Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0064404
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dc.titleGeneration and Characterisation of Keratin 7 (K7) Knockout Mice
dc.contributor.authorSandilands A.
dc.contributor.authorSmith F.J.D.
dc.contributor.authorLunny D.P.
dc.contributor.authorCampbell L.E.
dc.contributor.authorDavidson K.M.
dc.contributor.authorMacCallum S.F.
dc.contributor.authorCorden L.D.
dc.contributor.authorChristie L.
dc.contributor.authorFleming S.
dc.contributor.authorLane E.B.
dc.contributor.authorMcLean W.H.I.
dc.date.accessioned2019-11-04T04:06:00Z
dc.date.available2019-11-04T04:06:00Z
dc.date.issued2013
dc.identifier.citationSandilands A., Smith F.J.D., Lunny D.P., Campbell L.E., Davidson K.M., MacCallum S.F., Corden L.D., Christie L., Fleming S., Lane E.B., McLean W.H.I. (2013). Generation and Characterisation of Keratin 7 (K7) Knockout Mice. PLoS ONE 8 (5) : e64404. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0064404
dc.identifier.issn19326203
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/161311
dc.description.abstractKeratin 7 (K7) is a Type II member of the keratin superfamily and despite its widespread expression in different types of simple and transitional epithelia, its functional role in vivo remains elusive, in part due to the lack of any appropriate mouse models or any human diseases that are associated with KRT7 gene mutations. Using conventional gene targeting in mouse embryonic stem cells, we report here the generation and characterisation of the first K7 knockout mouse. Loss of K7 led to increased proliferation of the bladder urothelium although this was not associated with hyperplasia. K18, a presumptive type I assembly partner for K7, showed reduced expression in the bladder whereas K20, a marker of the terminally differentiated superficial urothelial cells was transcriptionally up-regulated. No other epithelia were seen to be adversely affected by the loss of K7 and western blot and immunofluorescence microscopy analysis revealed that the expression of K8, K18, K19 and K20 were not altered in the absence of K7, with the exception of the kidney where there was reduced K18 expression. © 2013 Sandilands et al.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20191101
dc.subjectcomplementary DNA
dc.subjectcytokeratin 7
dc.subjectmessenger RNA
dc.subjectanimal cell
dc.subjectarticle
dc.subjectcarboxy terminal sequence
dc.subjectcell proliferation
dc.subjectcontrolled study
dc.subjectembryo
dc.subjectembryonic stem cell
dc.subjectexon
dc.subjectgene mutation
dc.subjectgene targeting
dc.subjecthomozygosity
dc.subjectimmunofluorescence microscopy
dc.subjectknockout mouse
dc.subjectmouse
dc.subjectnonhuman
dc.subjectpolyacrylamide gel electrophoresis
dc.subjectpromoter region
dc.subjectprotein expression
dc.subjectreverse transcription polymerase chain reaction
dc.subjecturothelium
dc.subjectAnimals
dc.subjectCell Proliferation
dc.subjectFemale
dc.subjectFounder Effect
dc.subjectGene Expression Regulation
dc.subjectKeratin-18
dc.subjectKeratin-19
dc.subjectKeratin-20
dc.subjectKeratin-7
dc.subjectKeratin-8
dc.subjectMale
dc.subjectMice
dc.subjectMice, Knockout
dc.subjectProtein Binding
dc.subjectUrinary Bladder
dc.subjectUrothelium
dc.subjectMus
dc.typeArticle
dc.contributor.departmentPATHOLOGY
dc.description.doi10.1371/journal.pone.0064404
dc.description.sourcetitlePLoS ONE
dc.description.volume8
dc.description.issue5
dc.description.pagee64404
dc.published.statePublished
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