ArticleDevelopment (Cambridge, England)2008
Dap160/intersectin binds and activates aPKC to regulate cell polarity and cell cycle progression.
Article in Development (Cambridge, England), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- Polarity protein Par6 facilitates the processive phosphorylation of Lgl via a dynamic interaction with aPKC.Communications biology · 2025Article
- Haploinsufficiency of ITSN1 is associated with a substantial increased risk of Parkinson's disease.Cell reports · 2025Article
- Article
- Mask, the Drosophila ankyrin repeat and KH domain-containing protein, affects microtubule stability.Journal of cell science · 2021Article
- Asymmetric nuclear division in neural stem cells generates sibling nuclei that differ in size, envelope composition, and chromatin organization.Current biology : CB · 2021Article
- A polybasic domain in aPKC mediates Par6-dependent control of membrane targeting and kinase activity.The Journal of cell biology · 2020Article
- Mutations in ANKLE2, a ZIKA Virus Target, Disrupt an Asymmetric Cell Division Pathway in Drosophila Neuroblasts to Cause Microcephaly.Developmental cell · 2019Article
- aPKC: the Kinase that Phosphorylates Cell Polarity.F1000Research · 2018Review
- EGFR/ARF6 regulation of Hh signalling stimulates oncogenic Ras tumour overgrowth.Nature communications · 2017Article
- Rac1-mediated cytoskeleton rearrangements induced by intersectin-1s deficiency promotes lung cancer cell proliferation, migration and metastasis.Molecular cancer · 2016Article
- Molecular Control of Atypical Protein Kinase C: Tipping the Balance between Self-Renewal and Differentiation.Journal of molecular biology · 2016Review
- aPKC phosphorylates p27Xic1, providing a mechanistic link between apicobasal polarity and cell-cycle control.Developmental cell · 2014Article
- Oncogenic Ras stimulates Eiger/TNF exocytosis to promote growth.Development (Cambridge, England) · 2014Article
- Genetic and functional studies implicate synaptic overgrowth and ring gland cAMP/PKA signaling defects in the Drosophila melanogaster neurofibromatosis-1 growth deficiency.PLoS genetics · 2013Article
- Emerging roles for intersectin (ITSN) in regulating signaling and disease pathways.International journal of molecular sciences · 2013Review
- The Snail family member Worniu is continuously required in neuroblasts to prevent Elav-induced premature differentiation.Developmental cell · 2012Article
- Article
- Functional genomics identifies neural stem cell sub-type expression profiles and genes regulating neuroblast homeostasis.Developmental biology · 2012Article
- Apical-basal polarity in Drosophila neuroblasts is independent of vesicular trafficking.Molecular biology of the cell · 2011Article
- Intersecting pathways in cell biology.Science signaling · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The atypical protein kinase C (aPKC) is required for cell polarization of many cell types, and is upregulated in several human tumors. Despite its importance in cell polarity and growth control, relatively little is known about how aPKC activity is regulated. Here, we use a biochemical approach to identify Dynamin-associated protein 160 (Dap160; related to mammalian intersectin) as an aPKC-interacting protein in Drosophila. We show that Dap160 directly interacts with aPKC, stimulates aPKC activity in vitro and colocalizes with aPKC at the apical cortex of embryonic neuroblasts. In dap160 mutants, aPKC is delocalized from the neuroblast apical cortex and has reduced activity, based on its inability to displace known target proteins from the basal cortex. Both dap160 and aPKC mutants have fewer proliferating neuroblasts and a prolonged neuroblast cell cycle. We conclude that Dap160 positively regulates aPKC activity and localization to promote neuroblast cell polarity and cell cycle progression.
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Registered trials
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.