Key features and details
- Chicken polyclonal to 68kDa Neurofilament/NF-L
- Suitable for: WB
- Reacts with: Mouse, Rat, Chicken, Cow, Human
- Isotype: IgY
Product nameAnti-68kDa Neurofilament/NF-L antibody
See all 68kDa Neurofilament/NF-L primary antibodies
DescriptionChicken polyclonal to 68kDa Neurofilament/NF-L
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Mouse, Rat, Chicken, Cow, Human
Tissue, cells or virus corresponding to Cow 68kDa Neurofilament/NF-L.
- Rat cerebral cortex lysate. This antibody gave a positive result in IF/ICC when used in the following formaldehyde fixed cell lines: SKNSH.
Previously labelled as 68kDa Neurofilament.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferPreservative: 0.065% Sodium azide
Concentration information loading...
Our Abpromise guarantee covers the use of ab72997 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/10000. Detects a band of approximately 68 kDa (predicted molecular weight: 61 kDa).|
FunctionNeurofilaments usually contain three intermediate filament proteins: L, M, and H which are involved in the maintenance of neuronal caliber.
Involvement in diseaseDefects in NEFL are the cause of Charcot-Marie-Tooth disease type 1F (CMT1F) [MIM:607734]. CMT1F is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT1 group are characterized by severely reduced nerve conduction velocities (less than 38 m/sec), segmental demyelination and remyelination with onion bulb formations on nerve biopsy, slowly progressive distal muscle atrophy and weakness, absent deep tendon reflexes, and hollow feet. CMT1F is characterized by onset in infancy or childhood (range 1 to 13 years).
Defects in NEFL are the cause of Charcot-Marie-Tooth disease type 2E (CMT2E) [MIM:607684]. CMT2E is an autosomal dominant form of Charcot-Marie-Tooth disease type 2. Neuropathies of the CMT2 group are characterized by signs of axonal regeneration in the absence of obvious myelin alterations, normal or slightly reduced nerve conduction velocities, and progressive distal muscle weakness and atrophy.
Sequence similaritiesBelongs to the intermediate filament family.
DomainThe extra mass and high charge density that distinguish the neurofilament proteins from all other intermediate filament proteins are due to the tailpiece extensions. This region may form a charged scaffolding structure suitable for interaction with other neuronal components or ions.
Phosphorylated in the Head and Rod regions by the PKC kinase PKN1, leading to inhibit polymerization.
- Information by UniProt
- 68 kDa neurofilament protein antibody
- 68kDa Neurofilament antibody
- 68kDa neurofilament protein antibody
Anti-68kDa Neurofilament/NF-L antibody (ab72997) at 1/10000 dilution + Rat cerebral cortex lysate
Predicted band size: 61 kDa
Observed band size: 68 kDa why is the actual band size different from the predicted?
ICC/IF image of ab72997 stained SKNSH cells. The cells were 4% formaldehyde fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody ab72997 at 1/200 dilution overnight at +4°C. The secondary antibody (green) was DyLight® 488 goat anti- chicken IgY (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
ab72997 has been referenced in 7 publications.
- Karbassi E et al. Direct visualization of cardiac transcription factories reveals regulatory principles of nuclear architecture during pathological remodeling. J Mol Cell Cardiol 128:198-211 (2019). PubMed: 30742811
- Cerveró C et al. Glial Activation and Central Synapse Loss, but Not Motoneuron Degeneration, Are Prevented by the Sigma-1 Receptor Agonist PRE-084 in the Smn2B/- Mouse Model of Spinal Muscular Atrophy. J Neuropathol Exp Neurol 77:577-597 (2018). PubMed: 29767748
- Clements MP et al. The Wound Microenvironment Reprograms Schwann Cells to Invasive Mesenchymal-like Cells to Drive Peripheral Nerve Regeneration. Neuron 96:98-114.e7 (2017). IHC-Fr . PubMed: 28957681
- Lei Y et al. Gold nanoclusters-assisted delivery of NGF siRNA for effective treatment of pancreatic cancer. Nat Commun 8:15130 (2017). IHC ; Human . PubMed: 28440296
- Cerveró C et al. Chronic Treatment with the AMPK Agonist AICAR Prevents Skeletal Muscle Pathology but Fails to Improve Clinical Outcome in a Mouse Model of Severe Spinal Muscular Atrophy. Neurotherapeutics 13:198-216 (2016). PubMed: 26582176
- Szarek D et al. Lizard tail spinal cord: a new experimental model of spinal cord injury without limb paralysis. FASEB J 30:1391-403 (2016). PubMed: 26667043
- Tevosian SG et al. Adrenal Development in Mice Requires GATA4 and GATA6 Transcription Factors. Endocrinology 156:2503-17 (2015). PubMed: 25933105