Dysfunction and overexpression of ENaC-mediated sodium influx exacerbates activation of NLRP3-inflammasome mediated inflammation in cells with CF-associated mutations and is modulated by inhibition of these amiloride-sensitive sodium (Na+) channels.
In potassium-dependent NTPases, insertion of the activating potassium ion into the active site leads to rotation of the gamma-phosphate yielding a near-eclipsed, catalytically productive conformation of the triphosphate chain.
Sodium ions control the rates of both substrate binding and dissociation of an archaeal homologue of glutamate transporters in a manner that minimizes binding intermediates and maximizes transport efficiency.
Transient Ca elevations of cytoplasmic calcium in cardiac myocytes profoundly activate cardiac Na/K pump activity in parallel with physical-chemical changes of the sarcolemma but without involvement of conventional signaling mechanisms.
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