ArticleProceedings of the National Academy of Sciences of the United States of America2005
Insights into regulation of human Schwann cell proliferation by Erk1/2 via a MEK-independent and p56Lck-dependent pathway from leprosy bacilli.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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Who cites it
35 citing papers in PubMed, 95 citations in OpenAlex.
- Adenosine AFrontiers in pharmacology · 2024Article
- What happens when Schwann cells are exposed toIBRO neuroscience reports · 2023Review
- In vivo partial reprogramming by bacteria promotes adult liver organ growth without fibrosis and tumorigenesis.Cell reports. Medicine · 2022Article
- Peripheral Nerve Decellularization forACS biomaterials science & engineering · 2022Article
- The Armadillo as a Model for Leprosy Nerve Function Impairment: Preventative and Therapeutic Interventions.Frontiers in medicine · 2022Article
- Functional Impairment of Skin Appendages Due to Peripheral Nerve Involvement byOpen forum infectious diseases · 2020Article
- SPP1 promotes Schwann cell proliferation and survival through PKCα by binding with CD44 and αvβ3 after peripheral nerve injury.Cell & bioscience · 2020Article
- Cell Biology of Intracellular Adaptation ofMicrobiology spectrum · 2019Review
- Myelination key factor krox-20 is downregulated in Schwann cells and murine sciatic nerves infected by Mycobacterium leprae.International journal of experimental pathology · 2019Article
- Targeting of Ras-mediated FGF signaling suppresses Pten-deficient skin tumor.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Microprocessor complex subunit DiGeorge syndrome critical region gene 8 (Dgcr8) is required for schwann cell myelination and myelin maintenance.The Journal of biological chemistry · 2015Article
- Bacterial-induced cell reprogramming to stem cell-like cells: new premise in host-pathogen interactions.Current opinion in microbiology · 2015Review
- Nerve injury-induced c-Jun activation in Schwann cells is JNK independent.BioMed research international · 2014Article
- The armadillo as a model for peripheral neuropathy in leprosy.ILAR journal · 2014Review
- Fibroblast growth factor receptor like-1 (FGFRL1) interacts with SHP-1 phosphatase at insulin secretory granules and induces beta-cell ERK1/2 protein activation.The Journal of biological chemistry · 2013Article
- Article
- Dynamics of defense responses and cell fate change during Arabidopsis-Pseudomonas syringae interactions.PloS one · 2013Article
- Lck tyrosine kinase mediates β1-integrin signalling to regulate Schwann cell migration and myelination.Nature communications · 2013Article
- Reprogramming diminishes retention of Mycobacterium leprae in Schwann cells and elevates bacterial transfer property to fibroblasts.F1000Research · 2013Article
- Phenolic-glycolipid-1 and lipoarabinomannan preferentially modulate TCR- and CD28-triggered proximal biochemical events, leading to T-cell unresponsiveness in mycobacterial diseases.Lipids in health and disease · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activation of extracellular signal-regulated kinase (Erk) 1/2, which plays a critical role in diverse cellular processes, including cell proliferation, is known to be mediated by the canonical Raf-mitogen-activated protein kinase kinase (MEK) kinase cascade. Alternative MEK-independent signaling pathways for Erk1/2 activation in mammalian cells are not known. During our studies of human primary Schwann cell response to long-term infection of Mycobacterium leprae, the causative organism of leprosy, we identified that intracellular M. leprae activated Erk1/2 directly by lymphoid cell kinase (p56Lck), a Src family member, by means of a PKCepsilon-dependent and MEK-independent signaling pathway. Activation of this signaling induced nuclear accumulation of cyclin D1, G1/S-phase progression, and continuous proliferation, but without transformation. Thus, our data reveal a previously unknown signaling mechanism of glial cell proliferation, which might play a role in dedifferentiation as well as nerve regeneration and degeneration. Our findings may also provide a potential mechanism by which an obligate intracellular bacterial pathogen like M. leprae subverts nervous system signaling to propagate its cellular niche for colonization and long-term bacterial survival.
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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.