ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1997
Study of proline-directed protein kinases involved in phosphorylation of the heavy neurofilament subunit.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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Who cites it
23 citing papers in PubMed, 93 citations in OpenAlex.
- Neurofilaments and Neurofilament Proteins in Health and Disease.Cold Spring Harbor perspectives in biology · 2017Review
- Article
- Divergent and convergent roles for kinases and phosphatases in neurofilament dynamics.Journal of cell science · 2014Article
- Nuclear and cytosolic JNK signalling in neurons.Nature reviews. Neuroscience · 2014Review
- Signaling mechanisms and disrupted cytoskeleton in the diphenyl ditelluride neurotoxicity.Oxidative medicine and cellular longevity · 2014Review
- Topographic regulation of neuronal intermediate filaments by phosphorylation, role of peptidyl-prolyl isomerase 1: significance in neurodegeneration.Histochemistry and cell biology · 2013Review
- Neurofilaments at a glance.Journal of cell science · 2012Review
- Post-translational modification of Cu/Zn superoxide dismutase under anaerobic conditions.Biochemistry · 2012Article
- Activation of c-Jun N-terminal kinase (JNK) during mitosis in retinal progenitor cells.PloS one · 2012Article
- Declining phosphatases underlie aging-related hyperphosphorylation of neurofilaments.Neurobiology of aging · 2011Article
- Dynamic changes of neuroskeletal proteins in DRGs underlie impaired axonal maturation and progressive axonal degeneration in type 1 diabetes.Experimental diabetes research · 2009Article
- Neurofilament tail phosphorylation: identity of the RT-97 phosphoepitope and regulation in neurons by cross-talk among proline-directed kinases.Journal of neurochemistry · 2008Article
- Large scale hippocampal cellular distress may explain the behavioral consequences of repetitive traumatic experiences--a proteomic approach.Neurochemical research · 2008Article
- Review of the multiple aspects of neurofilament functions, and their possible contribution to neurodegeneration.Molecular neurobiology · 2008Review
- p35/cyclin-dependent kinase 5 phosphorylation of ras guanine nucleotide releasing factor 2 (RasGRF2) mediates Rac-dependent Extracellular Signal-regulated kinase 1/2 activity, altering RasGRF2 and microtubule-associated protein 1b distribution in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Decreased cyclin-dependent kinase 5 (cdk5) activity is accompanied by redistribution of cdk5 and cytoskeletal proteins and increased cytoskeletal protein phosphorylation in p35 null mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Effect of propionic and methylmalonic acids on the high molecular weight neurofilament subunit (NF-H) in rat cerebral cortex.Neurochemical research · 2002Article
- Effect of the branched-chain alpha-ketoacids accumulating in maple syrup urine disease on the high molecular weight neurofilament subunit (NF-H) in rat cerebral cortex.Metabolic brain disease · 2002Article
- Integrin alpha(1) beta(1)-mediated activation of cyclin-dependent kinase 5 activity is involved in neurite outgrowth and human neurofilament protein H Lys-Ser-Pro tail domain phosphorylation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Glutamate slows axonal transport of neurofilaments in transfected neurons.The Journal of cell biology · 2000Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high-molecular-mass neurofilament subunit (NFH) is normally hypophosphorylated in the neuronal perikaryon and undergoes extensive phosphorylation after entering the initial axon segment. Aberrant hyperphosphorylation of perikaryal NFH is a common feature of many neurological diseases. In a previous study (), we demonstrated a correlation between phosphorylation of perikaryal NFH and induction of stress-activated protein kinase (SAPK)-gamma. In this report, we present direct evidence showing that the in vivo activation of SAPKs by an upstream activator (MEKK-1) caused extensive NFH phosphorylation. We also show that stress-activated p38 kinases were not involved in the phosphorylation of perikaryal NFH in cultured dorsal root ganglion neurons and that this process was reversible. SAPKgamma was shown to be located in both the cell body and the neurites of the cultured neurons, suggesting that it is likely to be involved in the phosphorylation of cytoplasmic substrates. These could include neuritic NFH, which is highly phosphorylated despite the demonstrated lack of cyclin-dependent kinase-5 activity in these neurons. Neuritic NFH was also highly phosphorylated in neuronal cultures devoid of Schwann cells, indicating that this form of post-translational modification does not require cues stemming from Schwann cell-axon contacts. Collectively, these findings provide significant new insights into mechanisms involved in NFH phosphorylation in normal neurons and in disease states characterized by aberrant phosphorylation of neurofilaments.
Indexed as
Identifiers
9391002PMC6573415W2152629837What OpenQuestion holds
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.