ArticleDevelopmental neurobiology2008
A subset of signal transduction pathways is required for hippocampal growth cone collapse induced by ephrin-A5.
Article in Developmental neurobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Alzheimer's Disease and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Review
- Approaches to Manipulate Ephrin-A:EphA Forward Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2020Review
- Roles of Eph/ephrin bidirectional signaling during injury and recovery of the central nervous system.Neural regeneration research · 2018Review
- Roles of Eph/ephrin bidirectional signaling in central nervous system injury and recovery.Experimental and therapeutic medicine · 2018Article
- Redox-guided axonal regrowth requires cyclic GMP dependent protein kinase 1: Implication for neuropathic pain.Redox biology · 2017Article
- Inverse Expression Levels of EphrinA3 and EphrinA5 Contribute to Dopaminergic Differentiation of Human SH-SY5Y Cells.Journal of molecular neuroscience : MN · 2016Article
- The C. elegans NR4A nuclear receptor gene nhr-6 promotes cell cycle progression in the spermatheca lineage.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- The high molecular weight neurofilament subunit plays an essential role in axonal outgrowth and stabilization.Biology open · 2014Article
- Ephrin-A5/EphA4 signalling controls specific afferent targeting to cochlear hair cells.Nature communications · 2013Article
- Article
- Biophysics of substrate interaction: influence on neural motility, differentiation, and repair.Developmental neurobiology · 2011Review
- NO orchestrates the loss of synaptic boutons from adult "sick" motoneurons: modeling a molecular mechanism.Molecular neurobiology · 2011Review
- Ephrin-A5 suppresses neurotrophin evoked neuronal motility, ERK activation and gene expression.PloS one · 2011Article
- EphA3 functions are regulated by collaborating phosphotyrosine residues.Cell research · 2010Article
- Ephrin-B2 elicits differential growth cone collapse and axon retraction in retinal ganglion cells from distinct retinal regions.Developmental neurobiology · 2010Article
- A perspective on neuronal cell death signaling and neurodegeneration.Molecular neurobiology · 2010Article
- Nitric oxide induces pathological synapse loss by a protein kinase G-, Rho kinase-dependent mechanism preceded by myosin light chain phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Regulation of process retraction and cell migration by EphA3 is mediated by the adaptor protein Nck1.Biochemistry · 2009Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The Eph family tyrosine kinase receptors and their ligands, ephrins, play key roles in a wide variety of physiological and pathological processes including tissue patterning, angiogenesis, bone development, carcinogenesis, axon guidance, and neural plasticity. However, the signaling mechanisms underlying these diverse functions of Eph receptors have not been well understood. In this study, effects of Eph receptor activation on several important signal transduction pathways are examined. In addition, the roles of these pathways in ephrin-A5-induced growth cone collapse were assessed with a combination of biochemical analyses, pharmacological inhibition, and overexpression of dominant-negative and constitutively active mutants. These analyses showed that ephrin-A5 inhibits Erk activity but activates c-Jun N-terminal kinase. However, regulation of these two pathways is not required for ephrin-A5-induced growth cone collapse in hippocampal neurons. Artificial Erk activation by expression of constitutively active Mek1 and B-Raf failed to block ephrin-A5 effects on growth cones, and inhibitors of the Erk pathway also failed to inhibit collapse by ephrin-A5. Inhibition of JNK had no effects on ephrin-A5-induced growth cone collapse either. In addition, inhibitors to PKA and PI3-K showed no effects on ephrin-A5-induced growth cone collapse. However, pharmacological blockade of phosphotyrosine phosphatase activity, the Src family kinases, cGMP-dependent protein kinase, and myosin light chain kinase significantly inhibited ephrin-A5-induced growth cone collapse. These observations indicate that only a subset of signal transduction pathways is required for ephrin-A5-induced growth cone collapse.
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Registered trials
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