Carbon dioxide-dependent regulation of NF-κB family members RelB and p100 gives molecular insight into CO₂-dependent immune regulation.

ABSTRACT: CO₂ is a physiological gas normally produced in the body during aerobic respiration. Hypercapnia (elevated blood pCO₂ >≈50 mm Hg) is a feature of several lung pathologies, e.g. chronic obstructive pulmonary disease. Hypercapnia is associated with increased susceptibility to bacterial infections and suppression of inflammatory signaling. The NF-κB pathway has been implicated in these effects; however, the molecular mechanisms underpinning cellular sensitivity of the NF-κB pathway to CO₂ are not fully elucidated. Here, we identify several novel CO₂-dependent changes in the NF-κB pathway. NF-κB family members p100 and RelB translocate to the nucleus in response to CO₂ A cohort of RelB protein-protein interactions (e.g. with

SUBMITTER: Keogh CE 

PROVIDER: S-EPMC5500817 | biostudies-literature | 2017 Jul

REPOSITORIES: biostudies-literature