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Correction
for Harburger and Calderwood,
First published online April 22, 2009
doi: 10.1242/10.1242/jcs.052910
Author Correction |
There was an error published in J. Cell Sci. 122, 159-163.
It has been brought to our attention that there is an error in the poster published in association with this article. Non-phosphorylated ICAP1 is shown to bind to the cytoplasmic tails of integrin β-subunits, whereas Ca2+/calmodulin-dependent protein kinase II (CaMKII)-mediated phosphorylation of ICAP1 is depicted as driving dissociation of ICAP1 from integrin β-tails. Although ICAP1 is indeed a substrate for CaMKII, the phosphorylation of ICAP1 on Thr38 is likely to enhance ICAP1 binding to β1 tails rather than inhibit the interaction, and this might account for CaMKII-mediated inhibition of
5β1 activation (Bouvard et al., 1998
; Bouvard and Block, 1998
).
The authors apologise for this mistake and for any confusion caused.
References
Bouvard, D. and Block, M. R. (1998). Calcium/calmodulin-dependent protein kinase II controls integrin
5β1-mediated cell adhesion through the integrin cytoplasmic domain associated protein-1
. Biochem. Biophys. Res. Commun. 252, 46-50.[CrossRef][Medline]
Bouvard, D., Molla, A. and Block, M. R. (1998). Calcium/calmodulin-dependent protein kinase II controls
5β1 integrin-mediated inside-out signaling. J. Cell Sci. 111, 657-665.[Abstract]
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