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The helical binding interaction at the n-terminus of DDB2 allows for the protein to bind immediately after detecting UV damaged DNA. [3] DNA binds to DDB2 only when damaged by UV radiation. Binding with high affinity to a helical domain of DDB2 in the dimer form, UV-DDB, is facilitated by the n-terminal alpha helical paddle and beta wings of ...
UV light, specifically non-ionizing shorter-wavelength radiation such as UVC and UVB, causes direct DNA damage by initiating a synthesis reaction between two thymine molecules. The resulting dimer is very stable. Although they can be removed through excision repairs, when UV damage is extensive, the entire DNA molecule breaks down and the cell ...
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 ...
This process of absorption works to reduce the risk of DNA damage and the formation of pyrimidine dimers. UVA light makes up 95% of the UV light that reaches earth, whereas UVB light makes up only about 5%. UVB light is the form of UV light that is responsible for tanning and burning. Sunscreens work to protect from both UVA and UVB rays.
DNA damage inhibits M-CDKs which are a key component of progression into mitosis. In all eukaryotic cells, ATR and ATM are protein kinases that detect DNA damage. They bind to DNA damaged sites and activate Chk1, Chk2, and, in animal cells, p53. Together, these proteins make up the DNA damage response system.
A UV radiation induced thymine-thymine cyclobutane dimer (right) is the type of DNA damage which is repaired by DNA photolyase. Note: The above diagram is incorrectly labelled as thymine as the structures lack 5-methyl groups.
The methodology involves covalently linking a DNA-binding motif of the target sequence-specific DNA-binding protein with a photoactivatable crosslinking agent capable of reacting with DNA nucleotides when exposed to UV. This method provides information on the interaction between the DNA and protein in the crosslink. [27]
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 ...