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| Content Provider | Springer Nature : BioMed Central |
|---|---|
| Author | Qi, Yun-feng Huang, Yan-xin Wang, Hong-yan Zhang, Yu Bao, Yong-li Sun, Lu-guo Wu, Yin Yu, Chun-lei Song, Zhen-bo Zheng, Li-hua Sun, Ying Wang, Guan-nan Li, Yu-xin |
| Abstract | Background Interferon-gamma (IFN-gamma) and interleukin-6 (IL-6) are multifunctional cytokines that regulate immune responses, cell proliferation, and tumour development and progression, which frequently have functionally opposing roles. The cellular responses to both cytokines are activated via the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. During the past 10 years, the crosstalk mechanism between the IFN-gamma and IL-6 pathways has been studied widely and several biological hypotheses have been proposed, but the kinetics and detailed crosstalk mechanism remain unclear. Results Using established mathematical models and new experimental observations of the crosstalk between the IFN-gamma and IL-6 pathways, we constructed a new crosstalk model that considers three possible crosstalk levels: (1) the competition between STAT1 and STAT3 for common receptor docking sites; (2) the mutual negative regulation between SOCS1 and SOCS3; and (3) the negative regulatory effects of the formation of STAT1/3 heterodimers. A number of simulations were tested to explore the consequences of cross-regulation between the two pathways. The simulation results agreed well with the experimental data, thereby demonstrating the effectiveness and correctness of the model. Conclusion In this study, we developed a crosstalk model of the IFN-gamma and IL-6 pathways to theoretically investigate their cross-regulation mechanism. The simulation experiments showed the importance of the three crosstalk levels between the two pathways. In particular, the unbalanced competition between STAT1 and STAT3 for IFNR and gp130 led to preferential activation of IFN-gamma and IL-6, while at the same time the formation of STAT1/3 heterodimers enhanced preferential signal transduction by sequestering a fraction of the activated STATs. The model provided a good explanation of the experimental observations and provided insights that may inform further research to facilitate a better understanding of the cross-regulation mechanism between the two pathways. |
| Related Links | https://bmcbioinformatics.biomedcentral.com/counter/pdf/10.1186/1471-2105-14-41.pdf |
| Ending Page | 21 |
| Page Count | 21 |
| Starting Page | 1 |
| File Format | HTM / HTML |
| ISSN | 14712105 |
| DOI | 10.1186/1471-2105-14-41 |
| Journal | BMC Bioinformatics |
| Issue Number | 1 |
| Volume Number | 14 |
| Language | English |
| Publisher | BioMed Central |
| Publisher Date | 2013-02-06 |
| Access Restriction | Open |
| Subject Keyword | Bioinformatics Microarrays Computational Biology Computer Appl. in Life Sciences Algorithms Combine Stimulation Previous Experimental Observation SOCS3 mRNA Activate Receptor Complex STAT3 Homodimers Computational Biology/Bioinformatics |
| Content Type | Text |
| Resource Type | Article |
| Subject | Molecular Biology Biochemistry Computer Science Applications Applied Mathematics Structural Biology |
| Journal Impact Factor | 2.9/2023 |
| 5-Year Journal Impact Factor | 3.6/2023 |
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