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Merck
CN
  • FancJ regulates interstrand crosslinker induced centrosome amplification through the activation of polo-like kinase 1.

FancJ regulates interstrand crosslinker induced centrosome amplification through the activation of polo-like kinase 1.

Biology open (2013-10-30)
Jianqiu Zou, Fen Tian, Ji Li, Wyatt Pickner, Molly Long, Khosrow Rezvani, Hongmin Wang, Dong Zhang
摘要

DNA damage response (DDR) and the centrosome cycle are two of the most critical processes for maintaining a stable genome in animals. Sporadic evidence suggests a connection between these two processes. Here, we report our findings that six Fanconi Anemia (FA) proteins, including FancI and FancJ, localize to the centrosome. Intriguingly, we found that the localization of FancJ to the mother centrosome is stimulated by a DNA interstrand crosslinker, Mitomycin C (MMC). We further show that, in addition to its role in interstrand crosslinking (ICL) repair, FancJ also regulates the normal centrosome cycle as well as ICL induced centrosome amplification by activating the polo-like kinase 1 (PLK1). We have uncovered a novel function of FancJ in centrosome biogenesis and established centrosome amplification as an integral part of the ICL response.

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Sigma-Aldrich
单克隆抗-FLAG® M2 小鼠抗, clone M2, purified immunoglobulin (Purified IgG1 subclass), buffered aqueous solution (10 mM sodium phosphate, 150 mM NaCl, pH 7.4, containing 0.02% sodium azide)
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羟基脲, 98%, powder
Sigma-Aldrich
抗-PLK1抗体,克隆35-206, clone 35-206, Upstate®, from mouse
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抗-γ-微管蛋白 (DQ-19) 兔抗, IgG fraction of antiserum, buffered aqueous solution