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Cited by 472

The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.

Mitogen activated protein (MAP) kinase signal transduction pathways and novel anti-inflammatory targets

Open access
Hommes, D W, Peppelenbosch, M P, van Deventer, S J H·2003·Gut

Abstract

Over the last decade important advances have been made in our understanding of the molecular events underlying cellular responses to extracellular signals. Increased understanding of signal transduction mechanisms and gene regulation involved in immune responses has created opportunities for the discovery of novel therapeutic compounds useful in treating inflammatory disorders. One of the best studied signalling routes is the mitogen activated protein (MAP) kinase signal transduction pathway which plays a crucial role in many aspects of immune mediated inflammatory responses. Here, our current understanding of the MAP kinase pathway is reviewed, as well as recent advances in the design of novel agents that are able to modulate the activity of these signalling cascades.

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Metadata

Authors
Hommes, D. W., Peppelenbosch, M. P., & van Deventer, S. J. H.
Venue
Gut
Publisher
BMJ
Published
2003-01
Volume
52
Issue
1
Pages
144-151
ISSN
  • 0017-5749 (ISSN-L)
  • 1468-3288
OpenAlex
W2140677435
Cited by
472
References
71
FWCI
3.24
Type
journal article
Language
en
Open access
hybrid

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CoChat. (2026). Citation check: Mitogen activated protein (MAP) kinase signal transduction pathways and novel anti-inflammatory targets. https://app.cochat.ai/papers/10.1136/gut.52.1.144
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Hommes, D. W., Peppelenbosch, M. P., & van Deventer, S. J. H. (2003). Mitogen activated protein (MAP) kinase signal transduction pathways and novel anti-inflammatory targets. Gut. https://doi.org/10.1136/gut.52.1.144

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.