ArticleScientific reports2016
Tetraspanin CD82 Regulates the Spatiotemporal Dynamics of PKCα in Acute Myeloid Leukemia.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Tetraspanin CD82 shapes EGFR signaling outcomes through nanoscale receptor organization.The Journal of cell biology · 2026Article
- Protein palmitoylation in cancer: molecular functions and therapeutic potential.Molecular oncology · 2023Review
- CD82 palmitoylation site mutations at Cys5+Cys74 affect EGFR internalization and metabolism through recycling pathway.Acta biochimica et biophysica Sinica · 2022Article
- KAI1(CD82) is a key molecule to control angiogenesis and switch angiogenic milieu to quiescent state.Journal of hematology & oncology · 2021Article
- Proteoglycans regulate protein tyrosine phosphatase receptor σ organization on hematopoietic stem/progenitor cells.Experimental hematology · 2021Article
- Role of Metastasis Suppressor KAI1/CD82 in Different Cancers.Journal of oncology · 2021Review
- Site-specific functionality and tryptophan mimicry of lipidation in tetraspanin CD9.The FEBS journal · 2020Article
- Tetraspanin CD82 drives acute myeloid leukemia chemoresistance by modulating protein kinase C alpha and β1 integrin activation.Oncogene · 2020Article
- The tetraspanin CD82 regulates bone marrow homing and engraftment of hematopoietic stem and progenitor cells.Molecular biology of the cell · 2018Article
- Tetraspanins Function as Regulators of Cellular Signaling.Frontiers in cell and developmental biology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Patients with acute myeloid leukemia (AML) have increased myeloid cells within their bone marrow that exhibit aberrant signaling. Therefore, therapeutic targets that modulate disrupted signaling cascades are of significant interest. In this study, we demonstrate that the tetraspanin membrane scaffold, CD82, regulates protein kinase c alpha (PKCα)-mediated signaling critical for AML progression. Utilizing a palmitoylation mutant form of CD82 with disrupted membrane organization, we find that the CD82 scaffold controls PKCα expression and activation. Combining single molecule and ensemble imaging measurements, we determine that CD82 stabilizes PKCα activation at the membrane and regulates the size of PKCα membrane clusters. Further evaluation of downstream effector signaling identified robust and sustained activation of ERK1/2 upon CD82 overexpression that results in enhanced AML colony formation. Together, these data propose a mechanism where CD82 membrane organization regulates sustained PKCα signaling that results in an aggressive leukemia phenotype. These observations suggest that the CD82 scaffold may be a potential therapeutic target for attenuating aberrant signal transduction in AML.
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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.