RGD Reference Report - Brain armadillo protein delta-catenin interacts with Abl tyrosine kinase and modulates cellular morphogenesis in response to growth factors. - Rat Genome Database

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Brain armadillo protein delta-catenin interacts with Abl tyrosine kinase and modulates cellular morphogenesis in response to growth factors.

Authors: Lu, Q  Mukhopadhyay, NK  Griffin, JD  Paredes, M  Medina, M  Kosik, KS 
Citation: Lu Q, etal., J Neurosci Res. 2002 Mar 1;67(5):618-24.
RGD ID: 8693599
Pubmed: (View Article at PubMed) PMID:11891774
DOI: Full-text: DOI:10.1002/jnr.10151

delta-Catenin associates with adhesive junctions and facilitates cellular morphogenesis (Lu et al., 1999). Here we show that delta-catenin colocalizes with actin filaments and Abl tyrosine kinase in the growth cones of cultured hippocampal neurons. PC12 cells induced to express delta-catenin show accelerated neurite extension upon nerve growth factor (NGF) stimulation. STI571, an Abl family kinase inhibitor, further accentuates these stimulatory effects. delta-Catenin is a potent substrate for Abl in vitro using an immunocomplex assay and most of the Abl-induced tyrosine phosphorylation within cells is present in the N-terminus of delta-catenin. When delta-catenin-expressing epithelial cells are induced to scatter in response to hepatocyte growth factor (HGF), STI571 leads to the rapid redistribution of delta-catenin and changes in cellular morphology. We suggest that delta-catenin is a possible Abl substrate and acts downstream of Abl to orchestrate actin-based cellular morphogenesis.

Annotation

Gene Ontology Annotations    

Cellular Component
growth cone  (IDA)

Molecular Function

Objects Annotated

Genes (Rattus norvegicus)
Abl1  (ABL proto-oncogene 1, non-receptor tyrosine kinase)


Additional Information