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Article: The BCL7 gene family: Deletion of BCL7B in Williams syndrome

TitleThe BCL7 gene family: Deletion of BCL7B in Williams syndrome
Authors
Keywords5'-RACE
Gene expression
Hemizygous deletion
Translocation
Issue Date1998
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/gene
Citation
Gene, 1998, v. 224 n. 1-2, p. 35-44 How to Cite?
AbstractThe BCL7A gene, which maps to human chromosome 12q24.13, was cloned through its direct involvement with MYC and IGH in a three-way translocation in a Burkitt lymphoma cell line. Here, we describe the identification of two related human genes, BCL7B and BCL7C, which share 90% identity to the amino- terminal 51 amino acids of human BCL7A, as well as 41% identity in the same region to Drosophila melanogaster, Caenorhabditis elegans, and Brugia malayi EST sequences. This degree of relatedness in the amino-terminal domain suggests we have defined a new gene family of unknown function. There was little sequence conservation between the family members outside this conserved domain and no identified protein motifs could be deduced. Human BCL7B and BCL7C mapped to chromosome 7q11.23, and 16p11, respectively. No chromosomal rearrangements affecting BCL7B or BCL7C were detected in lymphoid malignancies. BCL7B did, however, map within the region of 7q11.23 which is commonly deleted in the congenital disorder, Williams syndrome.
Persistent Identifierhttp://hdl.handle.net/10722/44344
ISSN
2015 Impact Factor: 2.319
2015 SCImago Journal Rankings: 1.043
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJadayel, DMen_HK
dc.contributor.authorOsborne, LRen_HK
dc.contributor.authorCoignet, LJAen_HK
dc.contributor.authorZani, VJen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorScherer, SWen_HK
dc.contributor.authorDyer, MJSen_HK
dc.date.accessioned2007-09-12T03:51:48Z-
dc.date.available2007-09-12T03:51:48Z-
dc.date.issued1998en_HK
dc.identifier.citationGene, 1998, v. 224 n. 1-2, p. 35-44en_HK
dc.identifier.issn0378-1119en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44344-
dc.description.abstractThe BCL7A gene, which maps to human chromosome 12q24.13, was cloned through its direct involvement with MYC and IGH in a three-way translocation in a Burkitt lymphoma cell line. Here, we describe the identification of two related human genes, BCL7B and BCL7C, which share 90% identity to the amino- terminal 51 amino acids of human BCL7A, as well as 41% identity in the same region to Drosophila melanogaster, Caenorhabditis elegans, and Brugia malayi EST sequences. This degree of relatedness in the amino-terminal domain suggests we have defined a new gene family of unknown function. There was little sequence conservation between the family members outside this conserved domain and no identified protein motifs could be deduced. Human BCL7B and BCL7C mapped to chromosome 7q11.23, and 16p11, respectively. No chromosomal rearrangements affecting BCL7B or BCL7C were detected in lymphoid malignancies. BCL7B did, however, map within the region of 7q11.23 which is commonly deleted in the congenital disorder, Williams syndrome.en_HK
dc.languageengen_HK
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/geneen_HK
dc.relation.ispartofGeneen_HK
dc.subject5'-RACEen_HK
dc.subjectGene expressionen_HK
dc.subjectHemizygous deletionen_HK
dc.subjectTranslocationen_HK
dc.subject.mesh5¾-raceen_HK
dc.subject.meshGene expressionen_HK
dc.subject.meshHemizygous deletionen_HK
dc.subject.meshTranslocationen_HK
dc.subject.meshProteinsen_HK
dc.titleThe BCL7 gene family: Deletion of BCL7B in Williams syndromeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0378-1119&volume=224&issue=1-2&spage=35&epage=44&date=1998&atitle=The+BCL7+gene+family:+deletion+of+BCL7B+in+Williams+syndromeen_HK
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_subscribed_fulltexten_HK
dc.identifier.doi10.1016/S0378-1119(98)00514-9en_HK
dc.identifier.pmid9931421en_HK
dc.identifier.scopuseid_2-s2.0-0032509326en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032509326&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume224en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage35en_HK
dc.identifier.epage44en_HK
dc.identifier.isiWOS:000078028300005-
dc.publisher.placeNetherlandsen_HK
dc.identifier.scopusauthoridJadayel, DM=6602166929en_HK
dc.identifier.scopusauthoridOsborne, LR=35369973100en_HK
dc.identifier.scopusauthoridCoignet, LJA=7004542071en_HK
dc.identifier.scopusauthoridZani, VJ=55365649700en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridScherer, SW=35374654500en_HK
dc.identifier.scopusauthoridDyer, MJS=7201700604en_HK

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