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adenosine deaminase RNA specific

The ADAR gene provides instructions for making a protein called RNA-specific adenosine deaminase 1 (ADAR1). This protein is involved in making changes to (editing) RNA, a chemical cousin of DNA. Specifically, it attaches (binds) to RNA and changes an RNA building block (nucleotide) called adenosine to another nucleotide called inosine.

Normal function

The ADAR gene provides instructions for making a protein called RNA-specific adenosine deaminase 1 (ADAR1). This protein is involved in making changes to (editing) RNA, a chemical cousin of DNA. Specifically, it attaches (binds) to RNA and changes an RNA building block (nucleotide) called adenosine to another nucleotide called inosine.

The ADAR1 protein is involved in the control of the innate immune response, which is the immune system's early response to foreign invaders (pathogens). The immune system sometimes fails to recognise the body’s own RNA and may act as though it belongs to a pathogen that should be attacked. By changing adenosine to inosine, ADAR1 may prevent the immune system from targeting the body's own tissues.

The ADAR1 protein is also thought to inhibit the replication and spread of certain viruses, such as human immunodeficiency virus (HIV) and hepatitis C, by modifying their RNA. In addition, the ADAR1 protein controls the function of certain chemical messengers called neurotransmitters at particular sites in the body by modifying the RNA blueprint for the receptor proteins that interact with the neurotransmitters. Studies suggest that the ADAR1 protein may have other functions that are not well understood.

Conditions referring to this gene or chromosome

Altri nomi

ADAR1

adenosine deaminase acting on RNA 1-A

DRADA

DSH

DSRAD

dsRNA adenosine deaminase

dsRNA adeonosine deaminase

IFI-4

IFI4

interferon-induced protein 4

interferon-inducible protein 4

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Storia dell'articolo

Le informazioni su questa pagina sono scritte e revisionate da clinici qualificati.
  • 26 Sept 2024 | Ultima versione
  • 1 Sept 2024 | Pubblicato originariamente

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