ArticleThe Biochemical journal2001
Protein kinase C-delta C2-like domain is a binding site for actin and enables actin redistribution in neutrophils.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 50 citations in OpenAlex.
- The C2 Domain of PKC‑δ as a Dominant-Negative Modulator of Breast Cancer Cell Survival and Chemosensitivity.ACS omega · 2025Article
- Dual Regulation of Spine-Specific and Synapse-to-Nucleus Signaling by PKCδ during Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Antimicrobial agent triclosan suppresses mast cell signaling via phospholipase D inhibition.Journal of applied toxicology : JAT · 2019Article
- LysoPCs induce Hck- and PKCδ-mediated activation of PKCγ causing p47phox phosphorylation and membrane translocation in neutrophils.Journal of leukocyte biology · 2017Article
- Phosphorylation of E-cadherin at threonine 790 by protein kinase Cδ reduces β-catenin binding and suppresses the function of E-cadherin.Oncotarget · 2016Article
- The C2 Domain and Altered ATP-Binding Loop Phosphorylation at Ser³⁵⁹ Mediate the Redox-Dependent Increase in Protein Kinase C-δ Activity.Molecular and cellular biology · 2015Article
- Identification of lipocalin-2 as a PKCδ phosphorylation substrate in neutrophils.Journal of biomedical science · 2015Article
- Protein kinase C-delta regulates HIV-1 replication at an early post-entry step in macrophages.Retrovirology · 2012Article
- Article
- Subcellular localisation of the p40phox component of NADPH oxidase involves direct interactions between the Phox homology domain and F-actin.The international journal of biochemistry & cell biology · 2010Article
- The protein scaffold NHERF-1 controls the amplitude and duration of localized protein kinase D activity.The Journal of biological chemistry · 2009Article
- Structural basis of protein kinase C isoform function.Physiological reviews · 2008Review
- Serotonin modifies cytoskeleton and brush-border membrane architecture in human intestinal epithelial cells.American journal of physiology. Gastrointestinal and liver physiology · 2008Article
- Increased membrane affinity of the C1 domain of protein kinase Cdelta compensates for the lack of involvement of its C2 domain in membrane recruitment.The Journal of biological chemistry · 2006Article
- N-Formyl peptide receptor subtypes in human neutrophils activate L-plastin phosphorylation through different signal transduction intermediates.The Biochemical journal · 2004Article
- Effects of microinjected small GTPases on the actin cytoskeleton of human neutrophils.Journal of anatomy · 2003Article
- Activation of protein kinase C beta II by the stereo-specific phosphatidylserine receptor is required for phagocytosis of apoptotic thymocytes by resident murine tissue macrophages.The Journal of biological chemistry · 2002Article
- Involvement of protein kinase D in Fc gamma-receptor activation of the NADPH oxidase in neutrophils.The Biochemical journal · 2002Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils play a key role in host-defence mechanisms against invading pathogens, using their capacity to migrate, engulf micro-organisms and produce toxic radicals. Protein kinase C (PKC) isotypes are important intracellular regulators of these processes in neutrophils. PKC isotypes themselves are controlled by interactions with lipids, Ca(2+) and proteins. The C2-like domain of PKC-delta (deltaC2) has been identified as a protein-interaction domain in this PKC isotype. In the present paper we have investigated the contribution of protein interactions at this domain to the regulation/function of PKC-delta in neutrophils. Using affinity chromatography we identified actin as a deltaC2 binding partner in these cells. Fluorescein-labelled deltaC2, microinjected into immobilized neutrophils, interacts with filamentous actin (F-actin) inside the cell. PKC-delta co-localizes with F-actin in neutrophils, in lamellipodia at the leading edge of the cell. Stimulation with phorbol ester or IgG-opsonized Staphylococcus aureus results in co-ordinated redistribution of PKC-delta and F-actin, and a PKC-delta inhibitor inhibits these changes. Microinjection of deltaC2 also inhibits F-actin redistribution. Thus PKC-delta binds to F-actin through its C2 domain, and these interactions are important in regulating actin redistribution in neutrophils.
Indexed as
Identifiers
What OpenQuestion holds
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.