Anaspecmog The MOG peptide 35-55 is a specific fragment of the Myelin Oligodendrocyte Glycoprotein (MOG) that plays a pivotal role in understanding and modeling autoimmune neurological diseases, most notably multiple sclerosis (MS). This peptide, derived from a key component of the central nervous system's myelin sheath, is widely used in research settings to induce experimental autoimmune encephalomyelitis (EAE) in animal models. EAE closely mimics the pathological hallmarks of MS, including demyelination and inflammation, making MOG (35-55) an invaluable tool for investigating disease mechanisms and testing potential therapeutic interventions.
Myelin Oligodendrocyte Glycoprotein (MOG) is a protein found exclusively in the central nervous system (CNS). It is a minor component of the myelin sheath, which insulates nerve fibers and facilitates rapid signal transmission. In autoimmune conditions like MS, the immune system mistakenly attacks the myelin sheath, leading to demyelinationMOG (35-55), human - 1 mg. This damage disrupts nerve function and causes a wide range of neurological symptoms.
The MOG peptide 35-55, a specific sequence within the MOG protein, has been identified as an immunodominant epitope. This means it is particularly effective at eliciting an immune response, specifically the production of autoantibodies and T cell proliferation, when introduced into an organism. This characteristic makes it a powerful antigen for inducing EAE in laboratory animals.
Experimental Autoimmune Encephalomyelitis (EAE) is the most widely used animal model for studying MSMOG(35-55) amide Mouse, Rat. Write a review to earn BioPoints. Myelin ...PeptideServices;PeptideOverview ·PeptideManufacture · CustomPeptide.... By immunizing susceptible animals, such as mice and rats, with MOG (35-55) peptide, researchers can reliably induce a disease that shares many similarities with human multiple sclerosis. The induction of EAE via MOG (35-55) typically results in:
* Relapsing-Remitting Neurological Disease: Similar to the relapsing-remitting form of MS, EAE often presents with periods of symptom onset followed by recovery, and then subsequent relapses.
* Extensive Plaque-Like Demyelination: Histopathological examination of the CNS reveals lesions characterized by the loss of myelin, mirroring the plaques seen in MS patients.
* Inflammation: The immune response triggered by the peptide leads to inflammatory infiltrates within the CNS.
The ability of MOG (35-55) to induce these specific pathological outcomes makes it a critical reagent for researchers aiming to unravel the complex interplay between the immune system and the CNS in demyelinating diseases.MOG(35-55) amide Mouse, Rat. Write a review to earn BioPoints. Myelin ...PeptideServices;PeptideOverview ·PeptideManufacture · CustomPeptide... Studies using this peptide have been instrumental in identifying key immune cells, cytokines, and molecular pathways involved in MS pathogenesis.
The MOG (35-55) peptide serves several crucial functions in neuroscience research:
* Disease Modeling: As detailed above, it is the gold standard for inducing EAE, providing a robust platform for studying disease progression and the effects of therapeutic agents.MOG(35-55) is able to induce autoantibody production and relapsing-remitting neurological disease causing extensive plaque-like demyelination.
* Autoantibody Production: Immunization with MOG (35-55) can lead to the generation of autoantibodies against MOG, which are also found in some patients with MS and other demyelinating disorders like MOG antibody disease (MOGAD).
* T Cell Assays: The peptide is used in in vitro assays to study T cell responses, including proliferation and cytokine production, in response to MOG antigens. This helps in understanding T cell-mediated autoimmunity.
* Therapeutic Target Identification: By studying the immune responses elicited by MOG (35-55), researchers can identify potential targets for new therapies aimed at suppressing pathogenic immune reactions or promoting myelin repair. For example, some research explores how MOG (35-55) can be used to develop antigen-specific immunotherapies that aim to tolerize the immune system to MOG.MOG(35-55) (MOG(35-55)) TFA is a minor component of CNS myelin.MOG(35-55) (TFA) has encephalitogenic activity and induces T cell proliferative.
MOG (35-55) is available from various suppliers, often in different forms such as trifluoroacetate (TFA) salt, and may be specified for use in particular animal species (e.作者：S Bittner·2014·被引用次数：343—We here describe a protocol for immunization of C57BL/6 mice withMOG35-55 peptide10which results in a monophasic EAE with first symptoms after ...g.MOGProtein35-55is used as an antigen/immunogen to induce anti-MOGantibodies to induce experimental diseases such as experimental autoimmune ..., mouse, rat, human)Myelin Oligodendrocyte Glycoprotein (MOG)35-55 Mannan .... Purity, typically assessed by HPLC, is a critical factor for consistent and reproducible experimental results. Researchers must carefully consider the specific sequence, purity, and formulation of the peptide when designing their experimentsMOG(35-55) (mouse, rat) (trifluoroacetate salt): AnMOGantigenpeptide. Synonyms: MEVGWYRSPFSRVVHLYRNGK, Myelin Oligodendrocyte Glycoprotein (35-55).. The sequence MEVGWYRPPFSRVVHLYRNGK is often cited as the active encephalitogenic region.
Beyond its role in EAE, research into MOG antibodies and MOG antibody disease (MOGAD) has gained significant traction.Discover Rockland's Myelin oligodendrocyte glycoprotein (MOG)Peptide- 000-001-M42. Versatile and reliable for various research needs. While distinct from MS, MOGAD is another autoimmune demyelinating disorder where antibodies target MOG. Understanding the role of MOG peptides, including the 35-55 fragment, remains central to differentiating and managing these conditionsMOG 35–55 Peptide – Key Epitope in MS Research | p&e.
In conclusion, the MOG peptide 35-55 is far more than just a chemical compound; it is a vital research tool that has significantly advanced our understanding of multiple sclerosis and related autoimmune demyelinating diseases. Its ability to reliably induce EAE in animal models continues to drive progress in discovering novel treatments and ultimately improving the lives of individuals affected by these challenging neurological conditions.
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