2012Unpublished venueRequires access

Developing a novel integrated model of p38 MAPK and glucocorticoid signalling pathways

Alex S. Holehouse, Xian Yang, Ian M. Adcock, Yike Guo

Open publisher page 2 citations

Abstract

Glucocorticoid (GC) resistance is a key mechanism by which traditional asthma treatments become ineffective for patients, yet the molecular characteristics of the associated regulatory changes are largely unknown. Significant evidence suggests that crosstalk between p38 Mitogen Activated Protein Kinase (MAPK) and GC signalling pathways may contribute to this resistance. Based on a number of studies, a simplified GC signalling pathway model was developed and integrated with a pre-existing model of the p38 MAPK pathway. It is predicted that with experimental data, the validity and use of this model can be confirmed, corrections and updates can be made where necessary, and that through the two pathways' interface points the existence and scale of crosstalk can be examined.

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What this paper is about

Glucocorticoid (GC) resistance is a key mechanism by which traditional asthma treatments become ineffective for patients, yet the molecular characteristics of the associated regulatory changes are largely unknown. Significant evidence suggests that crosstalk between p38 Mitogen Activated Protein Kinase (MAPK) and GC signalling pathways may contribute to this resistance. Based on a number of studies, a simplified GC signalling pathway model was developed and integrated with a pre-existing model of the p38 MAPK pathway. It is predicted that with experimental data, the validity and use of this model can be confirmed, corrections and updates can be made where necessary, and that through the two pathways' interface points the existence and scale of crosstalk can be examined.

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OpenAlex reports 2 citations for this work. Citation counts describe recorded attention and do not establish research quality.

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Available abstract

Glucocorticoid (GC) resistance is a key mechanism by which traditional asthma treatments become ineffective for patients, yet the molecular characteristics of the associated regulatory changes are largely unknown. Significant evidence suggests that crosstalk between p38 Mitogen Activated Protein Kinase (MAPK) and GC signalling pathways may contribute to this resistance. Based on a number of studies, a simplified GC signalling pathway model was developed and integrated with a pre-existing model of the p38 MAPK pathway. It is predicted that with experimental data, the validity and use of this model can be confirmed, corrections and updates can be made where necessary, and that through the two pathways' interface points the existence and scale of crosstalk can be examined.

Key concepts: Crosstalk, MAPK/ERK pathway, p38 mitogen-activated protein kinases, Signalling pathways, Hedgehog signaling pathway, Signalling, Glucocorticoid, Kinase

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