| RRC ID |
41638
|
| 著者 |
Watanabe H, Yu D, Sasaki T, Shibuya H, Hosoi Y, Asada M, Komatsu K, Miura M.
|
| タイトル |
Insulin-like growth factor I receptor is expressed at normal levels in Nijmegen breakage syndrome cells.
|
| ジャーナル |
Biochem Biophys Res Commun
|
| Abstract |
Nijmegen breakage syndrome (NBS) is an autosomal recessive disorder sharing a pleiotropic phenotype with ataxia-telangiectasia (A-T), including increased radiosensitivity and cancer disposition. Insulin-like growth factor I receptor (IGF-IR) expression is reportedly decreased in A-T cells, which is thought to contribute to its increased radiosensitivity. In this study, we investigated whether the same mechanism underlies the radiosensitivity of NBS cells. GM7166VA7 cells lacking NBS1 protein displayed a phenotype of increased radiosensitivity, while the introduction of NBS1 cDNA conferred radioresistance comparable to normal cells. IGF-IR expression levels were essentially the same among normal, NBS, and NBS1-complemented NBS cells. There was no significant difference between NBS and NBS1-complemented cells in activation of major downstream pathways of IGF-IR upon IGF-I stimulation, including phosphatidylinositol-3(') kinase (PI3-K) and mitogen-activated protein kinase (MAPK). Collectively, IGF-IR-related events are unlikely to be disrupted in NBS cells, and therefore, defects in IGF-IR signaling do not explain the increased radiosensitivity of NBS cells.
|
| 巻・号 |
296(1)
|
| ページ |
62-6
|
| 公開日 |
2002-8-9
|
| DOI |
10.1016/s0006-291x(02)00817-3
|
| PII |
S0006291X02008173
|
| PMID |
12147227
|
| MeSH |
Cell Line, Transformed
Chromosome Breakage*
Humans
Insulin-Like Growth Factor I / metabolism
MAP Kinase Signaling System
Protein Binding
Radiation Tolerance / genetics
Receptor, IGF Type 1 / metabolism*
Signal Transduction
Syndrome
|
| IF |
2.985
|
| 引用数 |
2
|
|
WOS 分野
|
BIOPHYSICS
BIOCHEMISTRY & MOLECULAR BIOLOGY
|
| リソース情報 |
| ヒト・動物細胞 |
|
