MAL is a transcriptional coactivator for serum response factor (SRF), a transcription factor that activates the mitogen-responsive genes.
Background & Aims: SRF (Serum Response Factor), a widely expressed transcription factor, controls expression of mitogen-responsive and muscle-specific genes, thereby regulating the contractile actin microfilament.
The rapid responsiveness of these genes to growth factor stimulation is due to serum response elements (SREs) in the promoters of these genes [15].
This event involves the formation of a ternary complex, induced by the cooperative binding of TCFs with serum response factor (SRF) dimers [6] on serum response elements found in IEG promoters [7 9].
The c-fos promoter contains a serum response element (SRE) that mediates ternary complex formation with the Ets proteins SAP-1 or Elk-1 and the MADS-box protein, serum response factor (SRF).
A similar bias in domain specificity was also demonstrated in the serum response of AVA-vaccinated donors.
A transient increase in G-actin content, in turn, may initiate some signaling pathways (for instance, some serum response factor (SRF -dependent pathwaySRF -dependent
Formin homology 2 domain containing protein (FHOD1), a mammalian formin, regulates cytoskeletal architecture, enhances cell migration, and induces gene expression from the serum response element.
On the other hand, miR-133 enhances myoblast proliferation by repressing the serum response factor [59].
Similarly, a positive autoregulation was demonstrated for serum response factor (SRF) in muscle gene expression [6].
