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Other DNA damaging, cancer-causing agents include asbestos, which can cause damage through physical interaction with DNA or by indirectly setting off a reactive oxygen species, [10] excessive nickel exposure, which can repress the DNA damage-repair pathways, [11] aflatoxins, which are found in food, [9] and many more.
The double-helix model of DNA structure was first published in the journal Nature by James Watson and Francis Crick in 1953, [6] (X,Y,Z coordinates in 1954 [7]) based on the work of Rosalind Franklin and her student Raymond Gosling, who took the crucial X-ray diffraction image of DNA labeled as "Photo 51", [8] [9] and Maurice Wilkins, Alexander Stokes, and Herbert Wilson, [10] and base-pairing ...
A negatively supercoiled DNA molecule will produce either a one-start left-handed helix, the toroid, or a two-start right-handed helix with terminal loops, the plectoneme. Plectonemes are typically more common in nature, and this is the shape most bacterial plasmids will take.
In biochemistry and molecular genetics, an AP site (apurinic/apyrimidinic site), also known as an abasic site, is a location in DNA (also in RNA but much less likely) that has neither a purine nor a pyrimidine base, either spontaneously or due to DNA damage. It has been estimated that under physiological conditions 10,000 apurinic sites and 500 ...
The helix-turn-helix motif is a DNA-binding motif. The recognition and binding to DNA by helix-turn-helix proteins is done by the two α helices, one occupying the N-terminal end of the motif, the other at the C-terminus. In most cases, such as in the Cro repressor, the second helix contributes most to DNA recognition, and hence it is often ...
This build-up creates a torsional load that would eventually stop the replication fork. Topoisomerases are enzymes that temporarily break the strands of DNA, relieving the tension caused by unwinding the two strands of the DNA helix; topoisomerases (including DNA gyrase) achieve this by adding negative supercoils to the DNA helix. [42]
A DNA unwinding element (DUE or DNAUE) is the initiation site for the opening of the double helix structure of the DNA at the origin of replication for DNA synthesis. [1] It is A-T rich and denatures easily due to its low helical stability, [ 2 ] which allows the single-strand region to be recognized by origin recognition complex .
Uracil DNA glycosylase flips a uracil residue out of the duplex, shown in yellow. DNA glycosylases are responsible for initial recognition of the lesion. They flip the damaged base out of the double helix, as pictured, and cleave the N-glycosidic bond of the damaged base, leaving an AP site. There are two categories of glycosylases ...