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Neurofilaments are type IV intermediate filament heteropolymers composed of light, medium, and heavy chains. Additionally we are shipping Neurofilament, Light Polypeptide Antibodies (278) and Neurofilament, Light Polypeptide Kits (47) and many more products for this protein.
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Study found that NFL protein levels are at least doubled in pmn (show TBCE Proteins) mutant motoneurons and that NFL depletion rescues defective axon growth in cultured motoneurons and prolongs survival of pmn (show TBCE Proteins) mutant mice. This effect was found both in Nefl+/-;pmn (show TBCE Proteins) motoneurons in which elevated NF expression was brought back to wild-type control levels and in Nefl-/-;pmn (show TBCE Proteins) motoneurons in which axonal neurofilament was completely lost.
Nefl(N98S/+) mice had a noticeable tremor, and most animals showed a hindlimb clasping similar to human Charcot-Marie-Tooth Type 2E phenotype.
The finding of this study suggested that a lack of NFL protein alters the expression of cytoskeletal proteins and disrupts other NF subunits, causing intracellular aggregation but not gross structural changes in cortical neurons or cytoarchitecture.
Neurofilament light chain (NFL) and neuronal intermediate filament protein (show GFAP Proteins) alpha-internexin (show INA Proteins) accumulate in axon swellings in the spinal white matter in a superoxide dismutase (SOD)-1 (show SOD1 Proteins) mouse model.
Data suggest that tetrahydropapaveroline (an endogenous catechol) causes oxidative stress resulting in astrocyte/neuronal cell death via generation of reactive oxygen species and modification/aggregation of NF-L (as in neurodegenerative diseases).
Data show that mitochondria essentially stopped moving in neurons expressing neurofilament protein (NFL) mutants, probably a consequence of cytoskeletal disruption.
Myo Va interactions with intermediate filament proteins may serve similar roles in organizing organelle topography in different cell types.
NEFL transgenic mice exhibited extended duration of the hindlimb clasping response and gait anomalies, as well as sensorimotor deficits in stationary beam and suspended bar tests
Neuropathic effects of overexpressing NF-L can occur at the level of transgene RNA and are mediated by sequences in the NF-L 3' UTR
nNOS (show NOS1 Proteins) inhibitor, AR-R17477AR, prevents the loss of NF68 immunoreactivity induced by methamphetamine in the mouse striatum
CSF (show CSF2 Proteins) neurofilament light chain protein is an accurate marker for distinguishing Alzheimer's disease patients from healthy controls.
Cerebrospinal fluid neurofilament protein light is a useful tool for determining disease intensity in frontotemporal dementia and motor neuron disease patients.
Our results suggest that plasma NFL levels may not be a useful biomarker for the diagnosis of prodromal and dementia stages of AD.
In this Chinese Han population a novel Charcot-Marie-Tooth disease-associated gene mutations of NEFL (c.280C>T) was discovered.
We conclude that low BDNF (show BDNF Proteins) and high LCN2 (show LCN2 Proteins) and NF-L levels are associated with Multiple Sclerosis (MS) pathogenesis, and high IGFBP1level is a biomarker for female MS only, suggesting different MS progression pathways between the sexes. LCN2 (show LCN2 Proteins) is a candidate predictor of response to natalizumab treatment, and NF-L is a candidate predictor of clinically isolated syndrome's (CIS (show CISH Proteins)) conversion into MS.
This study showed tat (show TAT Proteins) Serum NfL concentration is increased in familial Alzheimer disease prior to symptom onset and correlates with measures of disease stage and severity. Serum NfL may thus be a feasible biomarker of early AD-related neurodegeneration.
Results show that both alphaS and NFL can be phosphorylated by CKII (show CSNK2A1 Proteins), PLK2 (show PLK2 Proteins) and PLK3 (show PLK3 Proteins), but Ser129 in alphaS is a preferential site for PLK2 (show PLK2 Proteins) and PLK3 (show PLK3 Proteins), demonstrating higher phosphorylation efficiency. Comparatively, CKII (show CSNK2A1 Proteins) preferentially phosphorylates Ser473 in NFL and this site can be phosphorylated by PLK1, 2 and 3, but these enzymes prefer to modify other sites within NFL.
Results provide evidence that in particular pNfH can be used as a good diagnostic biomarker of ALS (show IGFALS Proteins) at the diagnostic stage. Moreover, results indicate that NfL may be useful in monitoring disease progression in a subset of patients.
Level of neurofilament heavy chain and light chains were significantly elevated in the cerebrospinal fluid of Amyotrophic Lateral Sclerosis (ALS) patients compared to healthy controls/controls without parenchymal central nervous system involvement and ALS mimic disease patients.
Results from 2 independent prospective cohort studies show that serum NFL is a sensitive and dynamic biomarker for axonal injury in concussive traumatic brain injury. The marker should be useful to detect and monitor CNS injury in concussion
Neurofilaments are type IV intermediate filament heteropolymers composed of light, medium, and heavy chains. Neurofilaments comprise the axoskeleton and they functionally maintain the neuronal caliber. They may also play a role in intracellular transport to axons and dendrites. This gene encodes the light chain neurofilament protein. Mutations in this gene cause Charcot-Marie-Tooth disease types 1F (CMT1F) and 2E (CMT2E), disorders of the peripheral nervous system that are characterized by distinct neuropathies. A pseudogene has been identified on chromosome Y.
neurofilament, light polypeptide 68kDa
, neurofilament, light polypeptide
, neurofilament light polypeptide
, 68 kDa neurofilament protein
, neurofilament protein L
, neurofilament triplet L protein
, light molecular weight neurofilament protein
, neurofilament protein, light chain
, neurofilament subunit NF-L
, micro glutamic acid-rich protein
, neurofilament protein
, Neurofilament triplet L protein