LPSs are widely used to stimulate @entity2939 , but their effects on ion channels in immune cells are poorly known. In THP-1 cells and @entity1 blood monocytes treated with @entity558 , inwardly rectifying @entity3529 channel current (IKir, @entity558 ) newly emerged at 1 h, peaked at 4 h (-119    8.6 pA/pF), and decayed afterward (-32    6.7 pA/pF at 24 h). Whereas both the @entity12397 and @entity19378 mRNAs and proteins were observed, single-channel conductance (38 pS) of IKir, @entity558 and small interfering RNA-induced knockdown commonly indicated @entity19378 than @entity12397 . @entity558 -induced cytokine release and store-operated @entity141 entry were commonly decreased by @entity68248 , a Kir2 inhibitor. Immunoblot, confocal microscopy, and the effects of vesicular trafficking inhibitors commonly suggested plasma membrane translocation of @entity19378 by @entity558 . Both IKir, @entity558 and membrane translocation of @entity19378 were inhibited by @entity11009 ( @entity7131 [ @entity7131 ] inhibitor) or by transfection with small interfering RNA-specific @entity7131  . Interestingly, pharmacological activation of @entity7131 by @entity4515 induced both @entity12397 and @entity19378 currents. The spontaneously decayed IKir, @entity558 at 24 h was recovered by PI3K inhibitors but further suppressed by an inhibitor of @entity19065 (PIP3) phosphatase (phosphatase and tensin homolog). However, IKir, @entity558 at 24 h was not affected by Akt inhibitors, suggesting that the decreased @entity1078 availability, that is, conversion into PIP3 by PI3K, per se accounts for the decay of IKir, @entity558 . Taken together, to our knowledge these data are the first demonstrations that IKir is newly induced by @entity2939 stimulation via @entity7131 -dependent membrane trafficking of @entity19378 , and that conversion of @entity1078 to PIP3 modulates @entity19378 . The augmentation of @entity141 influx and cytokine release suggests a physiological role for @entity19378 in @entity2939 -stimulated monocytes.

Rise and Fall of @entity19378 Current by @entity2939 Signaling in @entity1 Monocytes: XXXX -Dependent Trafficking and PI3K-Mediated PIP2 Decrease.

@entity1 :: ('9606', 'Species') :: ['human'] @entity19065 :: ('MESH:C060974', 'Chemical') :: ['phosphatidylinositol(3,4,5)-trisphosphate'] @entity558 :: ('MESH:C536528', 'Disease') :: ['LPS'] @entity3529 :: ('D011188', 'Chemical') :: ['K(+)'] @entity1078 :: ('CHEBI:18348', 'Chemical') :: ['phosphatidylinositol(4,5)-bisphosphate'] @entity12397 :: ('3759', 'Gene') :: ['Kir2.1'] @entity4515 :: ('CHEBI:60755', 'Chemical') :: ['PMA'] @entity7131 :: ('MESH:D020151', 'Disease') :: ['protein kinase C', 'PKC'] @entity19378 :: ('3768', 'Gene') :: ['Kir2.2'] @entity11009 :: ('MESH:C070515', 'Chemical') :: ['GF109203X'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca(2+)'] @entity2939 :: ('7099', 'Gene') :: ['TLR4'] @entity68248 :: ('MESH:C546026', 'Chemical') :: ['ML-133']
@entity7131 :: (MESH:D020151,Disease) :: ['PKC']
