Computational definition of sequence motifs governing constitutive exon splicing.
Identifieur interne : 002390 ( PubMed/Corpus ); précédent : 002389; suivant : 002391Computational definition of sequence motifs governing constitutive exon splicing.
Auteurs : Xiang H-F Zhang ; Lawrence A. ChasinSource :
- Genes & development [ 0890-9369 ] ; 2004.
English descriptors
- KwdEn :
- 5' Untranslated Regions, Animals, Base Sequence, Cells, Cultured, Computer Simulation, Enhancer Elements, Genetic, Exons, Genes, Humans, I-kappa B Kinase, Introns, Mammals, Models, Genetic, Molecular Sequence Data, Mutation, Protein-Serine-Threonine Kinases (genetics), RNA Splicing, Regulatory Sequences, Ribonucleic Acid, Silencer Elements, Transcriptional, Transfection.
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical : 5' Untranslated Regions, I-kappa B Kinase, Regulatory Sequences, Ribonucleic Acid.
- Animals, Base Sequence, Cells, Cultured, Computer Simulation, Enhancer Elements, Genetic, Exons, Genes, Humans, Introns, Mammals, Models, Genetic, Molecular Sequence Data, Mutation, RNA Splicing, Silencer Elements, Transcriptional, Transfection.
Abstract
We have searched for sequence motifs that contribute to the recognition of human pre-mRNA splice sites by comparing the frequency of 8-mers in internal noncoding exons versus unspliced pseudo exons and 5' untranslated regions (5' untranslated regions [UTRs]) of transcripts of intronless genes. This type of comparison avoids the isolation of sequences that are distinguished by their protein-coding information. We classified sequence families comprising 2069 putative exonic enhancers and 974 putative exonic silencers. Representatives of each class functioned as enhancers or silencers when inserted into a test exon and assayed in transfected mammalian cells. As a class, the enhancer sequencers were more prevalent and the silencer elements less prevalent in all exons compared with introns. A survey of 58 reported exonic splicing mutations showed good agreement between the splicing phenotype and the effect of the mutation on the motifs defined here. The large number of effective sequences implied by these results suggests that sequences that influence splicing may be very abundant in pre-mRNA.
DOI: 10.1101/gad.1195304
PubMed: 15145827
Links to Exploration step
pubmed:15145827Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Computational definition of sequence motifs governing constitutive exon splicing.</title>
<author><name sortKey="Zhang, Xiang H F" sort="Zhang, Xiang H F" uniqKey="Zhang X" first="Xiang H-F" last="Zhang">Xiang H-F Zhang</name>
<affiliation><nlm:affiliation>Department of Biological Sciences, MC2433, Columbia University, New York, New York 10027, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Chasin, Lawrence A" sort="Chasin, Lawrence A" uniqKey="Chasin L" first="Lawrence A" last="Chasin">Lawrence A. Chasin</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2004">2004</date>
<idno type="RBID">pubmed:15145827</idno>
<idno type="pmid">15145827</idno>
<idno type="doi">10.1101/gad.1195304</idno>
<idno type="wicri:Area/PubMed/Corpus">002390</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002390</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Computational definition of sequence motifs governing constitutive exon splicing.</title>
<author><name sortKey="Zhang, Xiang H F" sort="Zhang, Xiang H F" uniqKey="Zhang X" first="Xiang H-F" last="Zhang">Xiang H-F Zhang</name>
<affiliation><nlm:affiliation>Department of Biological Sciences, MC2433, Columbia University, New York, New York 10027, USA.</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Chasin, Lawrence A" sort="Chasin, Lawrence A" uniqKey="Chasin L" first="Lawrence A" last="Chasin">Lawrence A. Chasin</name>
</author>
</analytic>
<series><title level="j">Genes & development</title>
<idno type="ISSN">0890-9369</idno>
<imprint><date when="2004" type="published">2004</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5' Untranslated Regions</term>
<term>Animals</term>
<term>Base Sequence</term>
<term>Cells, Cultured</term>
<term>Computer Simulation</term>
<term>Enhancer Elements, Genetic</term>
<term>Exons</term>
<term>Genes</term>
<term>Humans</term>
<term>I-kappa B Kinase</term>
<term>Introns</term>
<term>Mammals</term>
<term>Models, Genetic</term>
<term>Molecular Sequence Data</term>
<term>Mutation</term>
<term>Protein-Serine-Threonine Kinases (genetics)</term>
<term>RNA Splicing</term>
<term>Regulatory Sequences, Ribonucleic Acid</term>
<term>Silencer Elements, Transcriptional</term>
<term>Transfection</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>5' Untranslated Regions</term>
<term>I-kappa B Kinase</term>
<term>Regulatory Sequences, Ribonucleic Acid</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Base Sequence</term>
<term>Cells, Cultured</term>
<term>Computer Simulation</term>
<term>Enhancer Elements, Genetic</term>
<term>Exons</term>
<term>Genes</term>
<term>Humans</term>
<term>Introns</term>
<term>Mammals</term>
<term>Models, Genetic</term>
<term>Molecular Sequence Data</term>
<term>Mutation</term>
<term>RNA Splicing</term>
<term>Silencer Elements, Transcriptional</term>
<term>Transfection</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">We have searched for sequence motifs that contribute to the recognition of human pre-mRNA splice sites by comparing the frequency of 8-mers in internal noncoding exons versus unspliced pseudo exons and 5' untranslated regions (5' untranslated regions [UTRs]) of transcripts of intronless genes. This type of comparison avoids the isolation of sequences that are distinguished by their protein-coding information. We classified sequence families comprising 2069 putative exonic enhancers and 974 putative exonic silencers. Representatives of each class functioned as enhancers or silencers when inserted into a test exon and assayed in transfected mammalian cells. As a class, the enhancer sequencers were more prevalent and the silencer elements less prevalent in all exons compared with introns. A survey of 58 reported exonic splicing mutations showed good agreement between the splicing phenotype and the effect of the mutation on the motifs defined here. The large number of effective sequences implied by these results suggests that sequences that influence splicing may be very abundant in pre-mRNA.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15145827</PMID>
<DateCompleted><Year>2004</Year>
<Month>07</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0890-9369</ISSN>
<JournalIssue CitedMedium="Print"><Volume>18</Volume>
<Issue>11</Issue>
<PubDate><Year>2004</Year>
<Month>Jun</Month>
<Day>01</Day>
</PubDate>
</JournalIssue>
<Title>Genes & development</Title>
<ISOAbbreviation>Genes Dev.</ISOAbbreviation>
</Journal>
<ArticleTitle>Computational definition of sequence motifs governing constitutive exon splicing.</ArticleTitle>
<Pagination><MedlinePgn>1241-50</MedlinePgn>
</Pagination>
<Abstract><AbstractText>We have searched for sequence motifs that contribute to the recognition of human pre-mRNA splice sites by comparing the frequency of 8-mers in internal noncoding exons versus unspliced pseudo exons and 5' untranslated regions (5' untranslated regions [UTRs]) of transcripts of intronless genes. This type of comparison avoids the isolation of sequences that are distinguished by their protein-coding information. We classified sequence families comprising 2069 putative exonic enhancers and 974 putative exonic silencers. Representatives of each class functioned as enhancers or silencers when inserted into a test exon and assayed in transfected mammalian cells. As a class, the enhancer sequencers were more prevalent and the silencer elements less prevalent in all exons compared with introns. A survey of 58 reported exonic splicing mutations showed good agreement between the splicing phenotype and the effect of the mutation on the motifs defined here. The large number of effective sequences implied by these results suggests that sequences that influence splicing may be very abundant in pre-mRNA.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Xiang H-F</ForeName>
<Initials>XH</Initials>
<AffiliationInfo><Affiliation>Department of Biological Sciences, MC2433, Columbia University, New York, New York 10027, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chasin</LastName>
<ForeName>Lawrence A</ForeName>
<Initials>LA</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType>
<PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2004</Year>
<Month>05</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Genes Dev</MedlineTA>
<NlmUniqueID>8711660</NlmUniqueID>
<ISSNLinking>0890-9369</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D020121">5' Untranslated Regions</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D038621">Regulatory Sequences, Ribonucleic Acid</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber>
<NameOfSubstance UI="D017346">Protein-Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.10</RegistryNumber>
<NameOfSubstance UI="C496559">CHUK protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.10</RegistryNumber>
<NameOfSubstance UI="D051550">I-kappa B Kinase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.10</RegistryNumber>
<NameOfSubstance UI="C496560">IKBKB protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.11.10</RegistryNumber>
<NameOfSubstance UI="C496565">IKBKE protein, human</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D020121" MajorTopicYN="N">5' Untranslated Regions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003198" MajorTopicYN="N">Computer Simulation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004742" MajorTopicYN="N">Enhancer Elements, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005091" MajorTopicYN="Y">Exons</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005796" MajorTopicYN="N">Genes</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051550" MajorTopicYN="N">I-kappa B Kinase</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007438" MajorTopicYN="N">Introns</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008322" MajorTopicYN="N">Mammals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008957" MajorTopicYN="Y">Models, Genetic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012326" MajorTopicYN="Y">RNA Splicing</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D038621" MajorTopicYN="Y">Regulatory Sequences, Ribonucleic Acid</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D037941" MajorTopicYN="N">Silencer Elements, Transcriptional</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName>
</MeshHeading>
</MeshHeadingList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year>
<Month>5</Month>
<Day>18</Day>
<Hour>5</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2004</Year>
<Month>7</Month>
<Day>10</Day>
<Hour>5</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2004</Year>
<Month>5</Month>
<Day>18</Day>
<Hour>5</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">15145827</ArticleId>
<ArticleId IdType="doi">10.1101/gad.1195304</ArticleId>
<ArticleId IdType="pii">1195304</ArticleId>
<ArticleId IdType="pmc">PMC420350</ArticleId>
</ArticleIdList>
<ReferenceList><Reference><Citation>Genes Dev. 1998 Jul 1;12(13):1998-2012</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9649504</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Hum Mol Genet. 1998 May;7(5):919-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9536098</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1999 Jan;19(1):251-60</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9858549</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1999 Jan;19(1):261-73</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9858550</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1999 Mar;19(3):1705-19</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10022858</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1999 Mar;19(3):1853-63</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10022872</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2000 Feb;20(3):1063-71</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10629063</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Trends Biochem Sci. 2000 Mar;25(3):106-10</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10694877</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mutat Res. 2000 Feb;432(1-2):15-32</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10729708</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2000 Sep;20(17):6414-25</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10938119</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2000 Sep;20(18):6816-25</Citation>
<ArticleIdList><ArticleId IdType="pubmed">10958678</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nucleic Acids Res. 2001 Apr 1;29(7):1464-9</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11266547</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 2001 May;21(10):3281-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11313454</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Genet. 2001 Dec;29(4):412-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11726928</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Blood. 2002 Mar 1;99(5):1811-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11861299</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Genet. 2002 Apr;3(4):285-98</Citation>
<ArticleIdList><ArticleId IdType="pubmed">11967553</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Science. 2002 Aug 9;297(5583):1007-13</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12114529</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genome Biol. 2002 Oct 23;3(11):reviews0008</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12429065</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Struct Biol. 2003 Jan;10(1):33-7</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12447348</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nucleic Acids Res. 2003 Jul 1;31(13):3568-71</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12824367</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9440-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12883005</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Genet. 2003 Aug;34(4):460-3</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12833158</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Annu Rev Biochem. 2003;72:291-336</Citation>
<ArticleIdList><ArticleId IdType="pubmed">12626338</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genome Res. 2003 Dec;13(12):2637-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">14656968</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nucleic Acids Res. 2004;32(5):1783-91</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15034146</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Nat Rev Mol Cell Biol. 2004 Feb;5(2):89-99</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15040442</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genome Biol. 2004;5(4):218</Citation>
<ArticleIdList><ArticleId IdType="pubmed">15059251</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1989 Jul;9(7):2868-80</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2779551</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1990 Jan;10(1):84-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2136768</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Methods Enzymol. 1990;183:252-78</Citation>
<ArticleIdList><ArticleId IdType="pubmed">2314278</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1993 Jan;13(1):289-300</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8417332</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10091-5</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8234261</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1994 Mar;14(3):2140-6</Citation>
<ArticleIdList><ArticleId IdType="pubmed">8114744</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Biol Chem. 1995 Feb 10;270(6):2411-4</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7852296</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>EMBO J. 1995 Jul 17;14(14):3540-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7543047</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1995 Nov;15(11):6291-8</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7565782</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Genomics. 1995 May 20;27(2):348-51</Citation>
<ArticleIdList><ArticleId IdType="pubmed">7558004</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mol Cell Biol. 1997 Apr;17(4):2143-50</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9121463</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>J Mol Biol. 1997 Apr 25;268(1):78-94</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9149143</ArticleId>
</ArticleIdList>
</Reference>
<Reference><Citation>Mutat Res. 1998 Nov;411(3):179-214</Citation>
<ArticleIdList><ArticleId IdType="pubmed">9804951</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
</PubmedData>
</pubmed>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/MersV1/Data/PubMed/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002390 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd -nk 002390 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Sante |area= MersV1 |flux= PubMed |étape= Corpus |type= RBID |clé= pubmed:15145827 |texte= Computational definition of sequence motifs governing constitutive exon splicing. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Corpus/RBID.i -Sk "pubmed:15145827" \ | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Corpus/biblio.hfd \ | NlmPubMed2Wicri -a MersV1
![]() | This area was generated with Dilib version V0.6.33. | ![]() |