Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially
The immune checkpoint HLA-G prevents maternal rejection of the fetus and contributes in cancer invasion and acceptance of allografts. The 5' and 3' regulatory regions of the HLA-G gene are polymorphic and balancing selection probably maintains this variability. It is proposed that nucleoti...
Gespeichert in:
| Veröffentlicht in: | PloS one 2017-01, Vol.12 (1), p.e0169032-e0169032 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | e0169032 |
|---|---|
| container_issue | 1 |
| container_start_page | e0169032 |
| container_title | PloS one |
| container_volume | 12 |
| creator | Poras, Isabelle Yaghi, Layale Martelli-Palomino, Gustavo Mendes-Junior, Celso T Muniz, Yara Costa Netto Cagnin, Natalia F Sgorla de Almeida, Bibiana Castelli, Erick C Carosella, Edgardo D Donadi, Eduardo A Moreau, Philippe |
| description | The immune checkpoint HLA-G prevents maternal rejection of the fetus and contributes in cancer invasion and acceptance of allografts. The 5' and 3' regulatory regions of the HLA-G gene are polymorphic and balancing selection probably maintains this variability. It is proposed that nucleotide variations may affect the level of HLA-G expression. To investigate this issue we aimed to analyze how haplotypes of the 3' untranslated region (3'UTR) with highest worldwide frequencies, namely UTR-1, UTR-2, UTR-3, UTR-4, UTR-5, UTR-18 and UTR-7, impact the expression of a luciferase reporter gene in vitro. Experiments performed with the HLA-G positive cell lines JEG-3 (choricarcinoma) and FON (melanoma), and with the HLA-G negative cell lines M8 (melanoma) and U251MG (glioblastoma) showed that the HLA-G 3'UTR polymorphism influences the response to endogenous cellular factors and may vary according to the cell type. UTR-5 and UTR-7 impact the activity of luciferase the most whereas UTR-2, UTR-3, UTR-4, and UTR-18 have intermediate impact, and UTR-1 has the lowest impact. These results corroborate the previous associations between amounts of plasma sHLA-G levels and 3'UTR haplotypes in healthy individuals and reinforce that 3'UTR typing may be a predictor of the genetic predisposition of an individual to express different levels of HLA-G. |
| doi_str_mv | 10.1371/journal.pone.0169032 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1855068952</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A476237537</galeid><doaj_id>oai_doaj_org_article_1aaaf7d0fe554e0ab48548826b57fe03</doaj_id><sourcerecordid>A476237537</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5332-54a49d3714f96bd9d1937452442db3252aea54f4b2a3f2cf4d9433b0d6b03ab83</originalsourceid><addsrcrecordid>eNqNkl-LEzEUxQdR3HX1G4gGBBWkNZM_M5MXodTd7UJBEPc53Jkk7ZQ0qcmMUPzyZtrZpRUffEpIfvfcew8ny17neJrTMv-88X1wYKc77_QU54XAlDzJLnNByaQgmD49uV9kL2LcYMxpVRTPswtSYcaFEJfZ7wXsrO_2Ox2RN6hba7RYzia3iH5A964L4KKFTiv0Xa9a79IRU0OFOo-unfIr7Xwf0Q00nQ8HhUP1JwSJOVwnaK6tRcvWpQ5fW2N00K5rwdr9y-yZARv1q_G8yu5vrn_MF5Plt9u7-Ww5aThNC3AGTKi0MjOiqJVQaa2SccIYUTUlnIAGzgyrCVBDGsOUYJTWWBU1plBX9Cp7e9RNm0Y5-hZlXnGOi0pwkoi7I6E8bOQutFsIe-mhlYcHH1YSQtc2VsscAEypsNGcM42hZhVnVUWKmpdGY5q0vozd-nqrVaMHF-2Z6PmPa9dy5X9JTnBZMpwEPo4Cwf_sdezkto1NMhGcTmYPcwtWCYz_C-WUVJUoE_ruL_TfRozUCtKurTM-jdgMonLGyoLQktNB6_0JtdZgu3X0tu9SQuI5yI5gE3yMQZtHG3IshxQ_DCGHFMsxxanszamFj0UPsaV_ACE0648</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1855068952</pqid></control><display><type>article</type><title>Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Public Library of Science (PLoS)</source><creator>Poras, Isabelle ; Yaghi, Layale ; Martelli-Palomino, Gustavo ; Mendes-Junior, Celso T ; Muniz, Yara Costa Netto ; Cagnin, Natalia F ; Sgorla de Almeida, Bibiana ; Castelli, Erick C ; Carosella, Edgardo D ; Donadi, Eduardo A ; Moreau, Philippe</creator><creatorcontrib>Poras, Isabelle ; Yaghi, Layale ; Martelli-Palomino, Gustavo ; Mendes-Junior, Celso T ; Muniz, Yara Costa Netto ; Cagnin, Natalia F ; Sgorla de Almeida, Bibiana ; Castelli, Erick C ; Carosella, Edgardo D ; Donadi, Eduardo A ; Moreau, Philippe</creatorcontrib><description>The immune checkpoint HLA-G prevents maternal rejection of the fetus and contributes in cancer invasion and acceptance of allografts. The 5' and 3' regulatory regions of the HLA-G gene are polymorphic and balancing selection probably maintains this variability. It is proposed that nucleotide variations may affect the level of HLA-G expression. To investigate this issue we aimed to analyze how haplotypes of the 3' untranslated region (3'UTR) with highest worldwide frequencies, namely UTR-1, UTR-2, UTR-3, UTR-4, UTR-5, UTR-18 and UTR-7, impact the expression of a luciferase reporter gene in vitro. Experiments performed with the HLA-G positive cell lines JEG-3 (choricarcinoma) and FON (melanoma), and with the HLA-G negative cell lines M8 (melanoma) and U251MG (glioblastoma) showed that the HLA-G 3'UTR polymorphism influences the response to endogenous cellular factors and may vary according to the cell type. UTR-5 and UTR-7 impact the activity of luciferase the most whereas UTR-2, UTR-3, UTR-4, and UTR-18 have intermediate impact, and UTR-1 has the lowest impact. These results corroborate the previous associations between amounts of plasma sHLA-G levels and 3'UTR haplotypes in healthy individuals and reinforce that 3'UTR typing may be a predictor of the genetic predisposition of an individual to express different levels of HLA-G.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0169032</identifier><identifier>PMID: 28045999</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; 3' Untranslated Regions - genetics ; Allografts ; Alternatives ; Analysis ; Base Pairing - genetics ; Base Sequence ; Biology and Life Sciences ; Biotechnology ; Cancer ; Cell Line, Tumor ; DNA methylation ; Epidemiology ; Fetuses ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes, Reporter ; Genetics ; Glioblastoma ; Graft rejection ; Haplotypes ; Haplotypes - genetics ; Histocompatibility antigen HLA ; HLA antigens ; HLA-G Antigens - genetics ; Humans ; Hypoxia ; Immune checkpoint ; Immunology ; INDEL Mutation - genetics ; Infections ; Infectious diseases ; Luciferases - metabolism ; Melanoma ; MicroRNAs ; Mutagenesis, Site-Directed ; Polymorphism ; Polymorphism, Genetic ; Regulation ; Regulatory sequences ; Reporter gene ; Research and Analysis Methods ; Tissue typing ; Transcription (Genetics) ; Transcription factors</subject><ispartof>PloS one, 2017-01, Vol.12 (1), p.e0169032-e0169032</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Poras et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Poras et al 2017 Poras et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5332-54a49d3714f96bd9d1937452442db3252aea54f4b2a3f2cf4d9433b0d6b03ab83</citedby><cites>FETCH-LOGICAL-c5332-54a49d3714f96bd9d1937452442db3252aea54f4b2a3f2cf4d9433b0d6b03ab83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207740/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5207740/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28045999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Poras, Isabelle</creatorcontrib><creatorcontrib>Yaghi, Layale</creatorcontrib><creatorcontrib>Martelli-Palomino, Gustavo</creatorcontrib><creatorcontrib>Mendes-Junior, Celso T</creatorcontrib><creatorcontrib>Muniz, Yara Costa Netto</creatorcontrib><creatorcontrib>Cagnin, Natalia F</creatorcontrib><creatorcontrib>Sgorla de Almeida, Bibiana</creatorcontrib><creatorcontrib>Castelli, Erick C</creatorcontrib><creatorcontrib>Carosella, Edgardo D</creatorcontrib><creatorcontrib>Donadi, Eduardo A</creatorcontrib><creatorcontrib>Moreau, Philippe</creatorcontrib><title>Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The immune checkpoint HLA-G prevents maternal rejection of the fetus and contributes in cancer invasion and acceptance of allografts. The 5' and 3' regulatory regions of the HLA-G gene are polymorphic and balancing selection probably maintains this variability. It is proposed that nucleotide variations may affect the level of HLA-G expression. To investigate this issue we aimed to analyze how haplotypes of the 3' untranslated region (3'UTR) with highest worldwide frequencies, namely UTR-1, UTR-2, UTR-3, UTR-4, UTR-5, UTR-18 and UTR-7, impact the expression of a luciferase reporter gene in vitro. Experiments performed with the HLA-G positive cell lines JEG-3 (choricarcinoma) and FON (melanoma), and with the HLA-G negative cell lines M8 (melanoma) and U251MG (glioblastoma) showed that the HLA-G 3'UTR polymorphism influences the response to endogenous cellular factors and may vary according to the cell type. UTR-5 and UTR-7 impact the activity of luciferase the most whereas UTR-2, UTR-3, UTR-4, and UTR-18 have intermediate impact, and UTR-1 has the lowest impact. These results corroborate the previous associations between amounts of plasma sHLA-G levels and 3'UTR haplotypes in healthy individuals and reinforce that 3'UTR typing may be a predictor of the genetic predisposition of an individual to express different levels of HLA-G.</description><subject>3' Untranslated regions</subject><subject>3' Untranslated Regions - genetics</subject><subject>Allografts</subject><subject>Alternatives</subject><subject>Analysis</subject><subject>Base Pairing - genetics</subject><subject>Base Sequence</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>DNA methylation</subject><subject>Epidemiology</subject><subject>Fetuses</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Reporter</subject><subject>Genetics</subject><subject>Glioblastoma</subject><subject>Graft rejection</subject><subject>Haplotypes</subject><subject>Haplotypes - genetics</subject><subject>Histocompatibility antigen HLA</subject><subject>HLA antigens</subject><subject>HLA-G Antigens - genetics</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Immune checkpoint</subject><subject>Immunology</subject><subject>INDEL Mutation - genetics</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Luciferases - metabolism</subject><subject>Melanoma</subject><subject>MicroRNAs</subject><subject>Mutagenesis, Site-Directed</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Regulation</subject><subject>Regulatory sequences</subject><subject>Reporter gene</subject><subject>Research and Analysis Methods</subject><subject>Tissue typing</subject><subject>Transcription (Genetics)</subject><subject>Transcription factors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl-LEzEUxQdR3HX1G4gGBBWkNZM_M5MXodTd7UJBEPc53Jkk7ZQ0qcmMUPzyZtrZpRUffEpIfvfcew8ny17neJrTMv-88X1wYKc77_QU54XAlDzJLnNByaQgmD49uV9kL2LcYMxpVRTPswtSYcaFEJfZ7wXsrO_2Ox2RN6hba7RYzia3iH5A964L4KKFTiv0Xa9a79IRU0OFOo-unfIr7Xwf0Q00nQ8HhUP1JwSJOVwnaK6tRcvWpQ5fW2N00K5rwdr9y-yZARv1q_G8yu5vrn_MF5Plt9u7-Ww5aThNC3AGTKi0MjOiqJVQaa2SccIYUTUlnIAGzgyrCVBDGsOUYJTWWBU1plBX9Cp7e9RNm0Y5-hZlXnGOi0pwkoi7I6E8bOQutFsIe-mhlYcHH1YSQtc2VsscAEypsNGcM42hZhVnVUWKmpdGY5q0vozd-nqrVaMHF-2Z6PmPa9dy5X9JTnBZMpwEPo4Cwf_sdezkto1NMhGcTmYPcwtWCYz_C-WUVJUoE_ruL_TfRozUCtKurTM-jdgMonLGyoLQktNB6_0JtdZgu3X0tu9SQuI5yI5gE3yMQZtHG3IshxQ_DCGHFMsxxanszamFj0UPsaV_ACE0648</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Poras, Isabelle</creator><creator>Yaghi, Layale</creator><creator>Martelli-Palomino, Gustavo</creator><creator>Mendes-Junior, Celso T</creator><creator>Muniz, Yara Costa Netto</creator><creator>Cagnin, Natalia F</creator><creator>Sgorla de Almeida, Bibiana</creator><creator>Castelli, Erick C</creator><creator>Carosella, Edgardo D</creator><creator>Donadi, Eduardo A</creator><creator>Moreau, Philippe</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PIMPY</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20170101</creationdate><title>Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially</title><author>Poras, Isabelle ; Yaghi, Layale ; Martelli-Palomino, Gustavo ; Mendes-Junior, Celso T ; Muniz, Yara Costa Netto ; Cagnin, Natalia F ; Sgorla de Almeida, Bibiana ; Castelli, Erick C ; Carosella, Edgardo D ; Donadi, Eduardo A ; Moreau, Philippe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5332-54a49d3714f96bd9d1937452442db3252aea54f4b2a3f2cf4d9433b0d6b03ab83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>3' Untranslated regions</topic><topic>3' Untranslated Regions - genetics</topic><topic>Allografts</topic><topic>Alternatives</topic><topic>Analysis</topic><topic>Base Pairing - genetics</topic><topic>Base Sequence</topic><topic>Biology and Life Sciences</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>DNA methylation</topic><topic>Epidemiology</topic><topic>Fetuses</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Reporter</topic><topic>Genetics</topic><topic>Glioblastoma</topic><topic>Graft rejection</topic><topic>Haplotypes</topic><topic>Haplotypes - genetics</topic><topic>Histocompatibility antigen HLA</topic><topic>HLA antigens</topic><topic>HLA-G Antigens - genetics</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Immune checkpoint</topic><topic>Immunology</topic><topic>INDEL Mutation - genetics</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Luciferases - metabolism</topic><topic>Melanoma</topic><topic>MicroRNAs</topic><topic>Mutagenesis, Site-Directed</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Regulation</topic><topic>Regulatory sequences</topic><topic>Reporter gene</topic><topic>Research and Analysis Methods</topic><topic>Tissue typing</topic><topic>Transcription (Genetics)</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Poras, Isabelle</creatorcontrib><creatorcontrib>Yaghi, Layale</creatorcontrib><creatorcontrib>Martelli-Palomino, Gustavo</creatorcontrib><creatorcontrib>Mendes-Junior, Celso T</creatorcontrib><creatorcontrib>Muniz, Yara Costa Netto</creatorcontrib><creatorcontrib>Cagnin, Natalia F</creatorcontrib><creatorcontrib>Sgorla de Almeida, Bibiana</creatorcontrib><creatorcontrib>Castelli, Erick C</creatorcontrib><creatorcontrib>Carosella, Edgardo D</creatorcontrib><creatorcontrib>Donadi, Eduardo A</creatorcontrib><creatorcontrib>Moreau, Philippe</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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 Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</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>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Poras, Isabelle</au><au>Yaghi, Layale</au><au>Martelli-Palomino, Gustavo</au><au>Mendes-Junior, Celso T</au><au>Muniz, Yara Costa Netto</au><au>Cagnin, Natalia F</au><au>Sgorla de Almeida, Bibiana</au><au>Castelli, Erick C</au><au>Carosella, Edgardo D</au><au>Donadi, Eduardo A</au><au>Moreau, Philippe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>12</volume><issue>1</issue><spage>e0169032</spage><epage>e0169032</epage><pages>e0169032-e0169032</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The immune checkpoint HLA-G prevents maternal rejection of the fetus and contributes in cancer invasion and acceptance of allografts. The 5' and 3' regulatory regions of the HLA-G gene are polymorphic and balancing selection probably maintains this variability. It is proposed that nucleotide variations may affect the level of HLA-G expression. To investigate this issue we aimed to analyze how haplotypes of the 3' untranslated region (3'UTR) with highest worldwide frequencies, namely UTR-1, UTR-2, UTR-3, UTR-4, UTR-5, UTR-18 and UTR-7, impact the expression of a luciferase reporter gene in vitro. Experiments performed with the HLA-G positive cell lines JEG-3 (choricarcinoma) and FON (melanoma), and with the HLA-G negative cell lines M8 (melanoma) and U251MG (glioblastoma) showed that the HLA-G 3'UTR polymorphism influences the response to endogenous cellular factors and may vary according to the cell type. UTR-5 and UTR-7 impact the activity of luciferase the most whereas UTR-2, UTR-3, UTR-4, and UTR-18 have intermediate impact, and UTR-1 has the lowest impact. These results corroborate the previous associations between amounts of plasma sHLA-G levels and 3'UTR haplotypes in healthy individuals and reinforce that 3'UTR typing may be a predictor of the genetic predisposition of an individual to express different levels of HLA-G.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28045999</pmid><doi>10.1371/journal.pone.0169032</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-01, Vol.12 (1), p.e0169032-e0169032 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1855068952 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | 3' Untranslated regions 3' Untranslated Regions - genetics Allografts Alternatives Analysis Base Pairing - genetics Base Sequence Biology and Life Sciences Biotechnology Cancer Cell Line, Tumor DNA methylation Epidemiology Fetuses Gene expression Gene Expression Regulation, Neoplastic Genes, Reporter Genetics Glioblastoma Graft rejection Haplotypes Haplotypes - genetics Histocompatibility antigen HLA HLA antigens HLA-G Antigens - genetics Humans Hypoxia Immune checkpoint Immunology INDEL Mutation - genetics Infections Infectious diseases Luciferases - metabolism Melanoma MicroRNAs Mutagenesis, Site-Directed Polymorphism Polymorphism, Genetic Regulation Regulatory sequences Reporter gene Research and Analysis Methods Tissue typing Transcription (Genetics) Transcription factors |
| title | Haplotypes of the HLA-G 3' Untranslated Region Respond to Endogenous Factors of HLA-G+ and HLA-G- Cell Lines Differentially |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T17%3A14%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Haplotypes%20of%20the%20HLA-G%203'%20Untranslated%20Region%20Respond%20to%20Endogenous%20Factors%20of%20HLA-G+%20and%20HLA-G-%20Cell%20Lines%20Differentially&rft.jtitle=PloS%20one&rft.au=Poras,%20Isabelle&rft.date=2017-01-01&rft.volume=12&rft.issue=1&rft.spage=e0169032&rft.epage=e0169032&rft.pages=e0169032-e0169032&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0169032&rft_dat=%3Cgale_plos_%3EA476237537%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1855068952&rft_id=info:pmid/28045999&rft_galeid=A476237537&rft_doaj_id=oai_doaj_org_article_1aaaf7d0fe554e0ab48548826b57fe03&rfr_iscdi=true |