To determine how DNA damage regulates CBM complex, we co-expressed CARMA3 together with K48- and K63-linked ubiquitin, and found that DNA damage significantly induced K63-linked polyubiquitination (Fig. 1E).
We will also discuss how DNA damage regulates transcription, alters the chromatin environment and affects the mobility of chromosomes to promote the DDR, and how genome organization impacts DNA repair and chromosome translocations.
HIPK2 interacts physically and functionally with p53 and specifically phosphorylates p53 at serine 46 (Ser46) in response to severe DNA damage, regulating p53-induced apoptosis [11], [12].
Recent data show that JMY, a transcriptional co-factor that regulates the p53 response, represents a new class of multifunctional actin assembly factor [29], and that LIMK2, a p53-target gene upregulated by DNA damage, regulates actin dynamics [30].
BRCA2 recruits recombinase RAD51 to sites of damage, regulates its assembly into nucleoprotein filaments, and thereby promotes homologous recombination.
MiR-1246 takes part in DNA damage, regulates chloride transport and can be used as a circulating biomarker of malignant mammary epithelial cells.
However, it is yet not known as to how the extent of ROS produced during DNA damage regulates ATM function, if any, and the molecular mechanisms underlying this process.
DRAM1 (DNA damage-regulated autophagy modulator 1) is a TP53 target gene that modulates autophagy and apoptosis.
DRAM1 (DNA damage-regulated autophagy modulator 1) is a TP53 target gene coding a lysosomal membrane protein and has an essential role in TP53-mediated autophagy activation and apoptosis.
The induction of dram1 (DNA damage-regulated autophagy modulator 1) during infection suggests an immunological function of this autophagy modulator, and the zebrafish model could be further exploited to investigate therapeutic targeting of selective autophagy pathways (Mostowy et al., 2013; Meijer et al., 2014).
