Abstract
c-Abl plays important roles in cellular response to DNA damage. However, possible roles for Arg (Abl-related gene) in DNA damage response are unknown. Here, we show that ionizing radiation (IR)-induced Rad51 focus formation is reduced in Arg-deficient cells generated from a chicken B cell line by targeted disruption. This is consistent with the findings that Arg-deficient cells display hypersensitivity to IR, elevated frequencies of IR-induced chromosomal aberrations, and reduced targeted integration frequencies. All of these abnormalities in DNA damage repair are also observed in ATM-deficient cells but not in c-Abl-deficient cells. Finally, we show that Arg interacts with and phosphorylates Rad51 in 293T cells. These results suggest that Arg plays a role in homologous recombinational (HR) DNA repair by phosphorylating Rad51.
| Original language | English |
|---|---|
| Pages (from-to) | 697-702 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 299 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - 2002 |
| Externally published | Yes |
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Keywords
- c-Abl family
- Double-strand break
- Homologous recombinational DNA repair
- Rad51 focus
- Tyrosine phosphorylation
ASJC Scopus subject areas
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
Arg tyrosine kinase is involved in homologous recombinational DNA repair. / Li, Yingzhu; Shimizu, Hiroko; Xiang, Shuang Lin; Maru, Yoshiro; Takao, Noriaki; Yamamoto, Ken-ichi.
In: Biochemical and Biophysical Research Communications, Vol. 299, No. 5, 2002, p. 697-702.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Arg tyrosine kinase is involved in homologous recombinational DNA repair
AU - Li, Yingzhu
AU - Shimizu, Hiroko
AU - Xiang, Shuang Lin
AU - Maru, Yoshiro
AU - Takao, Noriaki
AU - Yamamoto, Ken-ichi
PY - 2002
Y1 - 2002
N2 - c-Abl plays important roles in cellular response to DNA damage. However, possible roles for Arg (Abl-related gene) in DNA damage response are unknown. Here, we show that ionizing radiation (IR)-induced Rad51 focus formation is reduced in Arg-deficient cells generated from a chicken B cell line by targeted disruption. This is consistent with the findings that Arg-deficient cells display hypersensitivity to IR, elevated frequencies of IR-induced chromosomal aberrations, and reduced targeted integration frequencies. All of these abnormalities in DNA damage repair are also observed in ATM-deficient cells but not in c-Abl-deficient cells. Finally, we show that Arg interacts with and phosphorylates Rad51 in 293T cells. These results suggest that Arg plays a role in homologous recombinational (HR) DNA repair by phosphorylating Rad51.
AB - c-Abl plays important roles in cellular response to DNA damage. However, possible roles for Arg (Abl-related gene) in DNA damage response are unknown. Here, we show that ionizing radiation (IR)-induced Rad51 focus formation is reduced in Arg-deficient cells generated from a chicken B cell line by targeted disruption. This is consistent with the findings that Arg-deficient cells display hypersensitivity to IR, elevated frequencies of IR-induced chromosomal aberrations, and reduced targeted integration frequencies. All of these abnormalities in DNA damage repair are also observed in ATM-deficient cells but not in c-Abl-deficient cells. Finally, we show that Arg interacts with and phosphorylates Rad51 in 293T cells. These results suggest that Arg plays a role in homologous recombinational (HR) DNA repair by phosphorylating Rad51.
KW - c-Abl family
KW - Double-strand break
KW - Homologous recombinational DNA repair
KW - Rad51 focus
KW - Tyrosine phosphorylation
UR - http://www.scopus.com/inward/record.url?scp=0036921395&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036921395&partnerID=8YFLogxK
U2 - 10.1016/S0006-291X(02)02692-X
DO - 10.1016/S0006-291X(02)02692-X
M3 - Article
C2 - 12470634
AN - SCOPUS:0036921395
VL - 299
SP - 697
EP - 702
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 5
ER -