Search results
Results from the WOW.Com Content Network
DNA gyrase, or simply gyrase, is an enzyme within the class of topoisomerase and is a subclass of Type II topoisomerases [1] that reduces topological strain in an ATP dependent manner while double-stranded DNA is being unwound by elongating RNA-polymerase [2] or by helicase in front of the progressing replication fork.
It was found that these "ghosts" could adsorb to bacteria that were susceptible to T2, although they contained no DNA and were simply the remains of the original viral capsule. They concluded that the protein protected the DNA from DNase, but that once the two were separated and the phage was inactivated, the DNase could hydrolyze the phage DNA.
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 ...
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 ...
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] Bare single-stranded DNA tends to fold back on itself forming secondary structures; these ...
Z-DNA is one of the many possible double helical structures of DNA. It is a left-handed double helical structure in which the helix winds to the left in a zigzag pattern, instead of to the right, like the more common B-DNA form. Z-DNA is thought to be one of three biologically active double-helical structures along with A-DNA and B-DNA.
XP is caused by a homozygous deficiency in UV DNA damage repair (GG-NER) which increases the patients' risk of skin cancer by 1000-fold. In heterozygous patients, the risk of cancer is sporadic but can be predicted based on analytical assessment of polymorphisms in XP related DNA repair genes purified from lymphocytes . [ 15 ]
The first column depicts mismatch repair in eukaryotes, while the second depicts repair in most bacteria. The third column shows mismatch repair, to be specific in E. coli. Micrograph showing loss of staining for MLH1 in colorectal adenocarcinoma in keeping with DNA mismatch repair (left of image) and benign colorectal mucosa (right of image).