ArticleBlood2009
Loss of pleckstrin defines a novel pathway for PKC-mediated exocytosis.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 55 citations in OpenAlex.
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- Identifying the HIV-Resistance-Related Factors and Regulatory Network via Multi-Omics Analyses.International journal of molecular sciences · 2024Article
- A selective review of inhibitors of protein kinase C gamma: a neuroplasticity-related common pathway for psychiatric illness.Frontiers in drug delivery · 2024Review
- Is autologous platelet activation the key step in ovarian therapy for fertility recovery and menopause reversal?BioMedicine · 2022Review
- M2 macrophage-related gene signature in chronic rhinosinusitis with nasal polyps.Frontiers in immunology · 2022Article
- DMAG, a novel countermeasure for the treatment of thrombocytopenia.Molecular medicine (Cambridge, Mass.) · 2021Article
- Pleckstrin Levels Are Increased in Patients with Chronic Periodontitis and RegulatedFrontiers in immunology · 2021Article
- Emerging Roles of Pleckstrin-2 Beyond Cell Spreading.Frontiers in cell and developmental biology · 2021Review
- Tumor Purity Coexpressed Genes Related to Immune Microenvironment and Clinical Outcomes of Lung Adenocarcinoma.Journal of oncology · 2021Article
- A multiscale biophysical model for the recruitment of actin nucleating proteins at the membrane interface.Soft matter · 2020Article
- A rare genomic duplication in 2p14 underlies autosomal dominant hearing loss DFNA58.Human molecular genetics · 2020Article
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- The Allelic Landscape of Human Blood Cell Trait Variation and Links to Common Complex Disease.Cell · 2016Article
- Toxicogenomics profiling of bone marrow from rats treated with topotecan in combination with oxaliplatin: a mechanistic strategy to inform combination toxicity.Frontiers in genetics · 2015Article
- Loss of ATE1-mediated arginylation leads to impaired platelet myosin phosphorylation, clot retraction, and in vivo thrombosis formation.Haematologica · 2014Article
- Review
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- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Pleckstrin, the platelet and leukocyte C kinase substrate, is a prominent substrate of PKC in platelets, monocytes, macrophages, lymphocytes, and granulocytes. Pleckstrin accounts for 1% of the total protein in these cells, but it is best known for containing the 2 prototypic Pleckstrin homology, or PH, domains. Overexpressed pleckstrin can affect polyphosphoinositide second messenger-based signaling events; however, its true in vivo role has been unknown. Here, we describe mice containing a null mutation within the pleckstrin gene. Platelets lacking pleckstrin exhibit a marked defect in exocytosis of delta and alpha granules, alphaIIbbeta3 activation, actin assembly, and aggregation after exposure to the PKC stimulant, PMA. Pleckstrin-null platelets aggregate normally in response to thrombin, but they fail to aggregate in response to thrombin in the presence of PI3K inhibitors, suggesting that a PI3K-dependent signaling pathway compensates for the loss of pleckstrin. Although pleckstrin-null platelets merged their granules in response to stimulation of PKC, they failed to empty their contents into the open canalicular system. This might be attributable to impaired actin assembly present in cells lacking pleckstrin. These data show that pleckstrin regulates the fusion of granules to the cell membrane and is an essential component of PKC-mediated exocytosis.
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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.