4oul: Difference between revisions
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== Function == | == Function == | ||
[[http://www.uniprot.org/uniprot/CAPR2_HUMAN CAPR2_HUMAN]] May regulate the transport and translation of mRNAs, modulating for instance the expression of proteins involved in synaptic plasticity in neurons. Involved in regulation of growth as erythroblasts shift from a highly proliferative state towards their terminal phase of differentiation. May be involved in apoptosis.<ref>PMID:14593112</ref> | [[http://www.uniprot.org/uniprot/CAPR2_HUMAN CAPR2_HUMAN]] May regulate the transport and translation of mRNAs, modulating for instance the expression of proteins involved in synaptic plasticity in neurons. Involved in regulation of growth as erythroblasts shift from a highly proliferative state towards their terminal phase of differentiation. May be involved in apoptosis.<ref>PMID:14593112</ref> | ||
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== Publication Abstract from PubMed == | |||
Previously, we have identified Caprin-2 as a new regulator in canonical Wnt signaling through a mechanism of facilitating LRP5/6 phosphorylation; moreover, we found that its C-terminal C1q-related domain (Cap2_CRD) is required for this process. Here, we determined the crystal structures of Cap2_CRD from human and zebrafish, which both associate as a homotrimer with calcium located at the symmetric center. Surprisingly, the calcium binding-deficient mutant exists as a more stable trimer than its wild-type counterpart. Further studies showed that this Caprin-2 mutant disabled in binding calcium maintains the activity of promoting LRP5/6 phosphorylation, whereas the mutations disrupting Cap2_CRD homotrimer did impair such activity. Together, our findings suggested that the C-terminal CRD domain of Caprin-2 forms a flexible homotrimer mediated by calcium and that such trimeric assembly is required for Caprin-2 to regulate canonical Wnt signaling. | |||
Structural insights into the C1q domain of Caprin-2 in canonical Wnt signaling.,Miao H, Jia Y, Xie S, Wang X, Zhao J, Chu Y, Zhou Z, Shi Z, Song X, Li L J Biol Chem. 2014 Dec 5;289(49):34104-13. doi: 10.1074/jbc.M114.591636. Epub 2014, Oct 20. PMID:25331957<ref>PMID:25331957</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
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== References == | == References == | ||
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