ArticleMolecular and cellular biology2009
Phosphoinositide (3,4,5)-triphosphate binding to phosphoinositide-dependent kinase 1 regulates a protein kinase B/Akt signaling threshold that dictates T-cell migration, not proliferation.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 77 citations in OpenAlex.
- Coordinated regulation of gene expression and microRNA changes in adipose tissue and circulating extracellular vesicles in response to pioglitazone treatment in humans with type 2 diabetes.Frontiers in endocrinology · 2022Trial
- Targeting Metabolic Pathways to Direct T-Cell Trafficking: Therapeutic Perspectives.Biomedicines · 2026Review
- Tumor Microenvironment Onmyoji: Cytokines with Dual Protumor and Antitumor Roles.Cancer communications (London, England) · 2026Review
- Recent insights into the role of Akt in CD4 T-cell activation and differentiation: alternative splicing and beyond.Immunometabolism (Cobham, Surrey) · 2023Review
- Trinity of inflammation, innate immune cells and cross-talk of signalling pathways in tumour microenvironment.Frontiers in pharmacology · 2023Review
- SUMOylation of PDPK1 Is required to maintain glycolysis-dependent CD4 T-cell homeostasis.Cell death & disease · 2022Article
- A human orthogonal IL-2 and IL-2Rβ system enhances CAR T cell expansion and antitumor activity in a murine model of leukemia.Science translational medicine · 2021Article
- Phosphoinositide 3-Kinase p110 Delta Differentially Restrains and Directs Naïve Versus Effector CD8Frontiers in immunology · 2021Article
- C-SH2 point mutation converts p85β regulatory subunit of phosphoinositide 3-kinase to an anti-aging gene.Scientific reports · 2019Article
- Differential T-cell receptor signals for T helper cell programming.Immunology · 2018Review
- Signaling and Function of Interleukin-2 in T Lymphocytes.Annual review of immunology · 2018Review
- Regulation of Effector and Memory CD8 T Cell Differentiation by IL-2-A Balancing Act.Frontiers in immunology · 2018Review
- Spatial alterations of De Novo purine biosynthetic enzymes by Akt-independent PDK1 signaling pathways.PloS one · 2018Article
- Control of amino acid transport coordinates metabolic reprogramming in T-cell malignancy.Leukemia · 2017Article
- Review
- Akt signaling is critical for memory CD8Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Potent and selective chemical probe of hypoxic signalling downstream of HIF-α hydroxylation via VHL inhibition.Nature communications · 2016Article
- The cytotoxic T cell proteome and its shaping by the kinase mTOR.Nature immunology · 2016Article
- Alternative Activation Mechanisms of Protein Kinase B Trigger Distinct Downstream Signaling Responses.The Journal of biological chemistry · 2015Article
- PI3Kδ Regulates the Magnitude of CD8+ T Cell Responses after Challenge with Listeria monocytogenes.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The present study explored the consequences of phosphoinositide (3,4,5)-triphosphate [PI(3,4,5)P(3)] binding to the pleckstrin homology (PH) domain of the serine/threonine kinase 3-phosphoinositide-dependent kinase 1 (PDK1). The salient finding is that PDK1 directly transduces the PI(3,4,5)P(3) signaling that determines T-cell trafficking programs but not T-cell growth and proliferation. The integrity of the PDK1 PH domain thus is not required for PDK1 catalytic activity or to support cell survival and the proliferation of thymic and peripheral T cells. However, a PDK1 mutant that cannot bind PI(3,4,5)P(3) cannot trigger the signals that terminate the expression of the transcription factor KLF2 in activated T cells and cannot switch the chemokine and adhesion receptor profile of naive T cells to the profile of effector T cells. The PDK1 PH domain also is required for the maximal activation of Akt/protein kinase B (PKB) and for the maximal phosphorylation and inactivation of Foxo family transcription factors in T cells. PI(3,4,5)P(3) binding to PDK1 and the strength of PKB activity thus can dictate the nature of the T-cell response. Low levels of PKB activity can be sufficient for T-cell proliferation but insufficient to initiate the migratory program of effector T cells.
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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.