Intermediate filament proteins participate in signal transduction

How timely transport of chemical signals between the distal end of long axonal processes and the cell bodies of neurons occurs is an interesting and unresolved issue. Recently, Perlson et al. presented evidence that cleavage products of newly synthesized vimentin, an intermediate filament (IF) prote...

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Bibliographic Details
Published in:Trends in cell biology 2005-11, Vol.15 (11), p.568-570
Main Authors: Helfand, Brian T., Chou, Ying-Hao, Shumaker, Dale K., Goldman, Robert D.
Format: Article
Language:English
Subjects:
Animals
Axonal Transport - physiology
beta Karyopherins - metabolism
Calpain - metabolism
Dyneins - metabolism
Intermediate Filament Proteins - metabolism
Intermediate Filament Proteins - physiology
Mice
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Models, Biological
Neurons - physiology
Phosphorylation
Sciatic Nerve - injuries
Sciatic Nerve - physiopathology
Signal Transduction - physiology
Vimentin - genetics
Vimentin - metabolism
Vimentin - physiology
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Summary:How timely transport of chemical signals between the distal end of long axonal processes and the cell bodies of neurons occurs is an interesting and unresolved issue. Recently, Perlson et al. presented evidence that cleavage products of newly synthesized vimentin, an intermediate filament (IF) protein, interact with mitogen-activated protein (MAP) kinases at sites of axon injury. These IF fragments appear to be required for the transport of these kinases to the cell body along microtubule tracks. The truncated vimentin is instrumental in signal propagation as it provides a scaffold that brings together activated MAP kinases (such as Erk 1 and Erk2), as well as importin β and cytoplasmic dynein. The authors propose that this all-in-one transport complex has the extraordinary ability to travel towards the cell body and enter the nucleus where the kinases activate and influence gene expression so that a neuron can generate a timely response to injury.
ISSN:0962-8924
1879-3088
DOI:10.1016/j.tcb.2005.09.009