Anti-68kDa Neurofilament antibody [EP675Y] (ab52989)
- Product nameAnti-68kDa Neurofilament antibody [EP675Y]See all 68kDa Neurofilament primary antibodies ...
- DescriptionRabbit monoclonal [EP675Y] to 68kDa Neurofilament
- Tested applicationsWB, IP, Flow Cyt more details
- Species reactivityReacts with: Mouse, Rat, Human
A synthetic peptide corresponding to residues near the C-term of human NF-L was used as immunogen
- Positive control
- SH-SY5Y cytoplasmic cell lysate
- General notesProduced under U.S. Patent No. 5,675,063.
- Storage instructionsStore at -20°C. Stable for 12 months at -20°C
- Storage bufferPBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%
- PurityTissue culture supernatant
- Clonality Monoclonal
- Clone numberEP675Y
Our Abpromise guarantee covers the use of ab52989 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
WB: 1/50000. Detects a band of approximately 68 kDa (predicted molecular weight: 61 kDa).
Is unsuitable for ICC.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
- 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.
- 68 kDa neurofilament protein antibody
- 68kDa neurofilament protein antibody
- CMT 1F antibody
- CMT 2E antibody
- CMT1F antibody
- CMT2E antibody
- FLJ53642 antibody
- Light molecular weight neurofilament protein antibody
- NEFL antibody
- Neurofilament light antibody
- Neurofilament light polypeptide 68kDa antibody
- Neurofilament light polypeptide antibody
- Neurofilament protein, light chain antibody
- Neurofilament subunit NF L antibody
- Neurofilament triplet L protein antibody
- NF 68 antibody
- NF L antibody
- NF-L antibody
- NF68 antibody
- NFL antibody
- NFL_HUMAN antibody
Anti-68kDa Neurofilament antibody [EP675Y] images
Anti-68kDa Neurofilament antibody [EP675Y] (ab52989) at 1/50000 dilution + SH-SY5Y cell lysate at 10 µg
goat anti-rabbit HRP labelled at 1/2000 dilution
Predicted band size : 61 kDa
Observed band size : 68 kDa (why is the actual band size different from the predicted?)
References for Anti-68kDa Neurofilament antibody [EP675Y] (ab52989)
This product has been referenced in:
- Zhao X et al. Neuronal PPARgamma deficiency increases susceptibility to brain damage after cerebral ischemia. J Neurosci 29:6186-95 (2009). WB ; Mouse . Read more (PubMed: 19439596) »