scholarly journals 1PT206 Cell adhesion molecule 1 (CADM1) on mast cells promotes interaction with dorsal root ganglion neurites by heterophilic binding to nectin-3(The 50th Annual Meeting of the Biophysical Society of Japan)

2012 ◽  
Vol 52 (supplement) ◽  
pp. S103
Author(s):  
Tadahide Furuno ◽  
Miho Sekimura ◽  
Keisuke Okamoto ◽  
Man Hagiyama ◽  
Akihiko Ito ◽  
...  
2009 ◽  
Vol 49 (supplement) ◽  
pp. S86
Author(s):  
Tadahide Furuno ◽  
Keisuke Okamoto ◽  
Miho Sekimura ◽  
Akihiko Ito ◽  
Naohide Hirashima ◽  
...  

Thorax ◽  
2010 ◽  
Vol 65 (Suppl 4) ◽  
pp. A17-A17
Author(s):  
E. P. Moiseeva ◽  
M. Leyland ◽  
P. Bradding

1998 ◽  
Vol 9 (2) ◽  
pp. 277-290 ◽  
Author(s):  
Paul M. Yip ◽  
Xiaoning Zhao ◽  
Anthony M.P. Montgomery ◽  
Chi-Hung Siu

The cell adhesion molecule L1 is a potent inducer of neurite outgrowth and it has been implicated in X-linked hydrocephalus and related neurological disorders. To investigate the mechanisms of neurite outgrowth stimulated by L1, attempts were made to identify the neuritogenic sites in L1. Fusion proteins containing different segments of the extracellular region of L1 were prepared and different neuronal cells were assayed on substrate-coated fusion proteins. Interestingly, both immunoglobulin (Ig)-like domains 2 and 6 (Ig2, Ig6) promoted neurite outgrowth from dorsal root ganglion cells, whereas neural retinal cells responded only to Ig2. L1 Ig2 contains a previously identified homophilic binding site, whereas L1 Ig6 contains an Arg-Gly-Asp (RGD) sequence. The neuritogenic activity of Ig6 was abrogated by mutations in the RGD site. The addition of RGD-containing peptides also inhibited the promotion of neurite outgrowth from dorsal root ganglion cells by glutathione S-transferase-Ig6, implicating the involvement of an integrin. The monoclonal antibody LM609 against αvβ3integrin, but not an anti-β1 antibody, inhibited the neuritogenic effects of Ig6. These data thus provide the first evidence that the RGD motif in L1 Ig6 is capable of promoting neurite outgrowth via interaction with the αvβ3integrin on neuronal cells.


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