Noble1991_CardiacActionPotential_SodiumCalciumExchange
Ontology highlight
ABSTRACT:
SUBMITTER: 
Camille Laibe
PROVIDER: MODEL1006230073 | BioModels | 2005-01-01
REPOSITORIES: BioModels
Dataset's files
Items per page: 5 1 - 5 of 11 |
Publications
The role of sodium-calcium exchange during the cardiac action potential.
Noble D D Noble S J SJ Bett G C GC Earm Y E YE Ho W K WK So I K IK
Annals of the New York Academy of Sciences 19910101
Similar Datasets
Project description:This a model from the article:
A model of sino-atrial node electrical activity based on a modification of the DiFrancesco-Noble (1984) equations.
Noble D, Noble SJ. Proc R Soc Lond B Biol Sci.
1984 Sep 22;222(1228):295-304. 6149553
,
Abstract:
DiFrancesco & Noble's (1984) equations (Phil. Trans. R. Soc. Lond. B (in the press.] have been modified to apply to the mammalian sino-atrial node. The modifications are based on recent experimental work. The modified equations successfully reproduce action potential and pacemaker activity in the node. Slightly different versions have been developed for peripheral regions that show a maximum diastolic potential near --75 mV and for central regions that do not hyperpolarize beyond --60 to --65 mV. Variations in extracellular potassium influence the frequency of pacemaker activity in the s.a. node model very much less than they do in the Purkinje fibre model. This corresponds well to the experimental observation that the node is less sensitive to external [K] than are Purkinje fibres. Activation of the Na-K exchange pump in the model by increasing intracellular sodium can suppress pacemaker activity. This phenomenon may contribute to the mechanism of overdrive suppression.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble D, Noble SJ. (1984) - version04
The original CellML model was created by:
Noble, Penny, J
penny.noble@dpag.ox.ac.uk
Oxford University
Department of Physiology, Anatomy & Genetics
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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.
2005-01-01 | MODEL0406151557 | BioModels
Project description:Liver fibrosis is a common pathological outcome of chronic liver injury triggered by diverse etiologies. To investigate the role of CEP72 in fibrogenesis under distinct fibrotic settings, we performed bulk mRNA sequencing of whole-liver total RNA from wild-type (WT) and Cep72 knockout (Cep72-KO) mice in two experimental models: Schistosoma japonicum (Sj) infection–induced liver fibrosis and carbon tetrachloride (CCl4)–induced liver fibrosis. For the Sj model, mice were percutaneously infected with 17 ± 1 Schistosoma japonicum cercariae per mouse and analyzed at 8 weeks post infection, generating four groups: 8W-NC (WT control), 8W-KO-NC (Cep72-KO control), 8W-Sj (WT + Sj infection), and 8W-Sj-KO (Cep72-KO + Sj infection) (n = 2 mice per group). For the CCl4 model, mice were treated for 8 weeks with intraperitoneal injections of 10% CCl4 at 10 μL/g body weight, twice per week, and samples were collected from 8W-CCL4 (WT + CCl4) and 8W-KO-CCL4 (Cep72-KO + CCl4) groups (n = 2 mice per group). Paired-end Illumina mRNA-seq was performed on extracted total RNA from whole liver tissue. This dataset enables comparative transcriptomic analyses to identify CEP72-associated gene expression programs and pathways involved in liver injury, inflammation, and fibrosis across parasitic and chemical models.
2026-07-01 | GSE318357 | GEO
Project description:This a model from the article:
Reconstruction of sino-atrial node pacemaker potential based on the voltage
clamp experiments.
Yanagihara K, Noma A, Irisawa H. Jpn J Physiol
1980;30(6):841-57 7265560
,
Abstract:
The pacemaker activity of the S-A node cell was explained by reconstructing the pacemaker potential using a Hodgkin-Huxley type mathematical model which was based on the reported voltage clamp data. In this model four dynamic currents, the sodium current iNa, the slow inward current, is, the potassium current, iK, and the hyperpolarization-activated current, ih, in addition to a time-dependent leak current, i1 were included. The model simulated the spontaneous action potential the current voltage relationship, and the voltage clamp experiment in normal Tyrode solution of the rabbit S-A node. Furthermore, the changes of activity induced by the potassium current blocker Ba2+, by applying constant current, acetylcholine, and epinephrine were also reconstructed. It was strongly suggested that the pacemaker depolarization in the S-A node cell is mainly due to a gradual increase of iS during diastole, and that the contribution of iK is much less compared to the potassium current iK2 in the Purkinje fiber pacemaker depolarization. The rising phase of the action potential was due to iS and the plateau phase is determined by both the inactivation of iS and activation of iK.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Yanagihara K, Noma A, Irisawa H. (1980) - version=1.0
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
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.
2005-01-01 | MODEL1006230072 | BioModels
Project description:This a model from the article:
Improved guinea-pig ventricular cell model incorporating a diadic space, IKr and
IKs, and length- and tension-dependent processes.
Noble D, Varghese A, Kohl P, Noble P. Can J Cardiol
1998 Jan;14(1):123-34 9487284
,
Abstract:
The guinea-pig ventricular cell model, originally developed by Noble et al in
1991, has been greatly extended to include accumulation and depletion of calcium
in a diadic space between the sarcolemma and the sarcoplasmic reticulum where,
according to contempory understanding, the majority of calcium-induced calcium
release is triggered. The calcium in this space is also assumed to play the
major role in calcium-induced inactivation of the calcium current. Delayed
potassium current equations have been developed to include the rapid (IKr) and
slow (IKs) components of the delayed rectifier current based on the data of of
Heath and Terrar, along with data from Sanguinetti and Jurkiewicz. Length- and
tension-dependent changes in mechanical and electrophysiological processes have
been incorporated as described recently by Kohl et al. Drug receptor
interactions have started to be developed, using the sodium channel as the first
target. The new model has been tested against experimental data on action
potential clamp, and on force-interval and duration-interval relations; it has
been found to reliably reproduce experimental observations.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble D, Varghese A, Kohl P, Noble P. (1998) - version=1.0
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
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.
2005-01-01 | MODEL1006230063 | BioModels
Project description:This a model from the article:
Improved guinea-pig ventricular cell model incorporating a diadic space, IKr and
IKs, and length- and tension-dependent processes.
Noble D, Varghese A, Kohl P, Noble P. Can J Cardiol
1998 Jan;14(1):123-34 9487284
,
Abstract:
The guinea-pig ventricular cell model, originally developed by Noble et al in
1991, has been greatly extended to include accumulation and depletion of calcium
in a diadic space between the sarcolemma and the sarcoplasmic reticulum where,
according to contempory understanding, the majority of calcium-induced calcium
release is triggered. The calcium in this space is also assumed to play the
major role in calcium-induced inactivation of the calcium current. Delayed
potassium current equations have been developed to include the rapid (IKr) and
slow (IKs) components of the delayed rectifier current based on the data of of
Heath and Terrar, along with data from Sanguinetti and Jurkiewicz. Length- and
tension-dependent changes in mechanical and electrophysiological processes have
been incorporated as described recently by Kohl et al. Drug receptor
interactions have started to be developed, using the sodium channel as the first
target. The new model has been tested against experimental data on action
potential clamp, and on force-interval and duration-interval relations; it has
been found to reliably reproduce experimental observations.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble D, Varghese A, Kohl P, Noble P. (1998) - version=1.0
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
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.
2005-01-01 | MODEL1006230089 | BioModels
Project description:This a model from the article:
Improved guinea-pig ventricular cell model incorporating a diadic space, IKr and
IKs, and length- and tension-dependent processes.
Noble D, Varghese A, Kohl P, Noble P. Can J Cardiol
1998 Jan;14(1):123-34 9487284
,
Abstract:
The guinea-pig ventricular cell model, originally developed by Noble et al in
1991, has been greatly extended to include accumulation and depletion of calcium
in a diadic space between the sarcolemma and the sarcoplasmic reticulum where,
according to contempory understanding, the majority of calcium-induced calcium
release is triggered. The calcium in this space is also assumed to play the
major role in calcium-induced inactivation of the calcium current. Delayed
potassium current equations have been developed to include the rapid (IKr) and
slow (IKs) components of the delayed rectifier current based on the data of of
Heath and Terrar, along with data from Sanguinetti and Jurkiewicz. Length- and
tension-dependent changes in mechanical and electrophysiological processes have
been incorporated as described recently by Kohl et al. Drug receptor
interactions have started to be developed, using the sodium channel as the first
target. The new model has been tested against experimental data on action
potential clamp, and on force-interval and duration-interval relations; it has
been found to reliably reproduce experimental observations.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Noble D, Varghese A, Kohl P, Noble P. (1998) - version=1.0
The original CellML model was created by:
Penny Noble
penny.noble@dpag.ox.ac.uk
The University of Oxford
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
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.
2005-01-01 | MODEL1006230080 | BioModels
Project description:This the model from the article:
Computer model of action potential of mouse ventricular myocytes.
Bondarenko VE, Szigeti GP, Bett GC, Kim SJ, Rasmusson RL Am. J. Physiol. Heart Circ. Physiol.
2004 Sep;287(3):H1378-403. Pubmed ID: 15142845
,
doi: 10.1152/ajpheart.00185.2003
.
Abstract:
We have developed a mathematical model of the mouse ventricular myocyte action potential (AP) from voltage-clamp data of the underlying currents and Ca 2+
transients. Wherever possible, we used Markov models to represent the molecular structure and function of ion channels. The model includes detailed intracellular Ca 2+
dynamics, with simulations of localized events such as sarcoplasmic Ca 2+
release into a small intracellular volume bounded by the sarcolemma and sarcoplasmic reticulum. Transporter-mediated Ca 2+
fluxes from the bulk cytosol are closely matched to the experimentally reported values and predict stimulation rate-dependent changes in Ca 2+
transients. Our model reproduces the properties of cardiac myocytes from two different regions of the heart: the apex and the septum. The septum has a relatively prolonged AP, which reflects a relatively small contribution from the rapid transient outward K +
current in the septum. The attribution of putative molecular bases for several of the component currents enables our mouse model to be used to simulate the behavior of genetically modified transgenic mice.
This SBML model has been converted from a CellML model (see: Bondarenko 2004 vers. 5 var. 1
) in the CellML repository
.
It has been slightly changed and a parameter E_try been introduced to make it valid SBML. The CellML model was orginally created by:
James Lawson
Auckland Bioengineering Institute
j.lawson(at)auckland.ac.nz
From the original CellML model:
The original CellML model version
"has been curated by Penny Noble from Oxford University and is known to run in COR and PCEnv. This model represents the APICAL CELL variant as described in Bondarenko et al.'s 2004 paper and all units are consistent. The model is able to reproduce the action potential traces from Figure 16 of the publication. This model has a PCEnv session file associated with it."
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.
.
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.
2005-01-01 | MODEL1150151512 | BioModels
Project description:Ikaros is a zinc finger transcription factor critical for proper hematopoietic development and tumor suppression in the lymphoid lineage. Here, we use the newly generated Ik-ZnF1-/- and Ik-ZnF4-/- mutant mice to study hematopoietic development in the BM. As an initial approach to study early hematopoietic development as well as non-lymphoid lineages, RNA-Seq was performed on "Hardy Fraction A" cells, without lineage depletion (B220+IgM-CD43+CD24-BP-1-), of wt and Ik-ZnF1-/- mice (two biological replicates of each). Ik-ZnF4-/- mice have extremely few cells in the "Hardy fraction A" gate, and only one RNA-Seq experiment was performed on this cell population, with strongly reduced reads/genome coverage.
2026-05-30 | GSE39069 | GEO
Project description:This a model from the article:
A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction.
Luo CH, Rudy Y. Circ Res.
1991 Jun;68(6):1501-26. 1709839
,
Abstract:
A mathematical model of the membrane action potential of the mammalian ventricular cell is introduced. The model is based, whenever possible, on recent single-cell and single-channel data and incorporates the possibility of changing extracellular potassium concentration [K]o. The fast sodium current, INa, is characterized by fast upstroke velocity (Vmax = 400 V/sec) and slow recovery from inactivation. The time-independent potassium current, IK1, includes a negative-slope phase and displays significant crossover phenomenon as [K]o is varied. The time-dependent potassium current, IK, shows only a minimal degree of crossover. A novel potassium current that activates at plateau potentials is included in the model. The simulated action potential duplicates the experimentally observed effects of changes in [K]o on action potential duration and rest potential. Physiological simulations focus on the interaction between depolarization and repolarization (i.e., premature stimulation). Results demonstrate the importance of the slow recovery of INa in determining the response of the cell. Simulated responses to periodic stimulation include monotonic Wenckebach patterns and alternans at normal [K]o, whereas at low [K]o nonmonotonic Wenckebach periodicities, aperiodic patterns, and enhanced supernormal excitability that results in unstable responses ("chaotic activity") are observed. The results are consistent with recent experimental observations, and the model simulations relate these phenomena to the underlying ionic channel kinetics.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Luo CH, Rudy Y. (1991) - version06
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
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.
2005-01-01 | MODEL0479527919 | BioModels
Project description:We aimed to clarify the function of YBX2, a germ cell-specific Y-box-binding protein, in endometrial cancer stem cells. Our data demonstrated that expression of YBX2 was essential for a stem cell-like phenotype of endometrial cancer cells. We analyzed enhanced gene expression of IK cells that overexpressed YBX2 (IK-YBX2 cells) by introduction of YBX2 using microarray analysis. The CT45A5 gene was the most upregulated in IK-YBX2 cells, compared with mock cells. Therefore, we focused on CT45A5, which is considered a stemness factor.
2017-12-31 | GSE97511 | GEO