<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Yamanaka, Masahiro</style></author><author><style face="normal" font="default" size="100%">Kato, Yukinari</style></author><author><style face="normal" font="default" size="100%">Angata, Takashi</style></author><author><style face="normal" font="default" size="100%">Narimatsu, Hisashi</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Deletion polymorphism of SIGLEC14 and its functional implications.</style></title><secondary-title><style face="normal" font="default" size="100%">Glycobiology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Glycobiology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antigens, CD</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, Differentiation, Myelomonocytic</style></keyword><keyword><style  face="normal" font="default" size="100%">B-Lymphocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Differentiation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Fusion</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Lectins</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipopolysaccharides</style></keyword><keyword><style  face="normal" font="default" size="100%">Macrophages</style></keyword><keyword><style  face="normal" font="default" size="100%">Monocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Cell Surface</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2009</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2009 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">841-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Human Siglec-14, a member of the Siglec family of sialic acid-binding lectins, shows extensive sequence similarity to human Siglec-5. To analyze respective expression patterns of Siglec-14 and Siglec-5, we developed specific antibodies against each of them. We found that the former was expressed on granulocytes and monocytes, while the latter was on granulocytes and B-cells. Surprisingly, some individuals lacked the expression of Siglec-14, while they all expressed Siglec-5. We found that a fusion between SIGLEC14 and SIGLEC5 genes, resulting in the functional deletion of SIGLEC14, underlies this phenotype. The presence of the &quot;SIGLEC14 null&quot; allele in all human populations we tested implies an ancient origin, while its allelic frequency is higher in Asians compared with Africans and Europeans. The forced expression of Siglec-14 in a monocytic cell line-enhanced TNF-alpha secretion elicited by lipopolysaccharide. These results imply that Siglec-14 may play some role in bacterial infection.&lt;/p&gt;
</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">&lt;p&gt;http://www.ncbi.nlm.nih.gov/pubmed/19369701?dopt=Abstract&lt;/p&gt;
</style></custom1></record></records></xml>