Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 17 (8), 321-7

Nuclear Receptors Versus Inflammation: Mechanisms of Transrepression


Nuclear Receptors Versus Inflammation: Mechanisms of Transrepression

Gabriel Pascual et al. Trends Endocrinol Metab.


Inflammation is a beneficial host response to external challenge or cellular injury that leads to the activation of a complex array of inflammatory mediators, finalizing the restoration of tissue structure and function. Although a beneficial response, prolonged inflammation can be detrimental to the host, contributing to the pathogenesis of many disease states. Considerable attention has been focused on the ability of several members of the nuclear receptor superfamily to inhibit transcriptional activation by signal-dependent transcription factors that include nuclear factor kappaB and activator protein 1, thereby, attenuating inflammatory responses to both acute and chronic challenge. An important general mechanism responsible for this activity is referred to as transrepression, in which nuclear receptors interfere with signal-dependent activation of inflammatory response genes through protein-protein interactions with coregulatory proteins and promoter-bound transcription factors, rather than direct, sequence-specific interactions with DNA.

Similar articles

See all similar articles

Cited by 69 PubMed Central articles

See all "Cited by" articles

Publication types

MeSH terms

LinkOut - more resources