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PDBsum entry 1q70

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Immune system PDB id
1q70

 

 

 

 

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Contents
Protein chain
119 a.a.
Theoretical model
PDB id:
1q70
Name: Immune system
Title: Homology model of the extracellular domain of human myelin oligodendrocyte glycoprotein
Structure: Myelin-oligodendrocyte glycoprotein. Chain: a. Fragment: extracellular domain
Source: Homo sapiens. Human
Authors: M.F.Mesleh,N.Belmar,C.W.Lu,V.V.Krishnan,R.S.Maxwell, C.P.Genain,M.Cosman
Key ref: M.F.Mesleh et al. (2002). Marmoset fine B cell and T cell epitope specificities mapped onto a homology model of the extracellular domain of human myelin oligodendrocyte glycoprotein. Neurobiol Dis, 9, 160-172. PubMed id: 11895369 DOI: 10.1006/nbdi.2001.0474
Date:
14-Aug-03     Release date:   04-Nov-03    
PROCHECK
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 Headers
 References

Protein chain
Q92892  (MOG_HUMAN) -  Myelin-oligodendrocyte glycoprotein from Homo sapiens
Seq:
Struc:
247 a.a.
119 a.a.
Key:    Secondary structure

 

 
DOI no: 10.1006/nbdi.2001.0474 Neurobiol Dis 9:160-172 (2002)
PubMed id: 11895369  
 
 
Marmoset fine B cell and T cell epitope specificities mapped onto a homology model of the extracellular domain of human myelin oligodendrocyte glycoprotein.
M.F.Mesleh, N.Belmar, C.W.Lu, V.V.Krishnan, R.S.Maxwell, C.P.Genain, M.Cosman.
 
  ABSTRACT  
 
Aberrant association of autoantibodies with myelin oligodendrocyte glycoprotein (MOG), an integral membrane protein of the central nervous system (CNS) myelin, has been implicated in the pathogenesis of multiple sclerosis (MS). Sensitization of nonhuman primates (Callithrix jacchus marmosets) against the nonglycosylated, recombinant N-terminal domain of rat MOG (residues 1-125) reproduces an MS-like disease in which MOG-specific autoantibodies directly mediate demyelination. To assess the interrelationship between MOG structure and the induction of autoimmune CNS diseases and to enable structure-based rational design of therapeutics, a homology model of human MOG(2-120) was constructed based on consensus residues found in immunoglobulin superfamily variable-type proteins having known structures. Possible sites for posttranslational modifications and dimerization have also been identified and analyzed. The B cell and T cell epitopes have been identified in rat MOG-immunized marmosets, and these sequences are observed to map primarily onto accessible regions in the model, which may explain their ability to generate potent antibody responses.
 

Literature references that cite this PDB file's key reference

  PubMed id Reference
20448482 S.A.Jagessar, Y.S.Kap, N.Heijmans, N.van Driel, L.van Straalen, J.J.Bajramovic, H.P.Brok, E.L.Blezer, J.Bauer, J.D.Laman, and B.A.'t Hart (2010).
Induction of progressive demyelinating autoimmune encephalomyelitis in common marmoset monkeys using MOG34-56 peptide in incomplete freund adjuvant.
  J Neuropathol Exp Neurol, 69, 372-385.  
19337065 B.A.'t Hart, and L.Massacesi (2009).
Clinical, pathological, and immunologic aspects of the multiple sclerosis model in common marmosets (Callithrix jacchus).
  J Neuropathol Exp Neurol, 68, 341-355.  
18388796 K.Hawker (2008).
B-cell-targeted treatment for multiple sclerosis: mechanism of action and clinical data.
  Curr Opin Neurol, 21, S19-S25.  
16903876 C.Delarasse, B.Della Gaspera, C.W.Lu, F.Lachapelle, A.Gelot, D.Rodriguez, A.Dautigny, C.Genain, and D.Pham-Dinh (2006).
Complex alternative splicing of the myelin oligodendrocyte glycoprotein gene is unique to human and non-human primates.
  J Neurochem, 98, 1707-1717.  
16461459 P.H.Lalive, T.Menge, C.Delarasse, B.Della Gaspera, D.Pham-Dinh, P.Villoslada, H.C.von Büdingen, and C.P.Genain (2006).
Antibodies to native myelin oligodendrocyte glycoprotein are serologic markers of early inflammation in multiple sclerosis.
  Proc Natl Acad Sci U S A, 103, 2280-2285.  
12060766 H.C.von Büdingen, S.L.Hauser, A.Fuhrmann, C.B.Nabavi, J.I.Lee, and C.P.Genain (2002).
Molecular characterization of antibody specificities against myelin/oligodendrocyte glycoprotein in autoimmune demyelination.
  Proc Natl Acad Sci U S A, 99, 8207-8212.  
The most recent references are shown first. Citation data come partly from CiteXplore and partly from an automated harvesting procedure. Note that this is likely to be only a partial list as not all journals are covered by either method. However, we are continually building up the citation data so more and more references will be included with time.

 

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