The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
The receptor for advanced glycation end‐products (RAGE) directly binds to ERK by a D‐domain‐like docking site
Abstract
The receptor for advanced glycation end‐products (RAGE)‐mediated cellular activation through the mitogen‐activated protein kinase (MAPK) cascade, activation of NF‐κB and Rho family small G‐proteins, cdc42/Rac, is implicated in the pathogenesis of inflammatory disorders and tumor growth/metastasis. However, the precise molecular mechanisms for the initiation of cell signaling by RAGE remain to be elucidated. In this study, proteins which directly bind to the cytoplasmic C‐terminus of RAGE were purified from rat lung extracts using an affinity chromatography technique and identified to be extracellular signal‐regulated protein kinase‐1 and ‐2 (ERK‐1/2). Their interactions were confirmed by immunoprecipitation of ERK‐1/2 from RAGE‐expressing HT1080 cell extracts with anti‐RAGE antibody. Furthermore, the augmentation of kinase activity of RAGE‐bound ERK upon the stimulation of cells with amphoterin was demonstrated by determining the phosphorylation level of myelin basic protein, an ERK substrate. In vitro binding studies using a series of C‐terminal deletion mutants of human RAGE revealed the importance of the membrane‐proximal cytoplasmic region of RAGE for the direct ERK–RAGE interaction. This region contained a sequence similar to the D‐domain, a ERK docking site which is conserved in some ERK substrates including MAPK‐interacting kinase‐1/2, mitogen‐ and stress‐activated protein kinase‐1, and ribosomal S6 kinase. These data suggest that ERK may play a role in RAGE signaling through direct interaction with RAGE.
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“The protein contains no obvious signalling domains90, although extracellular signal-regulated kinase (eRK) was shown to directly interact with the cytoplasmic tail of RAGe97.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [97]
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Cites
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Schmidt, A. M., Yan, S. D., Yan, S. F., & Stern, D. M. (2001) · Journal of Clinical Investigation · doi:10.1172/jci14002 · Cited by 1,256
Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases
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The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin
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Ligand-Induced, Receptor-Mediated Dimerization and Activation of EGF Receptor
Schlessinger, J. (2002) · Cell · doi:10.1016/s0092-8674(02)00966-2 · Cited by 995
Research works printed but not linked: 1
- Raabe T., 2002, Sci. STKE, 136, 1
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Sterile inflammation: sensing and reacting to damage
Chen, G. Y., & Nuñez, G. (2010) · Nature Reviews Immunology · doi:10.1038/nri2873 · Cited by 3,051
High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal
Lotze, M. T., & Tracey, K. J. (2005) · Nature reviews. Immunology · doi:10.1038/nri1594 · Cited by 2,490
HMGB1 and RAGE in Inflammation and Cancer
Sims, G. P., Rowe, D. C., Rietdijk, S. T., Herbst, R., & Coyle, A. J. (2010) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132603 · Cited by 1,436
Tian, J., Avalos, A. M., Mao, S.-Y., Chen, B., Senthil, K., Wu, H., Parroche, P., Drabic, S., Golenbock, D., Sirois, C., et al. (2007) · Nature Immunology · doi:10.1038/ni1457 · Cited by 1,372
Understanding RAGE, the receptor for advanced glycation end products
Bierhaus, A., Humpert, P. M., Morcos, M., Wendt, T., Chavakis, T., Arnold, B., Stern, D. M., & Nawroth, P. P. (2005) · Journal of Molecular Medicine · doi:10.1007/s00109-005-0688-7 · Cited by 1,297
Metadata
- Authors
- Ishihara, K., Tsutsumi, K., Kawane, S., Nakajima, M., & Kasaoka, T.
- Affiliations
- Novartis (Japan) (JP)
- ORCID
- Nakajima, Motowo
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2003-08-06
- Volume
- 550
- Issue
- 1-3
- Pages
- 107-113
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W1965497701
- Cited by
- 201
- References
- 47
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 5 · 2022: 10 · 2021: 8 · 2020: 7 · 2019: 6 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 6 · 2014: 12 · 2013: 10 · 2012: 9
- FWCI
- 4.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- receptor for advanced glycation end products, RAGE, ERK1/2, D domain, MAPK signaling, protein-protein interaction, myelin basic protein phosphorylation, amphoterin, RAGE signaling
- MeSH terms
- Receptor for Advanced Glycation End Products, Amino Acid Sequence, Animals, Binding Sites, Cell Extracts, Cells, Cultured, Cytoplasm, Myelin Basic Protein, Humans, Lung, Male, Phosphorylation, Receptors, Immunologic, Conserved Sequence, Rats, Wistar, Sequence Deletion, Protein Structure, Tertiary, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinases, HMGB1 Protein, Mitogen-Activated Protein Kinase 3, Mice, Rats
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