ArticleMolecular and cellular biology2006
A spatiotemporally coordinated cascade of protein kinase C activation controls isoform-selective translocation.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Angiotensin receptors and αPflugers Archiv : European journal of physiology · 2024Article
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- Activated Protein Kinase C (PKC) Is Persistently Trafficked with Epidermal Growth Factor (EGF) Receptor.Biomolecules · 2020Article
- TASK channels: channelopathies, trafficking, and receptor-mediated inhibition.Pflugers Archiv : European journal of physiology · 2020Review
- Phospho-substrate profiling of Epac-dependent protein kinase C activity.Molecular and cellular biochemistry · 2019Article
- Paclitaxel inhibits the activity and membrane localization of PKCα and PKCβI/II to elicit a decrease in stimulated calcitonin gene-related peptide release from cultured sensory neurons.Molecular and cellular neurosciences · 2017Article
- Article
- TRM6/61 connects PKCα with translational control through tRNAi(Met) stabilization: impact on tumorigenesis.Oncogene · 2016Article
- Differential Regulation of Multiple Steps in Inositol 1,4,5-Trisphosphate Signaling by Protein Kinase C Shapes Hormone-stimulated Ca2+ Oscillations.The Journal of biological chemistry · 2015Article
- Regulation of human organic anion transporter 3 by peptide hormone bradykinin.The Journal of pharmacology and experimental therapeutics · 2010Article
- Specific subcellular targeting of PKCalpha and PKCepsilon in normal and tumoral lactotroph cells by PMA-mitogenic stimulus.Journal of molecular histology · 2009Article
- A 20-amino acid module of protein kinase C{epsilon} involved in translocation and selective targeting at cell-cell contacts.The Journal of biological chemistry · 2009Article
- PCPH/ENTPD5 expression confers to prostate cancer cells resistance against cisplatin-induced apoptosis through protein kinase Calpha-mediated Bcl-2 stabilization.Cancer research · 2009Article
- Two conventional protein kinase C isoforms, alpha and beta I, are involved in the ATP-induced activation of volume-regulated anion channel and glutamate release in cultured astrocytes.Journal of neurochemistry · 2008Article
- Article
- Thyrotropin-releasing hormone (TRH) in the cerebellum.Cerebellum (London, England) · 2008Review
- BAFF controls B cell metabolic fitness through a PKC beta- and Akt-dependent mechanism.The Journal of experimental medicine · 2006Article
- A lipid-anchored neurokinin 1 receptor antagonist prolongs pain relief by a three-pronged mechanism of action targeting the receptor at the plasma membrane and in endosomes.The Journal of biological chemistryArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In pituitary GH3B6 cells, signaling involving the protein kinase C (PKC) multigene family can self-organize into a spatiotemporally coordinated cascade of isoform activation. Indeed, thyrotropin-releasing hormone (TRH) receptor activation sequentially activated green fluorescent protein (GFP)-tagged or endogenous PKCbeta1, PKCalpha, PKCepsilon, and PKCdelta, resulting in their accumulation at the entire plasma membrane (PKCbeta and -delta) or selectively at the cell-cell contacts (PKCalpha and -epsilon). The duration of activation ranged from 20 s for PKCalpha to 20 min for PKCepsilon. PKCalpha and -epsilon selective localization was lost in the presence of Gö6976, suggesting that accumulation at cell-cell contacts is dependent on the activity of a conventional PKC. Constitutively active, dominant-negative PKCs and small interfering RNAs showed that PKCalpha localization is controlled by PKCbeta1 activity and is calcium independent, while PKCepsilon localization is dependent on PKCalpha activity. PKCdelta was independent of the cascade linking PKCbeta1, -alpha, and -epsilon. Furthermore, PKCalpha, but not PKCepsilon, is involved in the TRH-induced beta-catenin relocation at cell-cell contacts, suggesting that PKCepsilon is not the unique functional effector of the cascade. Thus, TRH receptor activation results in PKCbeta1 activation, which in turn initiates a calcium-independent but PKCbeta1 activity-dependent sequential translocation of PKCalpha and -epsilon. These results challenge the current understanding of PKC signaling and raise the question of a functional dependence between isoforms.
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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.