deamination

The longer the strands are separated the greater the quantity of deamination.

The implications of deamination on 5-hydroxymethylcytosine, on the other hand, remains less understood.

Phenylacetone is the deamination product of amphetamine in the human body.

Deamination is the removal of an amine group from a molecule.

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

Only transcribed strand benefits from these deamination repair events.

The most common mutation is the deamination of cytosine to uracil.

An analogous process for organic nitrogen compounds is deamination.

Spontaneous deamination of 5-methylcytosine results in thymine and ammonia.

Deamination can be induced in solid or aqueous alanine by radiation.

Lactose non-fermenters may increase the pH by deamination of proteins.

Examples include fatty acids, glycerol, carbohydrates, deamination products, and ethanol.

It is prone to deamination by adenosine deaminase to a hypoxanthine.

Nitrogen is a component of amino acids and is released upon deamination.

Hypoxanthine is also a spontaneous deamination product of adenine.

Transitions can be caused by oxidative deamination and tautomerization.

CD2 is catalytically active and vital for deamination and motif specificity.

Another explanation is that the deamination repair joined to transcription does not occur on coding strand.

In similar manner, deamination of cytosine results in uracil.

They take part in the deamination of amino acids and synthesis of urea.

Nonetheless, the deamination process creates urea, which places low, but consistent, strain on the nephrons.

After all, the oxidative deamination you mentioned does not have much in common with the alkylation of bases via free radical reactions.

Excess amino acids are converted to other usable molecules by the liver in a process called deamination.

However, over evolutionary time methylated cytosines tend to turn into thymines because of spontaneous deamination.

There is no deamination step.