Dramatically reduced surface expression of NK cell receptor KIR2DS3 is attributed to multiple residues throughout the molecule
Using flow cytometry, fluorescent microscopy and examination of receptor glycosylation status, we demonstrate that an entire killer cell immunoglobulin-like receptor (KIR) locus ( KIR2DS3 )—assumed earlier to be surface expressed—appears to have little appreciable surface expression in transfected c...
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| Veröffentlicht in: | Genes and immunity 2009-03, Vol.10 (2), p.162-173 |
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| creator | VandenBussche, C J Mulrooney, T J Frazier, W R Dakshanamurthy, S Hurley, C K |
| description | Using flow cytometry, fluorescent microscopy and examination of receptor glycosylation status, we demonstrate that an entire killer cell immunoglobulin-like receptor (KIR) locus (
KIR2DS3
)—assumed earlier to be surface expressed—appears to have little appreciable surface expression in transfected cells. This phenotype was noted for receptors encoded by three allelic variants including the common
KIR2DS3*001
allele. Comparing the surface expression of KIR2DS3 with that of the better-studied KIR2DS1 molecule in two different cell lines, mutational analysis identified multiple polymorphic amino-acid residues that significantly alter the proportion of molecules present on the cell surface. A simultaneous substitution of five residues localized to the leader peptide (residues −18 and −7), second domain (residues 123 and 150) and transmembrane region (residue 234) was required to restore KIR2DS3 to the expression level of KIR2DS1. Corresponding simultaneous substitutions of KIR2DS1 to the KIR2DS3 residues resulted in a dramatically decreased surface expression. Molecular modeling was used to predict how these substitutions contribute to this phenotype. Alterations in receptor surface expression are likely to affect the balance of immune cell signaling impacting the characteristics of the response to pathogens or malignancy. |
| doi_str_mv | 10.1038/gene.2008.91 |
| format | Article |
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KIR2DS3
)—assumed earlier to be surface expressed—appears to have little appreciable surface expression in transfected cells. This phenotype was noted for receptors encoded by three allelic variants including the common
KIR2DS3*001
allele. Comparing the surface expression of KIR2DS3 with that of the better-studied KIR2DS1 molecule in two different cell lines, mutational analysis identified multiple polymorphic amino-acid residues that significantly alter the proportion of molecules present on the cell surface. A simultaneous substitution of five residues localized to the leader peptide (residues −18 and −7), second domain (residues 123 and 150) and transmembrane region (residue 234) was required to restore KIR2DS3 to the expression level of KIR2DS1. Corresponding simultaneous substitutions of KIR2DS1 to the KIR2DS3 residues resulted in a dramatically decreased surface expression. Molecular modeling was used to predict how these substitutions contribute to this phenotype. Alterations in receptor surface expression are likely to affect the balance of immune cell signaling impacting the characteristics of the response to pathogens or malignancy.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/gene.2008.91</identifier><identifier>PMID: 19005473</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Alleles ; Amino Acid Substitution ; Antibodies ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell lines ; Cell receptors ; Cell signaling ; Cell surface ; Cells ; Flow cytometry ; Gene Expression ; Gene Expression Regulation ; Genes ; Genotype & phenotype ; Glycosylation ; Human Genetics ; Humans ; Immune response ; Immunoglobulins ; Immunology ; Jurkat Cells ; Killer cell immunoglobulin-like receptors ; Killer Cells, Natural - immunology ; Killer Cells, Natural - metabolism ; Malignancy ; Models, Molecular ; Molecular modelling ; Natural killer cells ; Neoplasms - genetics ; Neoplasms - immunology ; Neoplasms - metabolism ; Oncology ; original-article ; Peptides ; Phenotypes ; Physiological aspects ; Polymorphism ; Potassium channels (inwardly-rectifying) ; Protein sorting signals ; Protein Structure, Tertiary - genetics ; Receptors, KIR - biosynthesis ; Receptors, KIR - genetics ; Receptors, KIR - immunology ; Signal Transduction ; Venus</subject><ispartof>Genes and immunity, 2009-03, Vol.10 (2), p.162-173</ispartof><rights>Macmillan Publishers Limited 2009</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Mar 2009</rights><rights>Macmillan Publishers Limited 2009.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c673t-6f0c27475417104c3bb4beb8af7eb82789a6202db32c81c83c9188efd244e2363</citedby><cites>FETCH-LOGICAL-c673t-6f0c27475417104c3bb4beb8af7eb82789a6202db32c81c83c9188efd244e2363</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gene.2008.91$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gene.2008.91$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,777,781,882,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19005473$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>VandenBussche, C J</creatorcontrib><creatorcontrib>Mulrooney, T J</creatorcontrib><creatorcontrib>Frazier, W R</creatorcontrib><creatorcontrib>Dakshanamurthy, S</creatorcontrib><creatorcontrib>Hurley, C K</creatorcontrib><title>Dramatically reduced surface expression of NK cell receptor KIR2DS3 is attributed to multiple residues throughout the molecule</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Using flow cytometry, fluorescent microscopy and examination of receptor glycosylation status, we demonstrate that an entire killer cell immunoglobulin-like receptor (KIR) locus (
KIR2DS3
)—assumed earlier to be surface expressed—appears to have little appreciable surface expression in transfected cells. This phenotype was noted for receptors encoded by three allelic variants including the common
KIR2DS3*001
allele. Comparing the surface expression of KIR2DS3 with that of the better-studied KIR2DS1 molecule in two different cell lines, mutational analysis identified multiple polymorphic amino-acid residues that significantly alter the proportion of molecules present on the cell surface. A simultaneous substitution of five residues localized to the leader peptide (residues −18 and −7), second domain (residues 123 and 150) and transmembrane region (residue 234) was required to restore KIR2DS3 to the expression level of KIR2DS1. Corresponding simultaneous substitutions of KIR2DS1 to the KIR2DS3 residues resulted in a dramatically decreased surface expression. Molecular modeling was used to predict how these substitutions contribute to this phenotype. Alterations in receptor surface expression are likely to affect the balance of immune cell signaling impacting the characteristics of the response to pathogens or malignancy.</description><subject>Alleles</subject><subject>Amino Acid Substitution</subject><subject>Antibodies</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell lines</subject><subject>Cell receptors</subject><subject>Cell signaling</subject><subject>Cell surface</subject><subject>Cells</subject><subject>Flow cytometry</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation</subject><subject>Genes</subject><subject>Genotype & phenotype</subject><subject>Glycosylation</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunoglobulins</subject><subject>Immunology</subject><subject>Jurkat Cells</subject><subject>Killer cell immunoglobulin-like receptors</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - metabolism</subject><subject>Malignancy</subject><subject>Models, Molecular</subject><subject>Molecular modelling</subject><subject>Natural killer cells</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - metabolism</subject><subject>Oncology</subject><subject>original-article</subject><subject>Peptides</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Polymorphism</subject><subject>Potassium channels (inwardly-rectifying)</subject><subject>Protein sorting signals</subject><subject>Protein Structure, Tertiary - genetics</subject><subject>Receptors, KIR - biosynthesis</subject><subject>Receptors, KIR - genetics</subject><subject>Receptors, KIR - immunology</subject><subject>Signal Transduction</subject><subject>Venus</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1ktlrFEEQhwdRTIy--SyNgiA4a187x4sQEo8lQSHR56anp2a2w8z02ockL_7t1rCL60qkobvo-upXB5VlzxldMCqqdz1MsOCUVouaPciOmSyLfClL-nC2iyKXVVkfZU9CuKGUFayoH2dHrKYUGXGc_Tr3etTRGj0Md8RDmwy0JCTfaQMEbjceQrBuIq4jXy6IgWFAysAmOk8uVlf8_FoQG4iO0dsmRQyOjoxpiHYzAKLBtgkCiWvvUr92KaIJZHQDmDTA0-xRp4cAz3bvSfb944dvZ5_zy6-fVmenl7kpShHzoqOGl7JcSlYyKo1oGtlAU-muxJuXVa0LTnnbCG4qZiphalZV0LVcSuCiECfZ-63uJjUjtAam6PWgNt6O2t8pp6069Ex2rXr3UwkcnywkCrzeCXj3AxuKarRhnoaewKWgOJWYhgsEX_0D3rjkJ2xO8QLL54LXM_XyvxRWXtX1stxL9XoAZafOYWlmzqtOWb2U2DdbIrW4h8LTwmiNm6Cz-H8Q8OYgAJkIt7HXKQS1ur46ZN9uWeNdCB66PyNjVM3rp-b1U_P6qZoh_uLvMe_h3b4hkG-BgK6pB7_v-17B398a5DQ</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>VandenBussche, C J</creator><creator>Mulrooney, T J</creator><creator>Frazier, W R</creator><creator>Dakshanamurthy, S</creator><creator>Hurley, C K</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20090301</creationdate><title>Dramatically reduced surface expression of NK cell receptor KIR2DS3 is attributed to multiple residues throughout the molecule</title><author>VandenBussche, C J ; Mulrooney, T J ; Frazier, W R ; Dakshanamurthy, S ; Hurley, C K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c673t-6f0c27475417104c3bb4beb8af7eb82789a6202db32c81c83c9188efd244e2363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Alleles</topic><topic>Amino Acid Substitution</topic><topic>Antibodies</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cell lines</topic><topic>Cell receptors</topic><topic>Cell signaling</topic><topic>Cell surface</topic><topic>Cells</topic><topic>Flow cytometry</topic><topic>Gene Expression</topic><topic>Gene Expression Regulation</topic><topic>Genes</topic><topic>Genotype & phenotype</topic><topic>Glycosylation</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunoglobulins</topic><topic>Immunology</topic><topic>Jurkat Cells</topic><topic>Killer cell immunoglobulin-like receptors</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - metabolism</topic><topic>Malignancy</topic><topic>Models, Molecular</topic><topic>Molecular modelling</topic><topic>Natural killer cells</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - metabolism</topic><topic>Oncology</topic><topic>original-article</topic><topic>Peptides</topic><topic>Phenotypes</topic><topic>Physiological aspects</topic><topic>Polymorphism</topic><topic>Potassium channels (inwardly-rectifying)</topic><topic>Protein sorting signals</topic><topic>Protein Structure, Tertiary - genetics</topic><topic>Receptors, KIR - biosynthesis</topic><topic>Receptors, KIR - genetics</topic><topic>Receptors, KIR - immunology</topic><topic>Signal Transduction</topic><topic>Venus</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>VandenBussche, C J</creatorcontrib><creatorcontrib>Mulrooney, T J</creatorcontrib><creatorcontrib>Frazier, W R</creatorcontrib><creatorcontrib>Dakshanamurthy, S</creatorcontrib><creatorcontrib>Hurley, C K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes and immunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>VandenBussche, C J</au><au>Mulrooney, T J</au><au>Frazier, W R</au><au>Dakshanamurthy, S</au><au>Hurley, C K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dramatically reduced surface expression of NK cell receptor KIR2DS3 is attributed to multiple residues throughout the molecule</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>10</volume><issue>2</issue><spage>162</spage><epage>173</epage><pages>162-173</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Using flow cytometry, fluorescent microscopy and examination of receptor glycosylation status, we demonstrate that an entire killer cell immunoglobulin-like receptor (KIR) locus (
KIR2DS3
)—assumed earlier to be surface expressed—appears to have little appreciable surface expression in transfected cells. This phenotype was noted for receptors encoded by three allelic variants including the common
KIR2DS3*001
allele. Comparing the surface expression of KIR2DS3 with that of the better-studied KIR2DS1 molecule in two different cell lines, mutational analysis identified multiple polymorphic amino-acid residues that significantly alter the proportion of molecules present on the cell surface. A simultaneous substitution of five residues localized to the leader peptide (residues −18 and −7), second domain (residues 123 and 150) and transmembrane region (residue 234) was required to restore KIR2DS3 to the expression level of KIR2DS1. Corresponding simultaneous substitutions of KIR2DS1 to the KIR2DS3 residues resulted in a dramatically decreased surface expression. Molecular modeling was used to predict how these substitutions contribute to this phenotype. Alterations in receptor surface expression are likely to affect the balance of immune cell signaling impacting the characteristics of the response to pathogens or malignancy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19005473</pmid><doi>10.1038/gene.2008.91</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Springer Nature - Complete Springer Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Alleles Amino Acid Substitution Antibodies Biomedical and Life Sciences Biomedicine Cancer Research Cell lines Cell receptors Cell signaling Cell surface Cells Flow cytometry Gene Expression Gene Expression Regulation Genes Genotype & phenotype Glycosylation Human Genetics Humans Immune response Immunoglobulins Immunology Jurkat Cells Killer cell immunoglobulin-like receptors Killer Cells, Natural - immunology Killer Cells, Natural - metabolism Malignancy Models, Molecular Molecular modelling Natural killer cells Neoplasms - genetics Neoplasms - immunology Neoplasms - metabolism Oncology original-article Peptides Phenotypes Physiological aspects Polymorphism Potassium channels (inwardly-rectifying) Protein sorting signals Protein Structure, Tertiary - genetics Receptors, KIR - biosynthesis Receptors, KIR - genetics Receptors, KIR - immunology Signal Transduction Venus |
| title | Dramatically reduced surface expression of NK cell receptor KIR2DS3 is attributed to multiple residues throughout the molecule |
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