Mouse Cdc21 only 0.5 kb upstream from Dna-pk cs in a head-to-head organization: an implication of co-evolution of ATM family members and cell cycle regulating genes

Mouse Cdc21 only 0.5 kb upstream from Dna-pk cs in a head-to-head organization: an implication... Short Communications Incorporating Mouse Genome Mammalian Genome 9, 769–772 (1998). © Springer-Verlag New York Inc. 1998 Mouse Cdc21 only 0.5 kb upstream from Dna-pk in a head-to-head cs organization: an implication of co-evolution of ATM family members and cell cycle regulating genes 1 2 1 1 1 1 Toshiyuki Saito, Yoichi Matsuda, Hideshi Ishii, Fumiaki Watanabe, Masahiko Mori, Akiko Hayashi, 1 1 1 1 1 1 Ryoko Araki, Akira Fujimori, Ryutaro Fukumura, Mitsuoki Morimyo, Koichi Tatsumi, Tada-aki Hori, Masumi Abe National Institute of Radiological Sciences, Inage-ku Anagawa 4-9-1, Chiba 263, Japan School of Agricultural Sciences, Nagoya University, Chikusa, Nagoya 464-01, Japan Received: 20 September 1997 / Accepted: 8 May 1998 The catalytic subunit of the DNA-dependent protein kinase (DNA- PK ) is a member of the ATM family, which in turn is a branch cs of the phosphatidylinositol 3-kinase (PI3K) superfamily (Hartley et al. 1995). The ATM family consists of relatively large proteins, all of which have motifs found in PI3Ks’ catalytic domains at their carboxy-terminal region. Many of the family members have been found to be involved in DNA repair, cell-cycle checkpoint control, and cell-cycle transition control (Zakian 1995). Furthermore, the ATM gene itself was demonstrated to be http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Mouse Cdc21 only 0.5 kb upstream from Dna-pk cs in a head-to-head organization: an implication of co-evolution of ATM family members and cell cycle regulating genes

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Publisher
Springer-Verlag
Copyright
Copyright © 1998 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003359900861
Publisher site
See Article on Publisher Site

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