Equine severe combined immunodeficiency: a defect in V(D)J recombination and DNA-dependent protein kinase activity
V(D)J rearrangement is the molecular mechanism by which an almost infinite array of specific immune receptors are generated. Defects in this process result in profound immunodeficiency as is the case in the C.B-17 SCID mouse or in RAG-1 (recombination-activating gene 1) or RAG-2 deficient mice. It h...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 1995-12, Vol.92 (25), p.11485-11489 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Wiler, R. (DNAX Corporation, Palo Alto, CA.) Leber, R Moore, B.B VanDyk, L.F Perryman, L.E Meek, K |
| description | V(D)J rearrangement is the molecular mechanism by which an almost infinite array of specific immune receptors are generated. Defects in this process result in profound immunodeficiency as is the case in the C.B-17 SCID mouse or in RAG-1 (recombination-activating gene 1) or RAG-2 deficient mice. It has recently become clear that the V(D)J recombinase most likely consists of both lymphoid-specific factors and ubiquitously expressed components of the DNA double-strand break repair pathway. The deficit in SCID mice is in a factor that is required for both of these pathways. In this report, we show that the factor defective in the autosomal recessive severe combined immunodeficiency of Arabian foals is required for (i) V(D)J recombination, (ii) resistance to ionizing radiation, and (iii) DNA-dependent protein kinase activity. |
| doi_str_mv | 10.1073/pnas.92.25.11485 |
| format | Article |
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(DNAX Corporation, Palo Alto, CA.) ; Leber, R ; Moore, B.B ; VanDyk, L.F ; Perryman, L.E ; Meek, K</creator><creatorcontrib>Wiler, R. (DNAX Corporation, Palo Alto, CA.) ; Leber, R ; Moore, B.B ; VanDyk, L.F ; Perryman, L.E ; Meek, K</creatorcontrib><description>V(D)J rearrangement is the molecular mechanism by which an almost infinite array of specific immune receptors are generated. Defects in this process result in profound immunodeficiency as is the case in the C.B-17 SCID mouse or in RAG-1 (recombination-activating gene 1) or RAG-2 deficient mice. It has recently become clear that the V(D)J recombinase most likely consists of both lymphoid-specific factors and ubiquitously expressed components of the DNA double-strand break repair pathway. The deficit in SCID mice is in a factor that is required for both of these pathways. In this report, we show that the factor defective in the autosomal recessive severe combined immunodeficiency of Arabian foals is required for (i) V(D)J recombination, (ii) resistance to ionizing radiation, and (iii) DNA-dependent protein kinase activity.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.92.25.11485</identifier><identifier>PMID: 8524788</identifier><language>eng</language><publisher>United States: National Academy of Sciences of the United States of America</publisher><subject>ADN ; Animals ; Base Sequence ; Biochemistry ; CABALLOS ; Cell Line ; Cell lines ; CHEVAL ; CHO Cells ; Cricetinae ; DEFAUT ; DEFECTOS ; DEFICIENCE IMMUNOLOGIQUE ; DEFICIENCIA INMUNOLOGICA ; DNA ; DNA Nucleotidyltransferases - genetics ; DNA-Activated Protein Kinase ; DNA-Binding Proteins ; Fibroblasts ; Fibroblasts - radiation effects ; Foals ; GENE ; Gene Rearrangement ; GENES ; Genes, Recessive ; Genetic mutation ; Homeodomain Proteins ; Horse Diseases - genetics ; Horses ; Immunity (Disease) ; Immunoblotting ; IMMUNOGLOBULINE ; INMUNOGLOBULINA ; Ligation ; Mice ; Mice, SCID - genetics ; Molecular Sequence Data ; MUTACION ; MUTATION ; Phenotype ; Polymerase Chain Reaction ; Protein-Serine-Threonine Kinases - genetics ; PROTEINA QUINASA ; PROTEINE KINASE ; Proteins ; Proteins - genetics ; RACE (ANIMAL) ; RADIACION IONIZANTE ; RADIATION IONISANTE ; Radiation Tolerance - genetics ; RAZAS (ANIMALES) ; RECOMBINACION ; RECOMBINAISON ; Recombination, Genetic ; Severe combined immunodeficiency ; Severe Combined Immunodeficiency - genetics ; Severe Combined Immunodeficiency - veterinary ; TRASTORNOS GENETICOS ; TROUBLE GENETIQUE ; VDJ Recombinases</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 1995-12, Vol.92 (25), p.11485-11489</ispartof><rights>Copyright 1995 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Dec 5, 1995</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c610t-e40ed17dfaa7f67ad64f63078cea57d2cd457291c92c8f0d25dd752b394c35313</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/92/25.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/2368922$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/2368922$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27903,27904,53770,53772,57996,58229</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8524788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wiler, R. (DNAX Corporation, Palo Alto, CA.)</creatorcontrib><creatorcontrib>Leber, R</creatorcontrib><creatorcontrib>Moore, B.B</creatorcontrib><creatorcontrib>VanDyk, L.F</creatorcontrib><creatorcontrib>Perryman, L.E</creatorcontrib><creatorcontrib>Meek, K</creatorcontrib><title>Equine severe combined immunodeficiency: a defect in V(D)J recombination and DNA-dependent protein kinase activity</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>V(D)J rearrangement is the molecular mechanism by which an almost infinite array of specific immune receptors are generated. Defects in this process result in profound immunodeficiency as is the case in the C.B-17 SCID mouse or in RAG-1 (recombination-activating gene 1) or RAG-2 deficient mice. It has recently become clear that the V(D)J recombinase most likely consists of both lymphoid-specific factors and ubiquitously expressed components of the DNA double-strand break repair pathway. The deficit in SCID mice is in a factor that is required for both of these pathways. In this report, we show that the factor defective in the autosomal recessive severe combined immunodeficiency of Arabian foals is required for (i) V(D)J recombination, (ii) resistance to ionizing radiation, and (iii) DNA-dependent protein kinase activity.</description><subject>ADN</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biochemistry</subject><subject>CABALLOS</subject><subject>Cell Line</subject><subject>Cell lines</subject><subject>CHEVAL</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>DEFAUT</subject><subject>DEFECTOS</subject><subject>DEFICIENCE IMMUNOLOGIQUE</subject><subject>DEFICIENCIA INMUNOLOGICA</subject><subject>DNA</subject><subject>DNA Nucleotidyltransferases - genetics</subject><subject>DNA-Activated Protein Kinase</subject><subject>DNA-Binding Proteins</subject><subject>Fibroblasts</subject><subject>Fibroblasts - radiation effects</subject><subject>Foals</subject><subject>GENE</subject><subject>Gene Rearrangement</subject><subject>GENES</subject><subject>Genes, Recessive</subject><subject>Genetic mutation</subject><subject>Homeodomain Proteins</subject><subject>Horse Diseases - genetics</subject><subject>Horses</subject><subject>Immunity (Disease)</subject><subject>Immunoblotting</subject><subject>IMMUNOGLOBULINE</subject><subject>INMUNOGLOBULINA</subject><subject>Ligation</subject><subject>Mice</subject><subject>Mice, SCID - genetics</subject><subject>Molecular Sequence Data</subject><subject>MUTACION</subject><subject>MUTATION</subject><subject>Phenotype</subject><subject>Polymerase Chain Reaction</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>PROTEINA QUINASA</subject><subject>PROTEINE KINASE</subject><subject>Proteins</subject><subject>Proteins - genetics</subject><subject>RACE (ANIMAL)</subject><subject>RADIACION IONIZANTE</subject><subject>RADIATION IONISANTE</subject><subject>Radiation Tolerance - genetics</subject><subject>RAZAS (ANIMALES)</subject><subject>RECOMBINACION</subject><subject>RECOMBINAISON</subject><subject>Recombination, Genetic</subject><subject>Severe combined immunodeficiency</subject><subject>Severe Combined Immunodeficiency - genetics</subject><subject>Severe Combined Immunodeficiency - veterinary</subject><subject>TRASTORNOS GENETICOS</subject><subject>TROUBLE GENETIQUE</subject><subject>VDJ Recombinases</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1vEzEQxVcIVELhjhAIiwMqhw3-XO8iLlVbvlTBAcrVcuzZ4rJrp7Y3Iv89DglR4QCn0ej93mhmXlU9JHhOsGQvl16neUfnVMwJ4a24Vc0I7kjd8A7frmYYU1m3nPK71b2UrjDGnWjxQXXQCspl286qeHY9OQ8owQoiIBPGRWktcuM4-WChd8aBN-tXSKPSgcnIefT16PTFBxRhi-vsgkfaW3T68bi2sARvwWe0jCFDob8XJAHSJruVy-v71Z1eDwke7OphdfHm7MvJu_r809v3J8fntWkIzjVwDJZI22st-0Zq2_C-YVi2BrSQlhrLhaQdMR01bY8tFdZKQRes44YJRthh9Xo7dzktRrCmrBT1oJbRjTquVdBO_al4901dhpXimNOm2J_v7DFcT5CyGl0yMAzaQ5iSklIyRgn_L0gkprxpuwI--wu8ClP05QeKYsJox7EoEN5CJoaUIvT7hQlWm8zVJnPVUUWF-pV5sTy5eejesAu56Ec7feP8rd6YoPppGDL8yAV9-m-0EI-3xFXKIe4RysqFlBb50VbudVD6MrqkLj53TflAS9lP6RXTbA</recordid><startdate>19951205</startdate><enddate>19951205</enddate><creator>Wiler, R. 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(DNAX Corporation, Palo Alto, CA.)</au><au>Leber, R</au><au>Moore, B.B</au><au>VanDyk, L.F</au><au>Perryman, L.E</au><au>Meek, K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Equine severe combined immunodeficiency: a defect in V(D)J recombination and DNA-dependent protein kinase activity</atitle><jtitle>Proceedings of the National Academy of Sciences - PNAS</jtitle><addtitle>Proc Natl Acad Sci U S A</addtitle><date>1995-12-05</date><risdate>1995</risdate><volume>92</volume><issue>25</issue><spage>11485</spage><epage>11489</epage><pages>11485-11489</pages><issn>0027-8424</issn><eissn>1091-6490</eissn><abstract>V(D)J rearrangement is the molecular mechanism by which an almost infinite array of specific immune receptors are generated. Defects in this process result in profound immunodeficiency as is the case in the C.B-17 SCID mouse or in RAG-1 (recombination-activating gene 1) or RAG-2 deficient mice. It has recently become clear that the V(D)J recombinase most likely consists of both lymphoid-specific factors and ubiquitously expressed components of the DNA double-strand break repair pathway. The deficit in SCID mice is in a factor that is required for both of these pathways. In this report, we show that the factor defective in the autosomal recessive severe combined immunodeficiency of Arabian foals is required for (i) V(D)J recombination, (ii) resistance to ionizing radiation, and (iii) DNA-dependent protein kinase activity.</abstract><cop>United States</cop><pub>National Academy of Sciences of the United States of America</pub><pmid>8524788</pmid><doi>10.1073/pnas.92.25.11485</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0027-8424 |
| ispartof | Proceedings of the National Academy of Sciences - PNAS, 1995-12, Vol.92 (25), p.11485-11489 |
| issn | 0027-8424 1091-6490 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_17024689 |
| source | MEDLINE; Jstor Complete Legacy; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry |
| subjects | ADN Animals Base Sequence Biochemistry CABALLOS Cell Line Cell lines CHEVAL CHO Cells Cricetinae DEFAUT DEFECTOS DEFICIENCE IMMUNOLOGIQUE DEFICIENCIA INMUNOLOGICA DNA DNA Nucleotidyltransferases - genetics DNA-Activated Protein Kinase DNA-Binding Proteins Fibroblasts Fibroblasts - radiation effects Foals GENE Gene Rearrangement GENES Genes, Recessive Genetic mutation Homeodomain Proteins Horse Diseases - genetics Horses Immunity (Disease) Immunoblotting IMMUNOGLOBULINE INMUNOGLOBULINA Ligation Mice Mice, SCID - genetics Molecular Sequence Data MUTACION MUTATION Phenotype Polymerase Chain Reaction Protein-Serine-Threonine Kinases - genetics PROTEINA QUINASA PROTEINE KINASE Proteins Proteins - genetics RACE (ANIMAL) RADIACION IONIZANTE RADIATION IONISANTE Radiation Tolerance - genetics RAZAS (ANIMALES) RECOMBINACION RECOMBINAISON Recombination, Genetic Severe combined immunodeficiency Severe Combined Immunodeficiency - genetics Severe Combined Immunodeficiency - veterinary TRASTORNOS GENETICOS TROUBLE GENETIQUE VDJ Recombinases |
| title | Equine severe combined immunodeficiency: a defect in V(D)J recombination and DNA-dependent protein kinase activity |
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