Accessibility navigation


Endosomes: a legitimate platform for the signaling train

Murphy, J. E., Padilla, B. E., Hasdemir, B., Cottrell, G. S. and Bunnett, N. W. (2009) Endosomes: a legitimate platform for the signaling train. Proceedings of the National Academy of Sciences of the United States of America, 106 (42). pp. 17615-17622. ISSN 1091-6490

Full text not archived in this repository.

It is advisable to refer to the publisher's version if you intend to cite from this work. See Guidance on citing.

To link to this item DOI: 10.1073/pnas.0906541106

Abstract/Summary

Although long regarded as a conduit for the degradation or recycling of cell surface receptors, the endosomal system is also an essential site of signal transduction. Activated receptors accumulate in endosomes, and certain signaling components are exclusively localized to endosomes. Receptors can continue to transmit signals from endosomes that are different from those that arise from the plasma membrane, resulting in distinct physiological responses. Endosomal signaling is widespread in metazoans and plants, where it transmits signals for diverse receptor families that regulate essential processes including growth, differentiation and survival. Receptor signaling at endosomal membranes is tightly regulated by mechanisms that control agonist availability, receptor coupling to signaling machinery, and the subcellular localization of signaling components. Drugs that target mechanisms that initiate and terminate receptor signaling at the plasma membrane are widespread and effective treatments for disease. Selective disruption of receptor signaling in endosomes, which can be accomplished by targeting endosomal-specific signaling pathways or by selective delivery of drugs to the endosomal network, may provide novel therapies for disease.

Item Type:Article
Refereed:Yes
Divisions:No Reading authors. Back catalogue items
ID Code:30256
Uncontrolled Keywords:Animals Endocytosis/physiology Endosomes/*physiology Humans MAP Kinase Signaling System/physiology Models, Biological Peptide Hydrolases/physiology Receptor Protein-Tyrosine Kinases/physiology Receptors, G-Protein-Coupled/physiology Signal Transduction/*physiology Toll-Like Receptors/physiology Ubiquitination/physiology
Additional Information:Murphy, Jane E Padilla, Benjamin E Hasdemir, Burcu Cottrell, Graeme S Bunnett, Nigel W DK39957/DK/NIDDK NIH HHS/ DK43207/DK/NIDDK NIH HHS/ DK57840/DK/NIDDK NIH HHS/ Proc Natl Acad Sci U S A. 2009 Oct 20;106(42):17615-22. Epub 2009 Oct 12.
Publisher:National Academy of Sciences

University Staff: Request a correction | Centaur Editors: Update this record

Page navigation