damage processing after S-phase inhibition, but their holnologs In budding yeast are not.