A genetic program that responds to ionizing radiation.
Abstract
The transcriptional response to ionizing radiation as assessed by measurement of total transcription in human cells is described here. IR exposure activated DNA damage molecules DDB2, DDIT2 and damage repair enzymes XPC and REV3L. In contrast, the stem loop binding protein and TOPBP1 interacting checkpoint and replication regulator TICRR were silenced demonstrating both importance of topoisomerase and SLBP in mediating transcriptional response to DNA damage. IR exposure in human cells resulted in halt in proliferation in conjunction with similar block in cycling indicated by MKI67 silencing and reduction in spindle regulators ESPL1, with concomitant activation of proliferation regulator BTG2. Ionizing radiation exposure was sufficient to induce nutrient sensor activation though TSC22D1. Ionizing radiation induced synthesis of ubiquitin C (UBC) and activated expression of the MHC receptor MR1. Cell death program was actively engaged by ionizing radiation indicated by activation of PDCD4 and BAX.
Fields of Study & Subjects
DNA Repair Mechanisms
Effects of Radiation Exposure
Cancer-related Molecular Pathways
Publication details
- Journal / source
- Zenodo (CERN European Organization for Nuclear Research)
- Publication date
- 15 January 2026
- Document type
- Preprint