Multiple sclerosis: Difference between revisions
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<scene name='Multiple_sclerosis/Ifnr_n_domain_labeled/1'>N-domain</scene>, with two disulfide bonds, a <scene name='Multiple_sclerosis/Ifnr_c_domain_labeled/1'>C-domain</scene>, with one disulfide bond, and a <scene name='Multiple_sclerosis/Ifnr_linker_region_labeled/1'>linker region</scene>. The <scene name='Multiple_sclerosis/Ifnr_termini_labeled/1'>termini regions</scene> of the receptor have no secondary structure, allowing for some serious flexibility, leading to <scene name='Multiple_sclerosis/Ifnr_clash_n-c/1'>eight clashes amongst the domains</scene>.<ref name="Interferon Receptor Structure">PMID:12842042</ref> | <scene name='Multiple_sclerosis/Ifnr_n_domain_labeled/1'>N-domain</scene>, with two disulfide bonds, a <scene name='Multiple_sclerosis/Ifnr_c_domain_labeled/1'>C-domain</scene>, with one disulfide bond, and a <scene name='Multiple_sclerosis/Ifnr_linker_region_labeled/1'>linker region</scene>. The <scene name='Multiple_sclerosis/Ifnr_termini_labeled/1'>termini regions</scene> of the receptor have no secondary structure, allowing for some serious flexibility, leading to <scene name='Multiple_sclerosis/Ifnr_clash_n-c/1'>eight clashes amongst the domains</scene>.<ref name="Interferon Receptor Structure">PMID:12842042</ref> | ||
Interferon-α <scene name='Multiple_sclerosis/Ifnawithreceptorcolored/1'>binds</scene> to an interferon receptor mainly with helices C and G. There are many <scene name='Multiple_sclerosis/Ifnawithreceptorintrxns/2'>residues</scene> within 4 angstroms of one another. These residues could form many <scene name='Multiple_sclerosis/Ifnawithreceptorintrxns/5'>different types of bonds</scene>, illustrated in white dotted lines. Given that interferon-α does not undergo many structural changes upon binding to interferon receptor II, Quadt-Akabayov et al. have concluded that the binding mechanism is similar to that of a lock and key.<ref name="Interferon Receptor Interferon Alpha">PMID:17001036</ref> | Interferon-α <scene name='Multiple_sclerosis/Ifnawithreceptorcolored/1'>binds</scene> to an interferon receptor mainly with helices C and G. There are many <scene name='Multiple_sclerosis/Ifnawithreceptorintrxns/2'>residues</scene> within 4 angstroms of one another. These residues could form many <scene name='Multiple_sclerosis/Ifnawithreceptorintrxns/5'>different types of bonds</scene>, illustrated in white dotted lines. Given that interferon-α does not undergo many structural changes upon binding to interferon receptor II, Quadt-Akabayov et al. have concluded that the binding mechanism is similar to that of a lock and key. While interferon-α and -β bind to the same receptors as one another, the affinities with which they bind to IFNAR1 and IFNAR2 differ. While the binding to IFNAR2 is stronger for both in comparison to IFNAR1, interferon-β has a much stronger affinity for IFNAR1 than interferon-α.<ref name="Interferon Receptor Interferon Alpha">PMID:17001036</ref> | ||
===Interferon | ===Interferon-β and MS=== | ||
Interferon-β was first approved for the treatment of MS in 1993. The drug has shown to be extremely effective on RRMS and SPMS, though more so on RRMS, with a reduction in relapse rate, decrease in disability progression, and MRI evidence of disease activity. While the exact mechanism of effectiveness is not known, it is quite clear that when administered, interferon-β is extremely effective at slowing the progression of the two less severe types of MS. Two types of interferon-βs exist on the market: interferon-β 1a and interferon-β 1b. Interferon-β 1a products ''Avonex'' and ''Rebif'' are recombinant peptides that are produced in Chinese hamster ovary cells and are identical to natural human Interferon-β. ''Avonex'' is injected intramuscularly once a week, while ''Rebif'' is injected subcutaneously three times a week. Interferon-β 1b products ''Betaseron'' and ''Extavia'' are produced recombinantly in ''Escherichia coli bacteria'' and administered subcutaneous injection every other day. The sequence is only one residue off from that of human Interferon-β. Interferon-β 1b is titrated to a target dose over 6 weeks. All four of these major market drugs bind to the same human interferon receptor.<ref>'MS:Pathogenesis and Treatment'</ref> | |||
== Other Treatments== | == Other Treatments== | ||
