ArticleThe Journal of biological chemistry2015
Protein Kinase C Phosphorylation of a γ-Protocadherin C-terminal Lipid Binding Domain Regulates Focal Adhesion Kinase Inhibition and Dendrite Arborization.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 59 citations in OpenAlex.
- PCDHGC3 silencing promotes clear cell renal cell carcinoma metastasis via mTOR/HIF2α activation, lipid metabolism rewiring, and ferroptosis evasion.Cell death & disease · 2026Article
- Protocadherin γC4 regulates neuronal survival and dendritic self-avoidance.Communications biology · 2026Article
- Reduced Neuronal Self-Avoidance in Mouse Starburst Amacrine Cells With Only One Pcdhg Isoform.Developmental neurobiology · 2026Article
- Article
- Surface delivery quantification reveals distinct trafficking efficiencies among clustered protocadherin isoforms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcriptomic Analysis Reveals Key Pathways Influenced by HIV-2 Vpx.International journal of molecular sciences · 2025Article
- Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Structural insights into the in situ assembly of clustered protocadherin γB4.Nature communications · 2025Article
- A C-terminal motif containing a PKC phosphorylation site regulates γ-Protocadherin-mediated dendrite arborization in the cerebral cortex in vivo.Developmental neurobiology · 2024Article
- A selective review of inhibitors of protein kinase C gamma: a neuroplasticity-related common pathway for psychiatric illness.Frontiers in drug delivery · 2024Review
- Loss of function of FIP200 in human pluripotent stem cell-derived neurons leads to axonal pathology and hyperactivity.Translational psychiatry · 2023Article
- A Unique Role for Protocadherin γC3 in Promoting Dendrite Arborization through an Axin1-Dependent Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Ubiquitination of the protocadherin-γA3 variable cytoplasmic domain modulates cell-cell interaction.Frontiers in cell and developmental biology · 2023Article
- FAK-Mediated Signaling Controls Amyloid Beta Overload, Learning and Memory Deficits in a Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- Trans-splicing facilitated by RNA pairing greatly expands sDscam isoform diversity but not homophilic binding specificity.Science advances · 2022Article
- How clustered protocadherin binding specificity is tuned for neuronal self-/nonself-recognition.eLife · 2022Article
- Mouse models for the study of clustered protocadherins.Current topics in developmental biology · 2022Article
- Wiring the Brain by Clustered Protocadherin Neural Codes.Neuroscience bulletin · 2021Review
- Article
- Expression of protocadherin-γC4 protein in the rat brain.The Journal of comparative neurology · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The γ-protocadherins (γ-Pcdhs) are a family of 22 adhesion molecules with multiple critical developmental functions, including the proper formation of dendritic arbors by forebrain neurons. The γ-Pcdhs bind to and inhibit focal adhesion kinase (FAK) via a constant C-terminal cytoplasmic domain shared by all 22 proteins. In cortical neurons lacking the γ-Pcdhs, aberrantly high activity of FAK and of PKC disrupts dendrite arborization. Little is known, however, about how γ-Pcdh function is regulated by other factors. Here we show that PKC phosphorylates a serine residue situated within a phospholipid binding motif at the shared γ-Pcdh C terminus. Western blots using a novel phospho-specific antibody against this site suggest that a portion of γ-Pcdh proteins is phosphorylated in the cortex in vivo. We find that PKC phosphorylation disrupts both phospholipid binding and the γ-Pcdh inhibition of (but not binding to) FAK. Introduction of a non-phosphorylatable (S922A) γ-Pcdh construct into wild-type cortical neurons significantly increases dendrite arborization. This same S922A construct can also rescue dendrite arborization defects in γ-Pcdh null neurons cell autonomously. Consistent with these data, introduction of a phosphomimetic (S/D) γ-Pcdh construct or treatment with a PKC activator reduces dendrite arborization in wild-type cortical neurons. Together, these data identify a novel mechanism through which γ-Pcdh control of a signaling pathway important for dendrite arborization is regulated.
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