ArticlePloS one2013
Phenotypical analysis of atypical PKCs in vivo function display a compensatory system at mouse embryonic day 7.5.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Protein Kinase C Family: Structures, Biological Functions, Diseases, and Pharmaceutical Interventions.MedComm · 2025Review
- Rare variants in PRKCI cause Van der Woude syndrome and other features of peridermopathy.American journal of human genetics · 2025Article
- Different Biomechanical Cell Behaviors in an Epithelium Drive Collective Epithelial Cell Extrusion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Tea polyphenols protect bovine intestinal epithelial cells from the adverse effects of heat-stressAnimal biotechnology · 2023Article
- Loss of polarity regulators initiates gasdermin-E-mediated pyroptosis in syncytiotrophoblasts.Life science alliance · 2023Article
- Dual inhibition of thioredoxin reductase and proteasome is required for auranofin-induced paraptosis in breast cancer cells.Cell death & disease · 2023Article
- Atypical protein kinase C is essential for embryonic vascular development in mice.Genesis (New York, N.Y. : 2000) · 2021Article
- Atypical protein kinase C iota (PKCλ/ι) ensures mammalian development by establishing the maternal-fetal exchange interface.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Mutations in ANKLE2, a ZIKA Virus Target, Disrupt an Asymmetric Cell Division Pathway in Drosophila Neuroblasts to Cause Microcephaly.Developmental cell · 2019Article
- Linking Cell Polarity to Cortical Development and Malformations.Frontiers in cellular neuroscience · 2019Review
- PKCε Inhibits Neuronal Dendritic Spine Development through Dual Phosphorylation of Ephexin5.Cell reports · 2018Article
- A Novel Atypical PKC-Iota Inhibitor, Echinochrome A, Enhances Cardiomyocyte Differentiation from Mouse Embryonic Stem Cells.Marine drugs · 2018Article
- The genetics of PKMζ and memory maintenance.Science signaling · 2017Review
- A Cdc42/RhoA regulatory circuit downstream of glycoprotein Ib guides transendothelial platelet biogenesis.Nature communications · 2017Article
- Article
- Prkci is required for a non-autonomous signal that coordinates cell polarity during cavitation.Developmental biology · 2016Article
- Compensation for PKMζ in long-term potentiation and spatial long-term memory in mutant mice.eLife · 2016Article
- Atypical PKC-iota Controls Stem Cell Expansion via Regulation of the Notch Pathway.Stem cell reports · 2015Article
- Regulation of mitochondrial function and cellular energy metabolism by protein kinase C-λ/ι: a novel mode of balancing pluripotency.Stem cells (Dayton, Ohio) · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe atypical protein kinases C (PKC) isoforms ι/λ and ζ play crucial roles in many cellular processes including development, cell proliferation, differentiation and cell survival. Possible redundancy between the two isoforms has always been an issue since most biochemical tools do not differentiate between the two proteins. Thus, much effort has been made during the last decades to characterize the functions of aPKCs using gene targeting approaches and depletion studies. However, little is known about the specific roles of each isoform in mouse development. METHODOLOGY/PRINCIPAL
findingsTo evaluate the importance of PKCι in mouse development we designed PKCι deletion mutants using the gene targeting approach. We show that the deletion of PKCι, results in a reduced size of the amniotic cavity at E7.5 and impaired growth of the embryo at E8.5 with subsequent absorption of the embryo. Our data also indicate an impaired localization of ZO-1 and disorganized structure of the epithelial tissue in the embryo. Importantly, using electron microscopy, embryoid body formation and immunofluorescence analysis, we found, that in the absence of PKCι, tight junctions and apico-basal polarity were still established. Finally, our study points to a non-redundant PKCι function at E9.5, since expression of PKCζ is able to rescue the E7.5 phenotype, but could not prevent embryonic lethality at a later time-point (E9.5).
conclusionOur data show that PKCι is crucial for mouse embryogenesis but is dispensable for the establishment of polarity and tight junction formation. We present a compensatory function of PKCζ at E7.5, rescuing the phenotype. Furthermore, this study indicates at least one specific, yet unknown, PKCι function that cannot be compensated by the overexpression of PKCζ at E9.5.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.