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Abelson interacting protein 1 (Abi-1) is essential for dendrite morphogenesis and synapse formation.

Authors: Proepper, C  Johannsen, S  Liebau, S  Dahl, J  Vaida, B  Bockmann, J  Kreutz, MR  Gundelfinger, ED  Boeckers, TM 
Citation: Proepper C, etal., EMBO J. 2007 Mar 7;26(5):1397-409. Epub 2007 Feb 15.
Pubmed: (View Article at PubMed) PMID:17304222
DOI: Full-text: DOI:10.1038/sj.emboj.7601569

Synaptogenesis and synaptic plasticity depend crucially on the dynamic and locally specific regulation of the actin cytoskeleton. We identified an important component for controlled actin assembly, abelson interacting protein-1 (Abi-1), as a binding partner for the postsynaptic density (PSD) protein ProSAP2/Shank3. During early neuronal development, Abi-1 is localized in neurites and growth cones; at later stages, the protein is enriched in dendritic spines and PSDs, as are components of a trimeric complex consisting of Abi-1, Eps8 and Sos-1. Abi-1 translocates upon NMDA application from PSDs to nuclei. Nuclear entry depends on abelson kinase activity. Abi-1 co-immunoprecipitates with the transcription factor complex of Myc/Max proteins and enhances E-box-regulated gene transcription. Downregulation of Abi-1 by small interfering RNA results in excessive dendrite branching, immature spine and synapse morphology and a reduction of synapses, whereas overexpression of Abi-1 has the opposite effect. Data show that Abi-1 can act as a specific synapto-nuclear messenger and is essentially involved in dendrite and synapse formation.

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CRRD Object Information
CRRD ID: 8553800
Created: 2014-05-08
Species: All species
Last Modified: 2014-05-08
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.