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transcription factor AP-2 alpha

L TFAP2A gene provides instructions for making a protein called transcription factor AP-2 alpha (AP-2α). As its name suggests, this protein is a transcription factor, which means it attaches (binds) to specific regions of DNA and helps control the activity of particular genes. Transcription factor AP-2α is one of a group of related proteins called AP-2 transcription factors. These proteins regulate genes that help control cell division and the self-destruction (apoptosis) of cells that are no longer needed.

Normal function

L TFAP2A gene provides instructions for making a protein called transcription factor AP-2 alpha (AP-2α). As its name suggests, this protein is a transcription factor, which means it attaches (binds) to specific regions of DNA and helps control the activity of particular genes. Transcription factor AP-2α is one of a group of related proteins called AP-2 transcription factors. These proteins regulate genes that help control cell division and the self-destruction (apoptosis) of cells that are no longer needed.

Transcription factor AP-2α is involved in development before birth. In particular, this protein is active in the neural crest, which is a group of cells in the early embryo that give rise to many tissues and organs. Among the embryonic structures formed from neural crest cells are the branchial arches, which develop into the bones and other tissues of the head and neck. The TFAP2A gene appears to be especially important for the development of tissues derived from the first and second branchial arches.

Conditions referring to this gene or chromosome

Altri nomi

activating enhancer-binding protein 2-alpha

activator protein 2

AP-2

AP-2 transcription factor

AP-2alpha

AP2-alpha

AP2A_HUMAN

AP2TF

BOFS

TFAP2

transcription factor AP-2 alpha (activating enhancer binding protein 2 alpha)

transcription factor AP-2-alpha

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Storia dell'articolo

Le informazioni su questa pagina sono scritte e revisionate da clinici qualificati.
  • 29 Set 2025 | Ultima versione
  • 1 Sept 2012 | Pubblicato originariamente

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