Iribe2006_CaMKIIkineticsModel

This a model from the article:
Modulatory effect of calmodulin-dependent kinase II (CaMKII) on sarcoplasmic
reticulum Ca2+ handling and interval-force relations: a modelling study.

Iribe G, Kohl P, Noble D. Philos Transact A Math Phys Eng Sci
2006 May 15;364(1842):1107-33 16608699
,
Abstract:

We hypothesize that slow inactivation of Ca2+/calmodulin-dependent kinase II
(CaMKII) and its modulatory effect on sarcoplasmic reticulum (SR) Ca2+ handling
are important for various interval-force (I-F) relations, in particular for the
beat interval dependency in transient alternans during the decay of
post-extrasystolic potentiation. We have developed a mathematical model of a
single cardiomyocyte to integrate various I-F relations, including alternans, by
incorporating a conceptual CaMKII kinetics model into the SR Ca2+ handling
model. Our model integrates I-F relations, such as the beat interval-dependent
twitch force duration, restitution and potentiation, positive staircase
phenomenon and alternans. We found that CaMKII affects more or less all I-F
relations, and it is a key factor for integration of the various I-F relations
in our model. Alternans arises, in the model, out of a steep relation between SR
Ca2+ load and release, owing to SR load-dependent changes in the releasability
of Ca2+ via the ryanodine receptor. Beat interval-dependent CaMKII activity,
owing to its kinetic properties and amplifying effect on SR Ca2+ load dependency
of Ca2+ release, replicated the beat interval dependency of alternans, as
observed experimentally. Additionally, our model enabled reproduction of the
effects of various interventions on alternans, such as the slowing or
accelerating of Ca2+ release and/or uptake. We conclude that a slow
time-dependent factor, represented in the model by CaMKII, is important for the
integration of I-F relations, including alternans, and that our model offers a
useful tool for further analysis of the roles of integrative Ca2+ handling in
myocardial I-F relations.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Iribe G, Kohl P, Noble D. (2006) - version=1.0

The original CellML model was created by:
Penny Noble

[e-mail]
The University of Oxford
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To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.