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Yamada2003_JAK_STAT_pathway


ABSTRACT: NCBS Curation Comments This model shows the control mechanism of Jak-Stat pathway, here SOCS1 (Suppressor of cytokine signaling-I) was identified as the negative regulator of Jak and STAT signal transduction pathway. Note: There are a few ambiguities in the paper like initial concentration of IFN and some reactions were missing in the paper that were employed for obtaining the results. The graphs are almost similar to the graphs as shown in the paper but still some ambiguities regarding the concentration are there. Thanks to Dr Satoshi Yamada for clarifying some of those ambiguities and providing the values used in simulations. Biomodels Curation Comments The model reproduces Fig 2 (A,C,E,G,I,K,M) of the paper. The set of equations present in the paper are inadequate to reproduce the figures mentioned . The model appears to have been fine tuned after correspondence between the curators at NCBS and the authors. There is however a slight discrepancy between the simulation results and the plots in the paper. The model was tested on MathSBML. This model originates from BioModels Database: A Database of Annotated Published Models. It is copyright (c) 2005-2006 The BioModels Team. For more information see the terms of use .

OTHER RELATED OMICS DATASETS IN: BIOMD0000000094

SUBMITTER: Sharat Vayttaden  

PROVIDER: BIOMD0000000093 | BioModels | 2007-03-07

REPOSITORIES: BioModels

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Publications

Control mechanism of JAK/STAT signal transduction pathway.

Yamada Satoshi S   Shiono Satoru S   Joo Akiko A   Yoshimura Akihiko A  

FEBS letters 20030101 1-3


Suppressor of cytokine signaling-1 (SOCS1) was identified as the negative regulator of Janus kinase (JAK) and signal transducer and activator of transcription (STAT) signal transduction pathway. However, the kinetics and control mechanism of the pathway have not yet been fully understood. We have developed the computer simulation of the JAK/STAT pathway. Without nuclear phosphatase, SOCS1's binding to JAK did not cause the decrease in nuclear phosphorylated STAT1. However, without SH2 domain-con  ...[more]

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