Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/88356
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dc.contributorDepartment of Health Technology and Informaticsen_US
dc.creatorCheung, Yen_US
dc.creatorWu, Zen_US
dc.creatorGarciaBarcelo, MMen_US
dc.creatorTam, PKHen_US
dc.creatorMa, ACHen_US
dc.creatorLui, VCHen_US
dc.date.accessioned2020-10-29T01:02:39Z-
dc.date.available2020-10-29T01:02:39Z-
dc.identifier.issn0022-3468en_US
dc.identifier.urihttp://hdl.handle.net/10397/88356-
dc.language.isoenen_US
dc.publisherW.B. Saundersen_US
dc.rights© 2020 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license(http://creativecommons.org/licenses/by-nc-nd/4.0/).en_US
dc.rightsThe following publication Cheung, Y., Wu, Z., Garcia-Barcelo, M. M., Tam, P. K. H., Ma, A. C. H., & Lui, V. C. H. (2021). Deletion of interleukin enhancer binding factor 2 (ILF2) resulted in defective biliary development and bile flow blockage. Journal of Pediatric Surgery, 56(2), 352-359, is available at https://doi.org/10.1016/j.jpedsurg.2020.06.032en_US
dc.subjectBile ducten_US
dc.subjectBiliary atresiaen_US
dc.subjectILF2en_US
dc.subjectLiveren_US
dc.subjectZebrafishen_US
dc.titleDeletion of interleukin enhancer binding factor 2 (ILF2) resulted in defective biliary development and bile flow blockageen_US
dc.typeJournal/Magazine Articleen_US
dc.identifier.spage352-
dc.identifier.epage359-
dc.identifier.volume56-
dc.identifier.issue2-
dc.identifier.doi10.1016/j.jpedsurg.2020.06.032en_US
dcterms.abstractPurpose: Biliary atresia (BA) is a devastating obstructive bile duct disease of newborns. BA has the highest incidence in Asians (1/5000), and its pathogenesis is unclear. We identified BA-private rare copy number variants (CNVs; 22 duplications and 6 deletions). ILF2 gene locates in the chromosome region (Chr1:153410347–153,634,058) which was deleted in a nonsyndromic BA patient. However, it is still not known whether ILF2 plays a role in hepatobiliary development and its deletion impacts on the bile duct development.en_US
dcterms.abstractMethods: To investigate if ILF2 is required for biliary development, we knock-out the zebrafish homologs of ILF2 by CRISPR/Cas9 approach, and discover that deletion of ILF2 causes a defective biliary development and a lack of bile flow from the liver to the gall bladder in zebrafish, which is a resemblance of phenotypes of BA.en_US
dcterms.abstractResults: Our data indicate that ILF2 gene is required for biliary development; deletion of ILF2 impairs bile duct development and could contribute to BA pathogenesis. This will be the first study to functionally evaluate the genes interfered by BA-private CNVs in hepatobiliary development and in BA pathogenesis.en_US
dcterms.abstractConclusions: Such functional study may reveal the potential value of these BA-private CNVs in the disease pathogenesis for BA. Level of evidence: N/A (animal and laboratory study).en_US
dcterms.accessRightsopen accessen_US
dcterms.bibliographicCitationJournal of pediatric surgery, 2020en_US
dcterms.bibliographicCitationJournal of pediatric surgery, 2020, v. 56, no. 2, p. 352-359-
dcterms.isPartOfJournal of pediatric surgeryen_US
dcterms.issued2020-
dc.identifier.scopus2-s2.0-85088219243-
dc.description.validate202010 bcmaen_US
dc.description.oaVersion of Recorden_US
dc.identifier.FolderNumberOA_Scopus/WOSen_US
dc.description.pubStatusPublisheden_US
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