FLAG-Peptide - DYKDDDDK

MOG (97-108) TCFFRDHSYQEE represents a short peptide sequence of the protein lipid part of the myelin sheath. Such proteins are obviously targets of the immune defense in multiple sclerosis. Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), is characterised by primary demyelination. It is widely thought that this is the result of an autoimmune attack against myelin components. Potential target antigens in MS are proteins of the myelin sheath such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), and proteolipid protein (PLP). Experimental autoimmune encephalomyelitis (EAE) has proven to be a particularly useful animal model. T cell epitopes of MOG for the induction of EAE in mice have been identified. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.

MOG (91-108) SDEGGYTCFFRDHSYQEE represents a short peptide sequence of the protein lipid part of the myelin sheath. Such proteins are obviously targets of the immune defense in multiple sclerosis. Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), is characterised by primary demyelination. It is widely thought that this is the result of an autoimmune attack against myelin components. Potential target antigens in MS are proteins of the myelin sheath such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), and proteolipid protein (PLP). Experimental autoimmune encephalomyelitis (EAE) has proven to be a particularly useful animal model. T cell epitopes of MOG for the induction of EAE in mice have been identified. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.

MOG (92-106) DEGGYTCFFRDHSYQ represents a short peptide sequence of the protein lipid part of the myelin sheath. Such proteins are obviously targets of the immune defense in multiple sclerosis. Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), is characterised by primary demyelination. It is widely thought that this is the result of an autoimmune attack against myelin components. Potential target antigens in MS are proteins of the myelin sheath such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), and proteolipid protein (PLP). Experimental autoimmune encephalomyelitis (EAE) has proven to be a particularly useful animal model. T cell epitopes of MOG for the induction of EAE in mice have been identified. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.

MOG (183-191) FVIVPVLGP represents a short peptide sequence of the protein lipid part of the myelin sheath. Such proteins are obviously targets of the immune defense in multiple sclerosis. Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), is characterised by primary demyelination. It is widely thought that this is the result of an autoimmune attack against myelin components. Potential target antigens in MS are proteins of the myelin sheath such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein (MBP), and proteolipid protein (PLP). Experimental autoimmune encephalomyelitis (EAE) has proven to be a particularly useful animal model. T cell epitopes of MOG for the induction of EAE in mice have been identified. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches. An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.

The MOG peptide fragment 35-55 (Myelin Oligodendrocyte Glycoprotein Peptide Fragment 35-55) induces experimental autoimmune encephalomyelitis in rodents. A single injection of this peptide produces a relapsing-remitting neurologic disease (multiple sclerosis, MS) with extensive plaque-like demyelination. Other experiments show that immunization with MOG (35-55) suppresses spontaneous regeneration of dopaminergic neurons injured with MPTP (a neurotoxin) >. Multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), is characterised by primary demyelination. It is widely thought that this is the result of an autoimmune attack against myelin components. Potential target antigens in MS are proteins of the myelin sheath > such as myelin oligodendrocyte glycoprotein (MOG), myelin basic protein ( MBP, 1-11 human: P2271 > 54-72 human: P2272 >), and proteolipid protein PLP, 139-151: P2273 > 178-191: P2274 >). Experimental autoimmune encephalomyelitis (EAE) has proven to be a particularly useful animal model for MS. T cell epitopes of MOG for the induction of EAE in mice have been identified. Several inhibitors of amyloid-beta aggregation have been published. Many of them are fragments and modified peptides derived from the native amyloid-beta sequence. Others were identified by phage display approaches.An overview about peptides that target amyloid-beta is described by Stains et al. (2007) ChemMedChem 2, 1674-1692.