MBP antibody | 26
Mouse anti Human MBP (aa67-74)
- Product Type
- Monoclonal Antibody
|Mouse anti MBP antibody, clone 26 recognizes an epitope between amino acids 67 and 74 of human myelin basic protein, also known as MBP, Myelin A1 protein or Myelin membrane encephalitogenic protein. MBP is a 304 amino acid ~33 kDa abundant component of the myelin membrane. There are 6 potential isoforms of MBP generated by alternative splicing, 4 of which lack the N-terminal region containing the immunogen sequence. Mouse anti MBP antibody, clone 26 is expected to recognize isoforms 1 and 2 (UniProt: P02686) . The N-terminal region of MBP is highly conserved and Mouse anti MBP antibody, clone 26 is expected to be broadly species cross reactive for isoforms maintaining the N-terminal region.|
- Target Species
- Product Form
- Tissue Culture Supernatant - liquid
- Tissue Culture Supernatant containing 0.1M Tris/HCl and foetal calf serum.
- Preservative Stabilisers
- <0.1% Sodium Azide (NaN3)
- Human myelin basic protein.
- Fusion Partners
- Spleen cells from immunized mice were fused with cells of the mouse SP2/0 myeloma cell line.
- For research purposes only
- 12 months from date of despatch
Avoid repeated freezing and thawing as this may denature the antibody. Storage in frost-free freezers is not recommended.
|Application Name||Verified||Min Dilution||Max Dilution|
|Immunohistology - Frozen|
References for MBP antibody
Groome, N. et al. (1988) New monoclonal antibodies reactive with defined sequential epitopes in human myelin basic protein.
J Neuroimmunol. 19 (4): 305-15.
No authors listed. (1984) Experimental allergic encephalomyelitis, a useful model for multiple sclerosis. A satellite conference of the International Society of Neurochemists. Seattle, Washington, July 16-19, 1983.
Prog Clin Biol Res. 146: 1-554.
Sanz-Rodriguez, M. et al. (2018) R-Ras1 and R-Ras2 Are Essential for Oligodendrocyte Differentiation and Survival for Correct Myelination in the Central Nervous System.
J Neurosci. 38 (22): 5096-110.
Alcover-Sanchez, B. et al. (2021) Absence of R-Ras1 and R-Ras2 causes mitochondrial alterations that trigger axonal degeneration in a hypomyelinating disease model.
Glia. 69 (3): 619-37.
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