Simplified representation of the DNA-damage-induced checkpoint response. Ionizing radiation induces DNA breaks. After the detection of a given damage by sensor proteins, this signal is transduced to the effector protein CHK2 via the transducer protein ATM. This ATM activation induces γ-H2AX formation, used as a biomarker for DNA breaks. Depending on the phase of the cell cycle the cell is in, this can lead to activation of p53 and inactivation of CDC25, which eventually leads to cell cycle arrest. Mediator proteins mostly are cell cycle specific and associate with damage sensors, signal transducers, or effectors at particular phases of the cell cycle and, thus, help provide signal transduction specificity. The effect of UV light is via the transducer protein ATR and the effector protein CHK1. MRE11 meiotic recombination 11, NBS1 Nijmegen breakage syndrome 1, ATM ataxia telangiectasia mutated, ATR ataxia telangiectasia related, γ-H2AX phosphorylated form of Histone variant 2AX, MDC1 mediator of DNA damage checkpoint 1, 63BP p63 binding protein, BRCA1 breast cancer 1, TopBP1 topoisomerase binding protein 1, CHK1 check 1, CHK2 check 2, CDC25 cell division cycle 25, G1 gap 1, S synthesis, G2 gap 2, M mitosis
Kiang, J.G., Olabisi, A.O.
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Kiang, J.G., Olabisi, A.O. Radiation: a poly-traumatic hit leading to multi-organ injury. Cell Biosci 9, 25 (2019). <a rel="nofollow" class="external free" href="https://doi.org/10.1186/s13578-019-0286-y">https://doi.org/10.1186/s13578-019-0286-y</a>