uracil

The lactam structure is the most common form of uracil.

In the gas phase, uracil has 4 sites that are more acidic than water.

The first site of ionization of uracil is not known.

The reactivity of uracil is unchanged even if the temperature changes.

The uracil causes higher amounts of 5-FU to stay inside the cells and kill them.

Following the stem-loop structure is a chain of uracil residues.

Chemically it is a derivative of nitrogen mustard and uracil.

These two bases are identical except that uracil lacks the 5' methyl group.

The bonds between uracil and adenine are very weak.

However, it is unstable, and can change into uracil (spontaneous deamination).

RNA also contains the base uracil in place of thymine.

The scientific goal in this case was to synthesize a drug which demonstrated specific uracil antagonism.

There are many laboratory syntheses of uracil available.

When elemental fluorine is reacted with uracil, 5-fluorouracil is produced.

Dihydrouracil is an intermediate in the catabolism of uracil.

As the name suggests, thymine may be derived by methylation of uracil at the 5th carbon.

Chemically, uracil is similar to thymine, differing only by a methyl group, and its production requires less energy.

The anticancer drug 5-fluorouracil can be produced by reacting xenon difluoride with uracil.

In similar manner, deamination of cytosine results in uracil.

If uracil is attached to a deoxyribose ring, it is known as a deoxyuridine.

Now accessible to the active site, the nucleotide interacts with the uracil binding motif.

Degradation of uracil produces the substrates aspartate, carbon dioxide, and ammonia.

Lindahl was the first to observe repair of uracil in DNA.

Family 2 excise uracil from mismatches with guanine.

It catalyzes the reduction of uracil and thymine.