Multiple sclerosis: Difference between revisions

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'''Please have patience as I edit this page over the next week! Thank you!'''--[[User:Kirsten Eldredge|Kirsten Eldredge]] 04:06, 21 April 2012 (IDT)
'''Please have patience as I edit this page over the next week! Thank you!'''--[[User:Kirsten Eldredge|Kirsten Eldredge]] 04:06, 21 April 2012 (IDT)
'''Multiple sclerosis (MS)'''- an autoimmune disease that effects every single victim differently. While some can go through their lives with relatively mild symptoms, others can become incapacitated within years or even months. Defined by Nylander and Hafler, MS is a "multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual."<ref name="MS Nylander & Hafler">PMID:22466660</ref> While the effects of the disease are well known, and various treatments exist for the disease, the exact identity of an antigen or infectious agent that causes the myriad of symptoms is unknown.
There are three ways in which MS is categorized: relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS). In RRMS, the patient experiences periods of time in which the symptoms considerably increase, although the neurological function of the patient usually returns to normal after the episode. Those with SPMS have symptoms like RRMS, but do not return to normal neurological function after the episode. In PPMS, the patient has an initial episode that never ends. That is, once the symptoms begin, there is no relapse in the neurological degradation.


<StructureSection load='1ifa' size='500' side='right' caption='Click on the green links to the left to see key structural features of Interferon Beta (PDB entry [[1ifa]])' scene='Multiple_sclerosis/Interferon_beta/1'>  
<StructureSection load='1ifa' size='500' side='right' caption='Click on the green links to the left to see key structural features of Interferon Beta (PDB entry [[1ifa]])' scene='Multiple_sclerosis/Interferon_beta/1'>  
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Interferon-β is a protein growth factor that stimulates an antiviral defense. Its encoding gene is one of only two known vertebrate structural genes that lacks introns.<ref name="Biochem Text">Voet, D., Voet, J.G., and C. Pratt. ''Fundamentals of Biochemistry'' 3rd Edition. Hoboken, NJ: John Wiley and Sons, 2008. Print.</ref>  
Interferon-β is a protein growth factor that stimulates an antiviral defense. Its encoding gene is one of only two known vertebrate structural genes that lacks introns.<ref name="Biochem Text">Voet, D., Voet, J.G., and C. Pratt. ''Fundamentals of Biochemistry'' 3rd Edition. Hoboken, NJ: John Wiley and Sons, 2008. Print.</ref>  


Interferon-β is a relatively simple biological response modifier, with several <scene name='Multiple_sclerosis/Interferon_beta_labeled/1'>identifiable regions</scene>. It consists of five <scene name='Multiple_sclerosis/Ifnb_helices_in_color/1'>alpha helices</scene>, as well as multiple interconnecting <scene name='Multiple_sclerosis/Interferon_beta_loops/2'>loop regions</scene>. Helices A, B and D run <scene name='Multiple_sclerosis/Ifnb_parallel_abd/3'>parallel to one another</scene>, and helices C and E run <scene name='Multiple_sclerosis/Ifnb_antiparallel/1'>anti-parallel</scene> to the other three helices, but <scene name='Multiple_sclerosis/Ifnb_antiparallel_ce/3'>parallel</scene> to one another. Helix A consists of residues 6-23; Helix B consists of residues 49-65; Helix C consists of residues 77-91; Helix D consists of residues 112-131; and Helix E consists of residues 135-155.<ref name="Structure">PMID:20616576</ref><ref name="UniProt">http://www.uniprot.org/uniprot/P00784</ref>
Interferon-β is a relatively simple biological response modifier, with several <scene name='Multiple_sclerosis/Interferon_beta_labeled/1'>identifiable regions</scene>. It consists of five <scene name='Multiple_sclerosis/Ifnb_helices_in_color/1'>alpha helices</scene>, as well as multiple interconnecting <scene name='Multiple_sclerosis/Interferon_beta_loops/2'>loop regions</scene>. Helices A, B and D run <scene name='Multiple_sclerosis/Ifnb_parallel_abd/3'>parallel to one another</scene>, and helices C and E run <scene name='Multiple_sclerosis/Ifnb_antiparallel/1'>anti-parallel</scene> to the other three helices, but <scene name='Multiple_sclerosis/Ifnb_antiparallel_ce/3'>parallel</scene> to one another. Helix A consists of residues 6-23; Helix B consists of residues 49-65; Helix C consists of residues 77-91; Helix D consists of residues 112-131; and Helix E consists of residues 135-155.<ref name="Structure Ifn B">PMID:20616576</ref><ref name="UniProt">http://www.uniprot.org/uniprot/P00784</ref>


Interferons alpha and beta interact with a receptor at the surface of <ref>[http://www.jbc.org/content/282/28/20045.full?sid=cbf08059-44d4-4957-8ea7-0351cab9c2ac] Samuel, C.E. "Interferons, Interferon Receptors, Signal Transducer and Transcriptional Activators, and Inteferon Regulatory Factors." ''J Biol Chem'' 2007 282: 20045-20046. First Published on May 14, 2007, doi:10.1074/jbc.R700025200</ref>  
Interferons alpha and beta interact with a receptor at the surface of <ref>[http://www.jbc.org/content/282/28/20045.full?sid=cbf08059-44d4-4957-8ea7-0351cab9c2ac] Samuel, C.E. "Interferons, Interferon Receptors, Signal Transducer and Transcriptional Activators, and Inteferon Regulatory Factors." ''J Biol Chem'' 2007 282: 20045-20046. First Published on May 14, 2007, doi:10.1074/jbc.R700025200</ref>  

Revision as of 00:25, 22 April 2012

Please have patience as I edit this page over the next week! Thank you!--Kirsten Eldredge 04:06, 21 April 2012 (IDT)

Multiple sclerosis (MS)- an autoimmune disease that effects every single victim differently. While some can go through their lives with relatively mild symptoms, others can become incapacitated within years or even months. Defined by Nylander and Hafler, MS is a "multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual."[1] While the effects of the disease are well known, and various treatments exist for the disease, the exact identity of an antigen or infectious agent that causes the myriad of symptoms is unknown.

There are three ways in which MS is categorized: relapsing-remitting (RRMS), secondary progressive (SPMS), and primary progressive (PPMS). In RRMS, the patient experiences periods of time in which the symptoms considerably increase, although the neurological function of the patient usually returns to normal after the episode. Those with SPMS have symptoms like RRMS, but do not return to normal neurological function after the episode. In PPMS, the patient has an initial episode that never ends. That is, once the symptoms begin, there is no relapse in the neurological degradation.

Interferon-β

Interferon-β is a protein growth factor that stimulates an antiviral defense. Its encoding gene is one of only two known vertebrate structural genes that lacks introns.[2]

Interferon-β is a relatively simple biological response modifier, with several . It consists of five , as well as multiple interconnecting . Helices A, B and D run , and helices C and E run to the other three helices, but to one another. Helix A consists of residues 6-23; Helix B consists of residues 49-65; Helix C consists of residues 77-91; Helix D consists of residues 112-131; and Helix E consists of residues 135-155.[3][4]

Interferons alpha and beta interact with a receptor at the surface of [5]

Interferon receptor

[6]

Interferon receptor bound to interferon alpha

A comparison of Interferon Alpha to Interferon Beta

Interferon Alpha

Drag the structure with the mouse to rotate

Interferon Beta

Drag the structure with the mouse to rotate


Click on the green links to the left to see key structural features of Interferon Beta (PDB entry 1ifa)

Drag the structure with the mouse to rotate

Other TreatmentsOther Treatments

CopaxoneCopaxone

ReferencesReferences

  1. ↑ Nylander A, Hafler DA. Multiple sclerosis. J Clin Invest. 2012 Apr 2;122(4):1180-8. doi: 10.1172/JCI58649. Epub 2012 Apr 2. PMID:22466660 doi:10.1172/JCI58649
  2. ↑ Voet, D., Voet, J.G., and C. Pratt. Fundamentals of Biochemistry 3rd Edition. Hoboken, NJ: John Wiley and Sons, 2008. Print.
  3. ↑ Kudo M. Management of hepatocellular carcinoma: from prevention to molecular targeted therapy. Oncology. 2010 Jul;78 Suppl 1:1-6. Epub 2010 Jul 8. PMID:20616576 doi:10.1159/000315222
  4. ↑ http://www.uniprot.org/uniprot/P00784
  5. ↑ [1] Samuel, C.E. "Interferons, Interferon Receptors, Signal Transducer and Transcriptional Activators, and Inteferon Regulatory Factors." J Biol Chem 2007 282: 20045-20046. First Published on May 14, 2007, doi:10.1074/jbc.R700025200
  6. ↑ Chill JH, Quadt SR, Levy R, Schreiber G, Anglister J. The human type I interferon receptor: NMR structure reveals the molecular basis of ligand binding. Structure. 2003 Jul;11(7):791-802. PMID:12842042

Relevant 3D StructuresRelevant 3D Structures

Interferon BetaInterferon Beta

1au1 - Homo sapiens

1ifa, 1wu3 - Mus musculus

Interferon ReceptorsInterferon Receptors

3s98, 3se3, 3se4, 1n6u, 1n6v, 2hym, 2kz1, 2lag, 3s8w, 3s9d - Homo sapiens

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Kirsten Eldredge
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