ArticleBlood2007
PI3K regulates pleckstrin-2 in T-cell cytoskeletal reorganization.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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
25 citing papers in PubMed, 44 citations in OpenAlex.
- PLEK2 promotes migration and invasion in pancreatic ductal adenocarcinoma by MMP1 through IL-17 pathway.Molecular and cellular biochemistry · 2025Article
- Pleckstrin-2 Mediates the Activation of AKT in Prostate Cancer and Is Repressed by Androgen Receptor.The American journal of pathology · 2024Article
- Pleckstrin-2-promoted PPM1B degradation plays an important role in transforming growth factor-β-induced breast cancer cell invasion and metastasis.Cancer science · 2023Article
- PI3K/AKT/mTOR Signaling Pathway in HPV-Driven Head and Neck Carcinogenesis: Therapeutic Implications.Biology · 2023Review
- Targeting pleckstrin-2/Akt signaling reduces proliferation in myeloproliferative neoplasm models.The Journal of clinical investigation · 2023Article
- Stabl: sparse and reliable biomarker discovery in predictive modeling of high-dimensional omic data.Research square · 2023Article
- Article
- PLEK2 promotes cancer stemness and tumorigenesis of head and neck squamous cell carcinoma via the c-Myc-mediated positive feedback loop.Cancer communications (London, England) · 2022Article
- PLEK2 promotes the proliferation and migration of non-small cell lung cancer cells in a BRD4-dependent manner.Molecular biology reports · 2022Article
- TGF-β-induced PLEK2 promotes metastasis and chemoresistance in oesophageal squamous cell carcinoma by regulating LCN2.Cell death & disease · 2021Article
- Expression and prognostic potential of PLEK2 in head and neck squamous cell carcinoma based on bioinformatics analysis.Cancer medicine · 2021Article
- PLEK2 promotes osteosarcoma tumorigenesis and metastasis by activating the PI3K/AKT signaling pathway.Oncology letters · 2021Article
- Targets and regulation of microRNA-652-3p in homoeostasis and disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Pleckstrin-2 is essential for erythropoiesis in β-thalassemic mice, reducing apoptosis and enhancing enucleation.Communications biology · 2021Article
- Pleckstrin-2 as a Prognostic Factor and Mediator of Gastric Cancer Progression.Gastroenterology research and practice · 2021Article
- Emerging Roles of Pleckstrin-2 Beyond Cell Spreading.Frontiers in cell and developmental biology · 2021Review
- Fission yeast Opy1 is an endogenous PI(4,5)PJournal of cell science · 2020Article
- Identification of a Robust Five-Gene Risk Model in Prostate Cancer: A Robust Likelihood-Based Survival Analysis.International journal of genomics · 2020Article
- PLEK2 promotes gallbladder cancer invasion and metastasis through EGFR/CCL2 pathway.Journal of experimental & clinical cancer research : CR · 2019Article
- Phospholipids: Pulling Back the Actin Curtain for Granule Delivery to the Immune Synapse.Frontiers in immunology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Pleckstrin-2 is composed of 2 pleckstrin homology (PH) domains and a disheveled-Egl-10-pleckstrin (DEP) domain. A lipid-binding assay revealed that pleckstrin-2 binds with greatest affinity to D3 and D5 phosphoinositides. Pleckstrin-2 expressed in Jurkat T cells bound to the cellular membrane and enhanced actin-dependent spreading only after stimulation of the T-cell antigen receptor or the integrin alpha4beta1. A pleckstrin-2 variant containing point mutations in both PH domains failed to associate with the Jurkat membrane and had no effect on spreading under the same conditions. Although still membrane bound, a pleckstrin-2 variant containing point mutations in the DEP domain demonstrated a decreased ability to induce membrane ruffles and spread. Pleckstrin-2 also colocalized with actin at the immune synapse and integrin clusters via its PH domains. Although pleckstrin-2 can bind to purified D3 and D5 phosphoinositides, the intracellular membrane association of pleckstrin-2 and cell spreading are dependent on D3 phosphoinositides, because these effects were disrupted by pharmacologic inhibition of phosphatidylinositol 3-kinase (PI3K). Our results indicate that pleckstrin-2 uses its modular domains to bind to membrane-associated phosphatidylinositols generated by PI3K, whereby it coordinates with the actin cytoskeleton in lymphocyte spreading and immune synapse formation.
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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.