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Peptides  >  Myelin Oligodendrocyte Glycoprotein (MOG)/Myelin Basic Proteins (MBP)  >>  MOG (35-55), mouse, rat

Product Name MOG (35 - 55), mouse, rat
MEVGWYRSPFSRVVHLYRNGK
Size 5 mg
Catalog # AS-60130-5
US$ $440
Purity % Peak Area By HPLC ≥ 95%
Description

Myelin oligodendrocyte glycoprotein (MOG) is a member of the immunoglobulin superfamily and is expressed exclusively in the central nervous system (1-3). MOG (35-55) is able to induce autoantibody production and relapsing-remitting neurological disease causing extensive plaque-like demyelination (1-2). Autoantibody response to MOG (35-55) has been observed in multiple sclerosis (MS) patients and MOG (35-55)-induced experimental autoimmune encephalomyelitis (EAE) C57/BL6 mice and Lewis rats (1-4).

Every lot of MOG (35-55) peptide is tested and proven to induce EAE. For the EAE results of the current lot, please email biology@anaspec.com.

MOG SAVINGS EVENT! Click here to learn more: SensoLyte MOG Kits, MOG 35-55 peptide, and MOG Recombinant Proteins

Detailed Information Datasheet
Flyer
Storage -20°C
References 1. Slavin, A. et al. Autoimmunity 28, 109 (1998).
2. Ichikawa, M. et al. Cellular Immunol 191, 97 (1999).
3. Kennel De March, A. et al. J Neuroimmunol 135, 117 (2003).
4. Robinson, W. et al. Nat Biotech 21, 1033 (2003).
Molecular Weight 2582
Sequence
(One-Letter Code)
MEVGWYRSPFSRVVHLYRNGK
Sequence
(Three-Letter Code)
H - Met - Glu - Val - Gly - Trp - Tyr - Arg - Ser - Pro - Phe - Ser - Arg - Val - Val - His - Leu - Tyr - Arg - Asn - Gly - Lys - OH
Product Citations Barkauskas, DS. et al. (2015). Focal transient CNS vessel leak provides a tissue niche for sequential immune cell accumulation during the asymptomatic phase of EAE induction. Exp Neurol doi:10.1016/j.expneurol.2015.02.018.
Aubé, B. et al. (2014). Neutrophils Mediate Blood–Spinal Cord Barrier Disruption in Demyelinating Neuroinflammatory Diseases. J Immunol doi: 10.4049/​jimmunol.1400401.
Cantor, JM. (2014). CD98 is a potential target for ablating B cell clonal expansion and autoantibody in multiple sclerosis. J Neuroimmunol doi: 10.1016/j.jneuroim.2014.06.015.
Krementsov, DN., et al. (2014). Sex‐specific control of central nervous system autoimmunity by p38 mitogen‐activated protein kinase signaling in myeloid cells. Ann Neurol 75, 50. doi: 10.1002/ana.24020.
Nagashima, H. et al. (2014). The adaptor TRAF5 limits the differentiation of inflammatory CD4+ T cells by antagonizing signaling via the receptor for IL-6. Nat Immunol 15, 449.
Ouyang, S. et al. (2014). Leukocyte infiltration into spinal cord of EAE mice is attenuated by removal of endothelial leptin signaling. Brain Behav Immun 40, 61.
Zhao, YG. et al. (2012). Dihydroartemisinin ameliorates inflammatory disease by its reciprocal effects on Th and regulatory T cell function via modulating the mammalian target of rapamycin pathway. J Immunol, 189, 4417. doi: 10.4049/jimmunol.1200919.
Polak, P. et al. (2011). Locus coeruleus damage and noradrenaline reductions in multiple sclerosis and experimental autoimmune encephalomyelitis. Brain 10.1093/brain/awq362. doi: 10.1093/brain/awq362.
Shohreh, R. et al. (2011). GH, but not GHRH, plays a role in the development of experimental autoimmune encephalomyelitis. Endocrinology 10.1210/en.2011-1317. doi: 10.1210/en.2011-1317.
Aizman, E. et al. (2010). The combined treatment of Copaxone and Salirasib attenuates experimental autoimmune encephalomyelitis (EAE) in mice. J Neuroimmunol 229, 192. doi: 10.1016/j.jneuroim.2010.08.022.
Simonini, MV. et al. (2010). Increasing CNS noradrenaline reduces EAE severity. J Neuroimmune Pharmacol 5, 252. doi: 10.1007/s11481-009-9182-2.
Simonini, M. et al. (2010). Regulation of oligodendrocyte progenitor cell maturation by PPARδ: effects on bone morphogenetic proteins. ASN Neuro 10.1042/AN20090033.
Toscano, MG. et al. (2010). Dendritic cells transduced with lentiviral vectors expressing VIP differentiate into VIP-secreting tolerogenic-like DCs. Mol Ther 18, 1035. doi: 10.1038/mt.2009.293.
Kawasaki, T. et al. (2009). A minimal regulatory domain in the C terminus of STIM1 binds to and activates ORAI1 CRAC channels. Biochem Biophys Res Commun 385, 49. doi: 10.1016/j.bbrc.2009.05.020.
Li, Q. et al. (2009). Augmenting DAF levels in vivo ameliorates experimental autoimmune encephalomyelitis. Mol Immunol 46, 2885. doi: 10.1016/j.molimm.2009.07.003.
Li, Q. et al. (2009). The complement inhibitor FUT-175 suppresses T cell autoreactivity in experimental autoimmune encephalomyelitis. Am J Pathol 175, 661. doi: 10.2353/ajpath.2009.081093.
Guo, B. et al. (2008). The type 1 IFN induction pathway constrains Th17-mediated autoimmune inflammation in mice. J Clin Invest 118, 1680. doi: 10.1172/JCI33342.
Sharp, AJ. et al. (2008). P2x7 deficiency suppresses development of experimental autoimmune encephalomyelitis. J Neuroinflammation 10.1186/1742-2094-5-33. doi: 10.1186/1742-2094-5-33.
Frausto, RF. et al. (2007). Myelin oligodendrocyte glycoprotein peptide-induced experimental allergic encephalomyelitis and T cell responses are unaffected by immunoproteasome deficiency. J Neuroimmunol 192, 124.
     
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