Neurofilament, Light Polypeptide Proteins (NEFL)

Neurofilaments are type IV intermediate filament heteropolymers composed of light, medium, and heavy chains. Additionally we are shipping Neurofilament, Light Polypeptide Antibodies (308) and Neurofilament, Light Polypeptide Kits (63) and many more products for this protein.

list all proteins Gene Name GeneID UniProt
NEFL 18039 P08551
NEFL 4747 P07196
NEFL 83613 P19527
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Top Neurofilament, Light Polypeptide Proteins at antibodies-online.com

Showing 8 out of 8 products:

Catalog No. Origin Source Conjugate Images Quantity Supplier Delivery Price Details
Escherichia coli (E. coli) Human His tag „Crystallography Grade“ protein due to multi-step, protein-specific purification process 1 mg Log in to see 30 to 35 Days
$5,370.21
Details
HEK-293 Cells Human Myc-DYKDDDDK Tag Validation with Western Blot 20 μg Log in to see 11 Days
$888.80
Details
Yeast Mouse His tag 100 μg Log in to see 8 to 11 Days
$578.60
Details
Wheat germ Human GST tag 2 μg Log in to see 11 to 12 Days
$230.67
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Yeast Rat His tag   1 mg Log in to see 60 to 71 Days
$3,545.67
Details
Escherichia coli (E. coli) Mouse His tag 100 μg Log in to see 15 to 18 Days
$560.00
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Escherichia coli (E. coli) Mouse Un-conjugated   100 μg Log in to see 11 to 18 Days
$582.75
Details
Escherichia coli (E. coli) Human Un-conjugated 100 μg Log in to see 15 to 18 Days
$608.00
Details

NEFL Proteins by Origin and Source

Origin Expressed in Conjugate
Mouse (Murine) ,

Human , ,
, ,
Rat (Rattus)

More Proteins for Neurofilament, Light Polypeptide (NEFL) Interaction Partners

Mouse (Murine) Neurofilament, Light Polypeptide (NEFL) interaction partners

  1. Study found that NFL protein levels are at least doubled in pmn mutant motoneurons and that NFL depletion rescues defective axon growth in cultured motoneurons and prolongs survival of pmn mutant mice. This effect was found both in Nefl+/-;pmn motoneurons in which elevated NF expression was brought back to wild-type control levels and in Nefl-/-;pmn motoneurons in which axonal neurofilament was completely lost.

  2. It may have a role in protecting neurites from dystrophy and in regulating cellular pathways related to the generation of Ab plaques.

  3. Nefl(N98S/+) mice had a noticeable tremor, and most animals showed a hindlimb clasping similar to human Charcot-Marie-Tooth Type 2E phenotype.

  4. Mice lacking NF-Lr ecapitulated the delayed synapse elimination phenotype observed in micelacking Nfasc155.

  5. 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.

  6. Neurofilament light chain (NFL) and neuronal intermediate filament protein alpha-internexin accumulate in axon swellings in the spinal white matter in a superoxide dismutase (SOD)-1 mouse model.

  7. 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).

  8. Data show that mitochondria essentially stopped moving in neurons expressing neurofilament protein (NFL) mutants, probably a consequence of cytoskeletal disruption.

  9. Myo Va interactions with intermediate filament proteins may serve similar roles in organizing organelle topography in different cell types.

  10. 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

  11. 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

  12. nNOS inhibitor, AR-R17477AR, prevents the loss of NF68 immunoreactivity induced by methamphetamine in the mouse striatum

  13. The 3' untranslated region of light neurofilament (NF-L) transcript enhances the reactivity of its own translated product and leads to loss of solubility and aggregation of NF-L protein and to coaggregation of mutant superoxide dismutase 1 (SOD1) protein

  14. copper-mediated NF-L modification may be closely related to oxidative reactions which play a critical role in neurodegenerative diseases

  15. We observed three overlapping phases in NF-L transgenic mice, including transient aggregate formation, reactive microgliosis, and progressive motor neuron loss.

  16. p190RhoGEF is involved in aggregation of NF-L protein and support a working hypothesis that aggregation of p190RhoGEF and NF-L is an upstream event triggering neurotoxicity in motor neuron disease.

  17. Mouse lactotrophs, gonadotrophs, thyrotrophs and somatotrophs express NF68 in a sexually dimorphic manner. Mouse pituitary cells from the proopiomelanocortin lineage nearly completely lack NF68 immunoreactivity.

  18. Alpha-internexin coassembles with all 3 neurofilament proteins into a single network of filaments in quadruple-transfected cells.

  19. NFL gene deficiency could retard MSCs proliferation and neuronal generation, even though the capability of neuronal lineage differentiation of MSCs may not be deterred.

  20. Disruption of neurofilament network with aggregation of NFL is a common triggering event of motor neuron degeneration in Charcot-Marie-Tooth disease.

Human Neurofilament, Light Polypeptide (NEFL) interaction partners

  1. NF-L may be involved in severity of neuronal injury following traumatic brain injury

  2. CSF neurofilament light chain protein is an accurate marker for distinguishing Alzheimer's disease patients from healthy controls.

  3. Cerebrospinal fluid neurofilament protein light is a useful tool for determining disease intensity in frontotemporal dementia and motor neuron disease patients.

  4. Our results suggest that plasma NFL levels may not be a useful biomarker for the diagnosis of prodromal and dementia stages of AD.

  5. In this Chinese Han population a novel Charcot-Marie-Tooth disease-associated gene mutations of NEFL (c.280C>T) was discovered.

  6. We conclude that low BDNF and high LCN2 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 is a candidate predictor of response to natalizumab treatment, and NF-L is a candidate predictor of clinically isolated syndrome's (CIS) conversion into MS.

  7. This study showed tat 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.

  8. Results show that both alphaS and NFL can be phosphorylated by CKII, PLK2 and PLK3, but Ser129 in alphaS is a preferential site for PLK2 and PLK3, demonstrating higher phosphorylation efficiency. Comparatively, CKII 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.

  9. Results provide evidence that in particular pNfH can be used as a good diagnostic biomarker of ALS at the diagnostic stage. Moreover, results indicate that NfL may be useful in monitoring disease progression in a subset of patients.

  10. fL is a weak independent risk factor in clinically isolated syndromes for conversion to multiple sclerosis. Its role as an axonal damage biomarker may be more relevant as suggested by its association with medium-term brain volume changes.

  11. 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.

  12. 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

  13. Findings support the potential value of serum NfL as a marker of neuroaxonal injury in early multiple sclerosis. Its reduction over time could represent regression to the mean, or a possible treatment effect of IFN-beta-1a. Association with whole brain atrophy and formation of acute white matter lesions has implications to use serum NfL as a biomarker of the overall consequences of brain damage and ongoing disease acti...

  14. Higher serum NfL concentrations are associated with more rapid brain atrophy and may therefore reflect disease intensity in dementia (FTD). Because blood sampling is less invasive and has better patient acceptability than lumbar puncture, serum NfL may provide important prognostic information and prove to be a useful outcome measure for clinical trials in FTD.

  15. We conclude that the NEFL N98S mutation is associated with a dominant intermediate Charcot-Marie-Tooth disease phenotype characterized by early-onset sensorimotor neuropathy delaying motor milestones, which may evolve into a severe and complex clinical picture including cerebellar ataxia.

  16. Plasma Concentration of the Neurofilament Light Protein (NFL) is a Biomarker of CNS Injury in HIV Infection

  17. The results showed an important role for miR-25 in regulating NEFL expression in Glioblastoma multiforme.

  18. Finally, we demonstrated that NEFL inhibited the NF-kappaB pathway, thereby suppressing the expression of uPA and decreasing NSCLC invasiveness and migration.

  19. Cerebrospinal fluid NFL concentration is increased by the early clinical stage of Alzheimer's Disease.

  20. The miR-381-NEFL axis is important for temozolomide resistance in glioblastoma multiforme.

Neurofilament, Light Polypeptide (NEFL) Protein Profile

Protein Summary

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.

Gene names and symbols associated with NEFL

  • neurofilament light (NEFL)
  • neurofilament, light polypeptide (NEFL)
  • neurofilament, light polypeptide b (neflb)
  • neurofilament, light polypeptide (Nefl)
  • neurofilament light (Nefl)
  • neurofilament, light L homeolog (nefl.L)
  • AI847934 protein
  • CMT1F protein
  • CMT2E protein
  • nefl protein
  • NF-L protein
  • NF68 protein
  • NFL protein
  • XNF-L protein
  • zgc:136626 protein

Protein level used designations for NEFL

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 , NF-L , micro glutamic acid-rich protein , neurofilament protein , Neurofilament triplet L protein

GENE ID SPECIES
464063 Pan troglodytes
477378 Canis lupus familiaris
641444 Macaca mulatta
664698 Danio rerio
18039 Mus musculus
4747 Homo sapiens
83613 Rattus norvegicus
281348 Bos taurus
100521224 Sus scrofa
397822 Xenopus laevis
419528 Gallus gallus
100173482 Pongo abelii
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