Cloning and Characterization of Three Novel Genes, ALS2CR1, ALS2CR2, and ALS2CR3, in the Juvenile Amyotrophic Lateral Sclerosis (ALS2) Critical Region at Chromosome 2q33–q34: Candidate Genes for ALS2
Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that manifests as selective upper and lower motor neuron degeneration. The autosomal recessive form of juvenile amyotrophic lateral sclerosis (ALS2) has previously been mapped to the 1.7-cM interval flanked by D2S116 and D2S223...
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| Veröffentlicht in: | Genomics (San Diego, Calif.) Calif.), 2001-01, Vol.71 (2), p.200-213 |
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| creator | Hadano, Shinji Yanagisawa, Yoshiko Skaug, Jennifer Fichter, Keith Nasir, Jamal Martindale, Duane Koop, Ben F. Scherer, Stephen W. Nicholson, Donald W. Rouleau, Guy A. Ikeda, Joh-E Hayden, Michael R. |
| description | Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that manifests as selective upper and lower motor neuron degeneration. The autosomal recessive form of juvenile amyotrophic lateral sclerosis (ALS2) has previously been mapped to the 1.7-cM interval flanked by D2S116 and D2S2237 on human chromosome 2q33–q34. We identified three novel full-length transcripts encoded by three distinct genes (HGMW-approved symbols ALS2CR1, ALS2CR2, and ALS2CR3) within the ALS2 critical region. The intron–exon organizations of these genes as well as those of CFLAR, CASP10, and CASP8, which were previously mapped to this region, were defined. These genes were evaluated for mutations in ALS2 patients, and no disease-associated sequence alterations in either exons or intron–exon boundaries were observed. Sequence analysis of overlapping RT-PCR products covering the whole coding sequence for each transcript revealed no aberrant mRNA sequences. These data strongly indicate that ALS2CR1, ALS2CR2, ALS2CR3, CFLAR, CASP10, and CASP8 are not causative genes for ALS2. |
| doi_str_mv | 10.1006/geno.2000.6392 |
| format | Article |
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The autosomal recessive form of juvenile amyotrophic lateral sclerosis (ALS2) has previously been mapped to the 1.7-cM interval flanked by D2S116 and D2S2237 on human chromosome 2q33–q34. We identified three novel full-length transcripts encoded by three distinct genes (HGMW-approved symbols ALS2CR1, ALS2CR2, and ALS2CR3) within the ALS2 critical region. The intron–exon organizations of these genes as well as those of CFLAR, CASP10, and CASP8, which were previously mapped to this region, were defined. These genes were evaluated for mutations in ALS2 patients, and no disease-associated sequence alterations in either exons or intron–exon boundaries were observed. Sequence analysis of overlapping RT-PCR products covering the whole coding sequence for each transcript revealed no aberrant mRNA sequences. These data strongly indicate that ALS2CR1, ALS2CR2, ALS2CR3, CFLAR, CASP10, and CASP8 are not causative genes for ALS2.</description><identifier>ISSN: 0888-7543</identifier><identifier>EISSN: 1089-8646</identifier><identifier>DOI: 10.1006/geno.2000.6392</identifier><identifier>PMID: 11161814</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>Adaptor Proteins, Signal Transducing ; ALS2CR1 gene ; ALS2CR2 gene ; ALS2CR3 gene ; Amyotrophic Lateral Sclerosis - genetics ; Base Sequence ; Biological and medical sciences ; Brain - metabolism ; Carrier Proteins ; CASP10 gene ; CASP8 and FADD-Like Apoptosis Regulating Protein ; CASP8 gene ; Caspase 10 ; Caspase 8 ; Caspase 9 ; Caspases - genetics ; CFLAR gene ; Chromosomes, Human, Pair 2 - genetics ; Cloning, Molecular ; Consensus Sequence ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; DNA Mutational Analysis ; Gene Library ; Humans ; Intracellular Signaling Peptides and Proteins ; Medical sciences ; Molecular Sequence Data ; Nerve Tissue Proteins - genetics ; Neurology ; Physical Chromosome Mapping ; Proteins ; RNA, Messenger - genetics</subject><ispartof>Genomics (San Diego, Calif.), 2001-01, Vol.71 (2), p.200-213</ispartof><rights>2001 Academic Press</rights><rights>2001 INIST-CNRS</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-eee9110869b7ea05f7ffb3cae5528e10a00b4c05da78250992234972c02ae3783</citedby><cites>FETCH-LOGICAL-c399t-eee9110869b7ea05f7ffb3cae5528e10a00b4c05da78250992234972c02ae3783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0888754300963924$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=990856$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11161814$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hadano, Shinji</creatorcontrib><creatorcontrib>Yanagisawa, Yoshiko</creatorcontrib><creatorcontrib>Skaug, Jennifer</creatorcontrib><creatorcontrib>Fichter, Keith</creatorcontrib><creatorcontrib>Nasir, Jamal</creatorcontrib><creatorcontrib>Martindale, Duane</creatorcontrib><creatorcontrib>Koop, Ben F.</creatorcontrib><creatorcontrib>Scherer, Stephen W.</creatorcontrib><creatorcontrib>Nicholson, Donald W.</creatorcontrib><creatorcontrib>Rouleau, Guy A.</creatorcontrib><creatorcontrib>Ikeda, Joh-E</creatorcontrib><creatorcontrib>Hayden, Michael R.</creatorcontrib><title>Cloning and Characterization of Three Novel Genes, ALS2CR1, ALS2CR2, and ALS2CR3, in the Juvenile Amyotrophic Lateral Sclerosis (ALS2) Critical Region at Chromosome 2q33–q34: Candidate Genes for ALS2</title><title>Genomics (San Diego, Calif.)</title><addtitle>Genomics</addtitle><description>Amyotrophic lateral sclerosis is a progressive neurodegenerative disease that manifests as selective upper and lower motor neuron degeneration. The autosomal recessive form of juvenile amyotrophic lateral sclerosis (ALS2) has previously been mapped to the 1.7-cM interval flanked by D2S116 and D2S2237 on human chromosome 2q33–q34. We identified three novel full-length transcripts encoded by three distinct genes (HGMW-approved symbols ALS2CR1, ALS2CR2, and ALS2CR3) within the ALS2 critical region. The intron–exon organizations of these genes as well as those of CFLAR, CASP10, and CASP8, which were previously mapped to this region, were defined. These genes were evaluated for mutations in ALS2 patients, and no disease-associated sequence alterations in either exons or intron–exon boundaries were observed. Sequence analysis of overlapping RT-PCR products covering the whole coding sequence for each transcript revealed no aberrant mRNA sequences. These data strongly indicate that ALS2CR1, ALS2CR2, ALS2CR3, CFLAR, CASP10, and CASP8 are not causative genes for ALS2.</description><subject>Adaptor Proteins, Signal Transducing</subject><subject>ALS2CR1 gene</subject><subject>ALS2CR2 gene</subject><subject>ALS2CR3 gene</subject><subject>Amyotrophic Lateral Sclerosis - genetics</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Brain - metabolism</subject><subject>Carrier Proteins</subject><subject>CASP10 gene</subject><subject>CASP8 and FADD-Like Apoptosis Regulating Protein</subject><subject>CASP8 gene</subject><subject>Caspase 10</subject><subject>Caspase 8</subject><subject>Caspase 9</subject><subject>Caspases - genetics</subject><subject>CFLAR gene</subject><subject>Chromosomes, Human, Pair 2 - genetics</subject><subject>Cloning, Molecular</subject><subject>Consensus Sequence</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>DNA Mutational Analysis</subject><subject>Gene Library</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>Nerve Tissue Proteins - genetics</subject><subject>Neurology</subject><subject>Physical Chromosome Mapping</subject><subject>Proteins</subject><subject>RNA, Messenger - genetics</subject><issn>0888-7543</issn><issn>1089-8646</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2KFDEUhYMoTju6dSkBQRS62vzUTzK7ptBRaRRmxnVIp251R6qS7qS6YVz5Dj6Vr-GTmJpqdSWukpDvnnM5B6GnlCwoIeXrDTi_YISQRcklu4dmlAiZiTIv76MZEUJkVZHzM_Qoxi-Jklywh-iMUlpSQfMZ-lF33lm3wdo1uN7qoM0AwX7Vg_UO-xbfbAMA_uiP0OFLcBDneLm6ZvUV_X1h87vh6cHn2Do8bAF_OBzB2Q7wsr_1Q_C7rTV4pZO67vC16SD4aCN-Oc69wnWwgzXp5wo2o7Me0jbB9z76HjDbc_7z2_c9zy9wncxsk3SmdXDrw533Y_Sg1V2EJ6fzHH1---amfpetPl2-r5erzHAphwwAJE0hlXJdgSZFW7XtmhsNRcEEUKIJWeeGFI2uBCuIlIzxXFbMEKaBV4KfoxeT7i74_QHioHobDXSdduAPUVWk5CwX5L8grQQRvOIJXEygSZHEAK3aBdvrcKsoUWPLamxZjS2rseU08OykfFj30PzFT7Um4PkJ0DGF2gbtjI1_OCmJKMpEiYmCFNfRQlDRWHAGGhvADKrx9l8b_AJ0x8B4</recordid><startdate>20010115</startdate><enddate>20010115</enddate><creator>Hadano, Shinji</creator><creator>Yanagisawa, Yoshiko</creator><creator>Skaug, Jennifer</creator><creator>Fichter, Keith</creator><creator>Nasir, Jamal</creator><creator>Martindale, Duane</creator><creator>Koop, Ben F.</creator><creator>Scherer, Stephen W.</creator><creator>Nicholson, Donald W.</creator><creator>Rouleau, Guy A.</creator><creator>Ikeda, Joh-E</creator><creator>Hayden, Michael R.</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20010115</creationdate><title>Cloning and Characterization of Three Novel Genes, ALS2CR1, ALS2CR2, and ALS2CR3, in the Juvenile Amyotrophic Lateral Sclerosis (ALS2) Critical Region at Chromosome 2q33–q34: Candidate Genes for ALS2</title><author>Hadano, Shinji ; Yanagisawa, Yoshiko ; Skaug, Jennifer ; Fichter, Keith ; Nasir, Jamal ; Martindale, Duane ; Koop, Ben F. ; Scherer, Stephen W. ; Nicholson, Donald W. ; Rouleau, Guy A. ; Ikeda, Joh-E ; Hayden, Michael R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-eee9110869b7ea05f7ffb3cae5528e10a00b4c05da78250992234972c02ae3783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adaptor Proteins, Signal Transducing</topic><topic>ALS2CR1 gene</topic><topic>ALS2CR2 gene</topic><topic>ALS2CR3 gene</topic><topic>Amyotrophic Lateral Sclerosis - genetics</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Brain - metabolism</topic><topic>Carrier Proteins</topic><topic>CASP10 gene</topic><topic>CASP8 and FADD-Like Apoptosis Regulating Protein</topic><topic>CASP8 gene</topic><topic>Caspase 10</topic><topic>Caspase 8</topic><topic>Caspase 9</topic><topic>Caspases - genetics</topic><topic>CFLAR gene</topic><topic>Chromosomes, Human, Pair 2 - genetics</topic><topic>Cloning, Molecular</topic><topic>Consensus Sequence</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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The autosomal recessive form of juvenile amyotrophic lateral sclerosis (ALS2) has previously been mapped to the 1.7-cM interval flanked by D2S116 and D2S2237 on human chromosome 2q33–q34. We identified three novel full-length transcripts encoded by three distinct genes (HGMW-approved symbols ALS2CR1, ALS2CR2, and ALS2CR3) within the ALS2 critical region. The intron–exon organizations of these genes as well as those of CFLAR, CASP10, and CASP8, which were previously mapped to this region, were defined. These genes were evaluated for mutations in ALS2 patients, and no disease-associated sequence alterations in either exons or intron–exon boundaries were observed. Sequence analysis of overlapping RT-PCR products covering the whole coding sequence for each transcript revealed no aberrant mRNA sequences. These data strongly indicate that ALS2CR1, ALS2CR2, ALS2CR3, CFLAR, CASP10, and CASP8 are not causative genes for ALS2.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>11161814</pmid><doi>10.1006/geno.2000.6392</doi><tpages>14</tpages></addata></record> |
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| ispartof | Genomics (San Diego, Calif.), 2001-01, Vol.71 (2), p.200-213 |
| issn | 0888-7543 1089-8646 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adaptor Proteins, Signal Transducing ALS2CR1 gene ALS2CR2 gene ALS2CR3 gene Amyotrophic Lateral Sclerosis - genetics Base Sequence Biological and medical sciences Brain - metabolism Carrier Proteins CASP10 gene CASP8 and FADD-Like Apoptosis Regulating Protein CASP8 gene Caspase 10 Caspase 8 Caspase 9 Caspases - genetics CFLAR gene Chromosomes, Human, Pair 2 - genetics Cloning, Molecular Consensus Sequence Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases DNA Mutational Analysis Gene Library Humans Intracellular Signaling Peptides and Proteins Medical sciences Molecular Sequence Data Nerve Tissue Proteins - genetics Neurology Physical Chromosome Mapping Proteins RNA, Messenger - genetics |
| title | Cloning and Characterization of Three Novel Genes, ALS2CR1, ALS2CR2, and ALS2CR3, in the Juvenile Amyotrophic Lateral Sclerosis (ALS2) Critical Region at Chromosome 2q33–q34: Candidate Genes for ALS2 |
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