c-Met recruits ICAM-1 as a coreceptor to compensate for the loss of CD44 in Cd44 null mice

@inproceedings{Olaku2011cMetRI,
  title={c-Met recruits ICAM-1 as a coreceptor to compensate for the loss of CD44 in Cd44 null mice},
  author={Vivienne Olaku and Alexandra Matzke and Claudia Mitchell and Susanne Hasenauer and Arul Sakkaravarthi and Giuseppina Pace and Helmut Ponta and V{\'e}ronique Orian-Rousseau},
  booktitle={Molecular biology of the cell},
  year={2011}
}
CD44 isoforms act as coreceptors for the receptor tyrosine kinases c-Met and VEGFR-2. However, Cd44 knockout mice do not show overt phenotypes, in contrast to Met and Vegfr-2 knockout mice. We hypothesized that CD44 is being compensated for by another factor in Cd44 null mice. Using RNAi technology and blocking experiments with antibodies, peptides, and purified ectodomains, as well as overexpression studies, we identified intercellular adhesion molecule-1 (ICAM-1) as a new coreceptor for c-Met… CONTINUE READING
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Peptides derived from exon v6 of the CD44 extracellular domain prevent activation of receptor tyrosine kinases and subsequently angiogenesis and metastatic spread of tumor cells

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