1. @entity141 - @entity70145 -dependent protein kinase II (CaMK) and a @entity70145 ( @entity70145 )-binding 'IQ' domain (IQ) are both implicated in @entity141 -dependent regulation of L-type @entity141 current (I( @entity9495 )). We used an IQ-mimetic peptide (IQmp), under conditions in which CaMK activity was controlled, to test the relationship between these @entity70145 -activated signalling elements in the regulation of L-type @entity141 channels (LTCCs) and I( @entity9495 ) in @entity95 ventricular myocytes. 2. A specific CaMK inhibitory peptide nearly abolished I( @entity9495 ) facilitation, but the facilitation was 'rescued' by cell dialysis with IQmp. 3. IQmp significantly enhanced I( @entity9495 ) facilitation and slowed the fast component of I( @entity9495 ) inactivation, compared with an inactive control peptide. Neither effect could be elicited by a more avid @entity70145 -binding peptide, suggesting that generalized @entity70145 buffering did not account for the effects of IQmp. 4. I( @entity9495 ) facilitation was abolished and the fast component of inactivation eliminated by @entity8452 , @entity5834 or @entity2426 , suggesting that the sarcoplasmic reticulum (SR) is an important source of @entity141 for I( @entity9495 ) facilitation and inactivation. IQmp did not restore I( @entity9495 ) facilitation under these conditions. 5. Engineered @entity141 -independent CaMK and IQmp each markedly increased LTCC open probability (P(o)) in excised cell membrane patches. The LTCC P(o) increases with CaMK and IQmp were non-additive, suggesting that CaMK and IQmp are components of a shared signalling pathway. 6. Both CaMK and IQmp induced a modal gating shift in LTCCs that favoured prolonged openings, indicating that CaMK and IQmp affect LTCCs through a common biophysical mechanism. 7. These findings support the hypothesis that CaMK is required for physiological I( @entity9495 ) facilitation in cardiac myocytes. Both CaMK and IQmp were able to induce a modal gating shift in LTCCs, suggesting that each of these signalling elements is important for @entity141 - @entity70145 -dependent LTCC facilitation in cardiac myocytes.

@entity70145 kinase and a @entity70145 -binding 'IQ' domain facilitate L-type @entity141 current in XXXX ventricular myocytes by a common mechanism.

@entity70145 :: ('100352392(Tax:9986)', 'Gene') :: ['calmodulin', 'CaM'] @entity2426 :: ('MESH:D019284', 'Chemical') :: ['thapsigargin'] @entity8452 :: ('MESH:D012433', 'Chemical') :: ['ryanodine'] @entity95 :: ('9986', 'Species') :: ['rabbit'] @entity5834 :: ('MESH:D002110', 'Chemical') :: ['caffeine'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca2+'] @entity9495 :: ('D002118', 'Chemical') :: ['Ca']
@entity95 :: (9986,Species) :: ['rabbit']
