Transcription factors

In a narrower sense, transcription factors are defined as proteins that influence the rate of transcription initiation (rate of mRNA production). Transcription factors are involved in the regulation of elongation and termination. They can bind to the DNA and activate or repress the promoter on the basis of specific binding domains (see domain below, see transactivation domain below). Some transcription factors do not bind directly to DNA, but to other DNA-binding proteins.

A distinction is made between general (basal) and tissue- or cell-specific transcription factors. Furthermore, there are transcription factors that facilitate the transcription of the gene (activators), but also those that prevent transcription (repressors).

General transcription factors are necessary for all transcription, they perform various tasks and bind either directly to DNA or to other DNA-binding proteins. They are ubiquitous, i.e. present equally in all cells of an organism. Transcription factors always occur as complexes with other proteins. By binding to the DNA, they provide a kind of "forum" for the RNA polymerase. The polymerase binds to this and transcription is initiated. Specific transcription factors tell the polymerase which gene to activate. The DNA regions to which they bind have a specific sequence (so-called cis-elements such as enhancers or silencers) that are recognized and bound by the transcription factor. The first step of transcription is initiation. Here, a DNA-dependent RNA polymerase creates an RNA whose nucleotide sequence is prescribed by the DNA. Specific transcription factors are usually activated by protein kinases (see MAP kinases below).

Examples of specific transcription factors:

• NF-kappaB (transcription factor of the Rel family)
• p53 (see below tumor suppressor genes)
• Fox proteins (see below forkhead box genes)
• GATA3 (master transcription factor of Th2 cells)

Various studies have shown that UV rays induce a transcription factor (AP-1) and can thus activate cell proliferation.

1. Berking C (2007) Photocarcinogenesis. dermatologist 58: 398-405