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DNA damage-inducible transcript 3, also known as C/EBP homologous protein (CHOP), is a pro-apoptotic transcription factor that is encoded by the DDIT3 gene. [ 5 ] [ 6 ] It is a member of the CCAAT/enhancer-binding protein (C/EBP) family of DNA-binding transcription factors. [ 6 ]
The SOS response is a global response to DNA damage in which the cell cycle is arrested and DNA repair and mutagenesis are induced. The system involves the RecA protein (Rad51 in eukaryotes). The RecA protein, stimulated by single-stranded DNA, is involved in the inactivation of the repressor of SOS response genes thereby inducing the response ...
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...
After DNA damage, cell cycle checkpoints are activated. Checkpoint activation pauses the cell cycle and gives the cell time to repair the damage before continuing to divide. DNA damage checkpoints occur at the G1/S and G2/M boundaries. An intra-S checkpoint also exists. Checkpoint activation is controlled by two master kinases, ATM and ATR.
Steps of the cell cycle. The G 2-M checkpoint occurs between the G 2 and M phases. G2-M arrest. The G 2-M DNA damage checkpoint is an important cell cycle checkpoint in eukaryotic organisms that ensures that cells don't initiate mitosis until damaged or incompletely replicated DNA is sufficiently repaired.
A–T has been described as a genome instability syndrome, a DNA repair disorder and a DNA damage response (DDR) syndrome. ATM , the gene responsible for this multi-system disorder, encodes a protein of the same name which coordinates the cellular response to DNA double strand breaks (DSBs). [ 27 ]
FUS/TLS was initially identified as a fusion protein (FUS-CHOP) produced as a result of chromosomal translocations in human cancers, especially liposarcomas. [6] [9] In these instances, the promoter and N-terminal part of FUS/TLS is translocated to the C-terminal domain of various DNA-binding transcription factors (e.g. CHOP) conferring a strong transcriptional activation domain onto the ...
These reactive chemical species can reach DNA by diffusion and the bimolecular reaction damages the DNA (oxidative stress). Unlike direct DNA damage which causes sunburn, indirect DNA damage does not result in any warning signal or pain in the human body. The bimolecular reactions that cause the indirect DNA damage are illustrated in the figure: