Inactivation of the EGF-TM7 receptor EMR4 after the Pan-Homo divergence

被引：36

作者：

Hamann, J

Kwakkenbos, MJ

de Jong, EC

Heus, H

Olsen, AS

van Lier, RAW

机构：

[1] Univ Amsterdam, Acad Med Ctr, Expt Immunol Lab, NL-1100 DE Amsterdam, Netherlands

[2] Univ Amsterdam, Acad Med Ctr, Dept Cell Biol & Histol, NL-1105 AZ Amsterdam, Netherlands

[3] NV Organon, Target Discovery Unit, NL-5340 BH Oss, Netherlands

[4] US DOE, Joint Genome Inst, Walnut Creek, CA 94598 USA

来源：

EUROPEAN JOURNAL OF IMMUNOLOGY | 2003年 / 33卷 / 05期

关键词：

class B GPCR; EGF-TM7; family; EMR4; frameshift mutation;

D O I：

10.1002/eji.200323881

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

We here report on the identification of a novel human EGF-TM7 receptor, designated EMR4. Like most EGF-TM7 receptor genes, EMR4 is localized on the short arm of chromosome 19, in close proximity to EMR1. Remarkably, due to a one-nucleotide deletion in exon 8, translation of human EMR4 would result in a truncated 232-amino acid protein lacking the entire seven-span transmembrane region. This deletion is not present in nonhuman primates, including chimpanzees, suggesting that EMR4 became nonfunctional only after human speciation, about five million years ago. Thus, EMR4 surprisingly accounts for a genetic difference between humans and primates related to immunity.

引用

页码：1365 / 1371

页数：7

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