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A point mutation in the amino terminus of TLR7 abolishes signaling without affecting ligand binding.

Abstract:

TLR7 is the mammalian receptor for ssRNA and some nucleotide-like small molecules. We have generated a mouse by N-nitrose-N'-ethyl urea mutagenesis in which threonine 68 of TLR7 was substituted with isoleucine. Cells bearing this mutant TLR7 lost the sensitivity to the small-molecule TLR7 agonist resiquimod, hence the name TLR7(rsq1). In this work, we report the characterization of this mutant protein. Similar to the wild-type counterpart, TLR7(rsq1) localizes to the endoplasmic reticulum and...

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Publisher copy:
10.4049/jimmunol.1003585

Authors


Iavarone, C More by this author
Ramsauer, K More by this author
Kubarenko, AV More by this author
Debasitis, JC More by this author
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Journal:
Journal of immunology (Baltimore, Md. : 1950)
Volume:
186
Issue:
7
Pages:
4213-4222
Publication date:
2011-04-05
DOI:
EISSN:
1550-6606
ISSN:
0022-1767
URN:
uuid:a49fe24a-4be7-4aa7-90bd-af567412dabc
Source identifiers:
418822
Local pid:
pubs:418822

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