ArticleThe Journal of physiology2006
Signalling during hypoxia in human T lymphocytes--critical role of the src protein tyrosine kinase p56Lck in the O2 sensitivity of Kv1.3 channels.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 44 citations in OpenAlex.
- Deviation from physiologically appropriate oxygen levels alters proliferation, cytokine production and proximal antigen receptor signalling in CD4+ memory T cells.Frontiers in immunology · 2026Article
- Effects of Preoperative Nutritional Status and Lymphocyte Count on the Development of Early-term Atrial Fibrillation After Coronary Artery Bypass Grafting: A Retrospective Study.Brazilian journal of cardiovascular surgery · 2024Article
- The Phosphorylation of Kv1.3: A Modulatory Mechanism for a Multifunctional Ion Channel.Cancers · 2023Review
- How the Potassium Channel Response of T Lymphocytes to the Tumor Microenvironment Shapes Antitumor Immunity.Cancers · 2022Review
- The LCK-14-3-3ζ-TRPM8 axis regulates TRPM8 function/assembly and promotes pancreatic cancer malignancy.Cell death & disease · 2022Article
- Oxygen-dependent regulation of ion channels: acute responses, post-translational modification, and response to chronic hypoxia.Pflugers Archiv : European journal of physiology · 2021Review
- A defect in KCa3.1 channel activity limits the ability of CD8Science signaling · 2018Article
- Novel "Elements" of Immune Suppression within the Tumor Microenvironment.Cancer immunology research · 2017Review
- Potassium channels Kv1.3 and KCa3.1 cooperatively and compensatorily regulate antigen-specific memory T cell functions.Nature communications · 2017Article
- Kv1.3 Channels Mark Functionally Competent CD8+ Tumor-Infiltrating Lymphocytes in Head and Neck Cancer.Cancer research · 2017Article
- Can Some Marine-Derived Fungal Metabolites Become Actual Anticancer Agents?Marine drugs · 2015Review
- The C-terminus SH3-binding domain of Kv1.3 is required for the actin-mediated immobilization of the channel via cortactin.Molecular biology of the cell · 2015Article
- Placing ion channels into a signaling network of T cells: from maturing thymocytes to healthy T lymphocytes or leukemic T lymphoblasts.BioMed research international · 2015Review
- Ghrelin increases lymphocytes in chronic normobaric hypoxia.Advanced pharmaceutical bulletin · 2014Article
- Oxidative modulation of voltage-gated potassium channels.Antioxidants & redox signaling · 2014Review
- Significance of preoperative total lymphocyte count as a prognostic criterion in adult cardiac surgery.Anesthesiology and pain medicine · 2014Article
- Selective inhibition of KCa3.1 channels mediates adenosine regulation of the motility of human T cells.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Selective inhibition of CCR7(-) effector memory T cell activation by a novel peptide targeting Kv1.3 channel in a rat experimental autoimmune encephalomyelitis model.The Journal of biological chemistry · 2012Article
- Modulation of Kv1.3 channels by protein kinase A I in T lymphocytes is mediated by the disc large 1-tyrosine kinase Lck complex.American journal of physiology. Cell physiology · 2012Article
- Modulation of T cell activation by localized K⁺ accumulation at the immunological synapse--a mathematical model.Journal of theoretical biology · 2012Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
T lymphocytes encounter hypoxia when they migrate to pathological sites such as tumours and wounds. The inability of T cells to provide an efficient defence at these sites can in part be explained by the hypoxic environment. Kv 1.3 channels, important components of the T cell activation process are inhibited by hypoxia and their inhibition accounts for a hypoxia-induced decrease in T cell proliferation. Although Kv 1.3 channels play a key role in T cell O(2) sensing, the signalling mechanisms mediating their response to hypoxia are still not understood. In this study, we show that the src-protein tyrosine kinase p56Lck (Lck) is required for Kv 1.3 channel response to hypoxia. Pre-exposure to the src inhibitor PP2 abolished the hypoxia-induced inhibition of Kv 1.3 channels in primary human T lymphocytes. Moreover, Kv 1.3 channel sensitivity to hypoxia was lost in Lck-deficient Jurkat T cells. Further studies with recombinant Kv 1.3 channels showed that Kv 1.3 channels lack intrinsic O(2) sensitivity, but delivery of Lck into the cells and transfection of a constitutively active Lck (Y505FLck) restored their sensitivity to hypoxia. Although Lck is necessary for the Kv 1.3 channel response to hypoxia, it does not directly inhibit Kv 1.3 channels. Indeed, under normal oxygen tension, delivery of active Lck into L929 cells and overexpression of Y505FLck did not decrease recombinant Kv 1.3 currents. On the contrary, activation of endogenous src kinases increased wild-type Kv 1.3 currents in T lymphocytes. Our findings indicate that Lck is required for the acute response to hypoxia of human T lymphocytes as it is necessary to confer O(2) sensitivity on Kv 1.3 channels.
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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.