http://purl.uniprot.org/citations/24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/24391875 | http://www.w3.org/2000/01/rdf-schema#comment | "Cell polarity plays a critical role in neuronal differentiation during development of the central nervous system (CNS). Recent studies have established the significance of atypical protein kinase C (aPKC) and its interacting partners, which include PAR-3, PAR-6 and Lgl, in regulating cell polarization during neuronal differentiation. However, their roles in neuronal maintenance after CNS development remain unclear. Here we performed conditional deletion of aPKCλ, a major aPKC isoform in the brain, in differentiated neurons of mice by camk2a-cre or synapsinI-cre mediated gene targeting. We found significant reduction of aPKCλ and total aPKCs in the adult mouse brains. The aPKCλ deletion also reduced PAR-6β, possibly by its destabilization, whereas expression of other related proteins such as PAR-3 and Lgl-1 was unaffected. Biochemical analyses suggested that a significant fraction of aPKCλ formed a protein complex with PAR-6β and Lgl-1 in the brain lysates, which was disrupted by the aPKCλ deletion. Notably, the aPKCλ deletion mice did not show apparent cell loss/degeneration in the brain. In addition, neuronal orientation/distribution seemed to be unaffected. Thus, despite the polarity complex disruption, neuronal deletion of aPKCλ does not induce obvious cell loss or disorientation in mouse brains after cell differentiation."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.org/dc/terms/identifier | "doi:10.1371/journal.pone.0084036"xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Hirose T."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Yamanaka T."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Ohno S."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Hattori N."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Akimoto K."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Kurosawa M."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Nukina N."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/author | "Tosaki A."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/date | "2013"xsd:gYear |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/name | "PLoS One"xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/pages | "e84036"xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/title | "Loss of aPKClambda in differentiated neurons disrupts the polarity complex but does not induce obvious neuronal loss or disorientation in mouse brains."xsd:string |
http://purl.uniprot.org/citations/24391875 | http://purl.uniprot.org/core/volume | "8"xsd:string |
http://purl.uniprot.org/citations/24391875 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24391875 |
http://purl.uniprot.org/citations/24391875 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3UR71-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3UR74-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3URM8-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3URM9-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3Z6L5-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A0E3Z795-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |
http://purl.uniprot.org/uniprot/#_A0A1D5RLU4-mappedCitation-24391875 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/24391875 |