Please use this identifier to cite or link to this item:
https://doi.org/10.1371/journal.pone.0064404
DC Field | Value | |
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dc.title | Generation and Characterisation of Keratin 7 (K7) Knockout Mice | |
dc.contributor.author | Sandilands A. | |
dc.contributor.author | Smith F.J.D. | |
dc.contributor.author | Lunny D.P. | |
dc.contributor.author | Campbell L.E. | |
dc.contributor.author | Davidson K.M. | |
dc.contributor.author | MacCallum S.F. | |
dc.contributor.author | Corden L.D. | |
dc.contributor.author | Christie L. | |
dc.contributor.author | Fleming S. | |
dc.contributor.author | Lane E.B. | |
dc.contributor.author | McLean W.H.I. | |
dc.date.accessioned | 2019-11-04T04:06:00Z | |
dc.date.available | 2019-11-04T04:06:00Z | |
dc.date.issued | 2013 | |
dc.identifier.citation | Sandilands 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.issn | 19326203 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/161311 | |
dc.description.abstract | Keratin 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.rights | Attribution 4.0 International | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.source | Unpaywall 20191101 | |
dc.subject | complementary DNA | |
dc.subject | cytokeratin 7 | |
dc.subject | messenger RNA | |
dc.subject | animal cell | |
dc.subject | article | |
dc.subject | carboxy terminal sequence | |
dc.subject | cell proliferation | |
dc.subject | controlled study | |
dc.subject | embryo | |
dc.subject | embryonic stem cell | |
dc.subject | exon | |
dc.subject | gene mutation | |
dc.subject | gene targeting | |
dc.subject | homozygosity | |
dc.subject | immunofluorescence microscopy | |
dc.subject | knockout mouse | |
dc.subject | mouse | |
dc.subject | nonhuman | |
dc.subject | polyacrylamide gel electrophoresis | |
dc.subject | promoter region | |
dc.subject | protein expression | |
dc.subject | reverse transcription polymerase chain reaction | |
dc.subject | urothelium | |
dc.subject | Animals | |
dc.subject | Cell Proliferation | |
dc.subject | Female | |
dc.subject | Founder Effect | |
dc.subject | Gene Expression Regulation | |
dc.subject | Keratin-18 | |
dc.subject | Keratin-19 | |
dc.subject | Keratin-20 | |
dc.subject | Keratin-7 | |
dc.subject | Keratin-8 | |
dc.subject | Male | |
dc.subject | Mice | |
dc.subject | Mice, Knockout | |
dc.subject | Protein Binding | |
dc.subject | Urinary Bladder | |
dc.subject | Urothelium | |
dc.subject | Mus | |
dc.type | Article | |
dc.contributor.department | PATHOLOGY | |
dc.description.doi | 10.1371/journal.pone.0064404 | |
dc.description.sourcetitle | PLoS ONE | |
dc.description.volume | 8 | |
dc.description.issue | 5 | |
dc.description.page | e64404 | |
dc.published.state | Published | |
Appears in Collections: | Staff Publications Elements |
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