Overexpression of the immediate early response 5 gene increases the radiosensitivity of HeLa cells.

The effects of the immediate early response 5 () gene on the sensitivity of HeLa cells to radiation remain unclear. In the present study, stably transfected HeLa cells resulting in the knockdown or overexpression of were investigated. In addition, xenografts of normal, -silenced and -overexpressed HeLa cells were injected into nude mice and examined.

IER5 is involved in DNA Double-Strand Breaks Repair in Association with PAPR1 in Hela Cells.

The immediate early response gene 5 (5) is a radiation response gene induced in a dose-independent manner, and has been suggested to be a molecular biomarker for biodosimetry purposes upon radiation exposure. Here, we investigated the function of IER5 in DNA damage response and repair. We found that interference on IER5 expression significantly decreased the efficiency of repair of DNA double-strand breaks induced by ionizing radiations in Hela cells.

Radiation-induced expression of is dose-dependent and not associated with the clinical outcomes of radiotherapy in cervical cancer.

This study aimed to investigate the expression of the immediate-early response 5 (IER5) gene in cervical cancer tissues and explore the association between the expression of IER5 and the clinical outcomes of radiotherapy. We collected specimens by surgery or biopsy and obtained 53 specimens from tissues after radiotherapy and 16 specimens from tissues before radiotherapy. Immunohistochemistry and western blotting were used to assess the protein expression levels of IER5.

Induced expression of the IER5 gene by gamma-ray irradiation and its involvement in cell cycle checkpoint control and survival.

The immediate-early response gene 5 (IER5) was previously shown, using microarray analysis, to be upregulated by ionizing radiation. Here we further characterized the dose- and time-dependency of radiation-induced expression of IER5 at doses from 0.5 to 15 Gy by quantitative real-time PCR analyses in HeLa cells and human lymphoblastoid AHH-1 cells.