[9] In addition, subcellular localization of the NR4A1 protein appears to play a key role in the survival and death of cells.

This process is mediated by the NF-κB (nuclear factor-kappa B) complex, a ubiquitous transcription factor involved in cellular response to stress.

These include physiological stimuli such as "fatty acids, stress, prostaglandins, growth factors, calcium, inflammatory cytokines, peptide hormones, phorbol esters, and neurotransmitters" and physical stimuli including "magnetic fields, mechanical agitation (causing fluid shear stress), and membrane depolarization".

Mechanistically, NR4A1 is preferentially recruited to binding sites of the transcription factor AP-1, where it represses effector gene expression by inhibiting AP-1 function.

[17] The binding sites on the response elements for NR4A1, which are common to the two other members of the NR4A family, are:[7] Nuclear receptor 4A1 has the systematic HUGO gene symbol NR4A1.

Nuclear receptor 4A1 has a high degree of structural similarity with other family members at the DNA-binding domain with 91-95% sequence conservation.

They are immediate early genes activated in a ligand-independent manner that bind at the homologous sites on response elements.

[11] NR4A1 has homologous genes in a range of species including neuronal growth factor-induced clone B in rats, Nur77 in mice and TR3 in humans.