Control mechanism of JAK/STAT signal transduction pathway

  title={Control mechanism of JAK/STAT signal transduction pathway},
  author={Satoshi Yamada and Satoru Shiono and Akiko Joo and Akihiko Yoshimura},
  journal={FEBS Letters},

Computational and mathematical models of the JAK-STAT signal transduction pathway

A deterministic mathematical model is implemented using the ODEs solver CO-PASI, and a stochastic computational model is built using the Stochastic Pi Machine (SPiM) that has the potential to contribute to cancer research.

Effect of SHP-2, SOCS3, and PP2 on IL-6 signal transduction in hepatocytes

A mathematical model has been developed that integrates signaling through both JAK/STAT and MAPK pathways and it is shown that SHP-2 and SOCS3 do not just influence the pathway that they are mainly associated with, but also have a profound effect on the other pathway due to interactions of the pathways.

Mathematical Model of IL-6 signal transduction in Hepatocytes

It can be determined that the influence of SOCS3 and SHP-2 on signaling induced by IL-6 is not independent of each other and the developed model used to analyze the interactions between the two pathways is found to predict behavior inline with the experimental studies.

Systems biology of JAK/STAT signalling.

A data-based model of the core module of the JAK2/STAT5 signalling pathway showed that rapid nucleocytoplasmic cycling of STAT5 is an essential pathway property.

Modeling regulatory mechanisms in IL‐6 signal transduction in hepatocytes

A mathematical model has been developed that integrates signaling through both the JAK/STAT and the MAPK pathway and suggests that interactions between SHP‐2 and SOCS3 influence signaling through theJAK/ STAT and theMAPK pathways.

Robustness Analysis of the IFN-γ Induced JAK-STAT Signaling Pathway

The study demonstrates that the JAK-STAT signaling pathway is robust with respect to its “signal time” and “Signal duration”, but sensitive with respectto its ”signal amplitude”.

Model-driven experimental analysis of the function of SHP-2 in IL-6-induced Jak/STAT signaling.

An identifiable model of early Jak/STAT signaling is proposed that describes the data and proves to be predictive and implies that the stepwise association of IL-6 with gp80 and gp130 and STAT3 dimerization at the receptor are essential for the dynamics of early pathway activation.



The Jak-STAT pathway.

Suppressors of Cytokine Signaling (SOCS): Inhibitors of the JAK/STAT Pathway

The SOCS family consists of eight proteins: CIS and SOCS1-SOCS7, which contain a central SH2 domain, a conserved C-terminus referred to as the SOCS box, and a unique N- terminus, and some of the biochemical and genetic studies investigating the physiologic role of SOCS in regulating cytokine activity are summarized.

Negative regulation of cytokine signaling pathways.

Biochemical characterization as well as gene disruption studies indicate that JAB/SOCS1/SSI-1 is an important negative regulator of interferon gamma signaling.

Modulation of STAT signaling by STAT-interacting proteins

The roles of STAT-interacting proteins in the regulation of STAT signaling are reviewed, finding a number of proteins function to modulate STAT signaling at various steps and mediate the crosstalk of STATs with other cellular signaling pathways.

The STAT family of proteins in cytokine signaling.

  • K. Shuai
  • Biology
    Progress in biophysics and molecular biology
  • 1999

Choice of STATs and other substrates specified by modular tyrosine-based motifs in cytokine receptors

Selecting particular substrates that characterize responses to the ciliary neurotrophic factor-interleukin-6 cytokine family depended not on which Jak was activated, but was instead determined by specific tyrosine-based motifs in the receptor components--gp130 and LIFR--shared by these cytokines.

Shp-2 Tyrosine Phosphatase Functions as a Negative Regulator of the Interferon-Stimulated Jak/STAT Pathway

It is proposed that Shp-2 acts to promote cell growth and survival through two mechanisms, i.e., the stimulation of growth factor-initiated mitogenic pathways and the suppression of cytotoxic effect elicited by cytokines, such as IFNs.

A new protein containing an SH2 domain that inhibits JAK kinases

A new SH2-domain-containing protein is isolated, JAB, which is a JAK-binding protein that interacts with the Jak2 tyrosine-kinase JH1 domain, and JAB and CIS appear to function as negative regulators in the JAK signalling pathway.