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Gene Review

MBP  -  myelin basic protein

Homo sapiens

Synonyms: Myelin A1 protein, Myelin basic protein, Myelin membrane encephalitogenic protein
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Disease relevance of MBP

  • Following administration of the MBP peptide, together with adjuvant and pertussis toxin, transgenic mice developed focal CNS inflammation and demyelination that led to clinical manifestations and disease courses resembling those seen in MS [1].
  • In zones surrounding areas of demyelination, virus containing oligodendroglia were most numerous and MAG staining of periaxonal regions was decreased, but there was little change in MBP staining [2].
  • Forty-nine of 55 patients with optic neuritis had increased CSF anti-MBP and the remaining 6 had increased anti-PLP [3].
  • Numbers of cells responding to AChR in MS and MBP in myasthenia gravis did not differ from numbers found in absence of antigen [4].
  • In demyelinated regions, both MAG and MBP staining were severely altered; also there was much less JC virus staining [2].

Psychiatry related information on MBP

  • No MBP-specific AFCs were detected in CNS tissue sections of 11 patients with other neurological diseases, such as Parkinson's and Alzheimer's disease, or in brain tissue sections of eight deceased persons without neurological diseases [5].
  • Although our data indicate that intrathecal anti-MBP IgG may occur early during HIV-1 infection and that they are more common in patients with HIV-1-associated cognitive/motor complex, the possible demyelinating role of these antibodies remains to be demonstrated [6].
  • To define further this restricted heterogeneity and to direct further efforts to identify an antigenic target of CSF oligoclonal bands, the presence of idiotope (Id)-bearing antibodies sharing an Id with a murine monoclonal antibody to myelin basic protein peptide 80-89 was examined in the CSF of MS patients [7].
  • Myelin basic protein antibodies in catatonic schizophrenia [8].
  • Myelin basic protein (MBP) antibodies were determined by solid-phase radioimmunoassay in the serum and cerebrospinal fluid of 10 patients with catatonia, 10 patients with other forms of schizophrenia, and 10 psychiatrically healthy controls [8].

High impact information on MBP


Chemical compound and disease context of MBP


Biological context of MBP

  • In contrast, OIND are characterized by similar frequencies of serum IgG antibody responses to MOG-Ig (53%) and MBP (47%), whereas serum IgG responses to MOG-Ig are rare in ONND (3%) and rheumatoid arthritis (10%) [16].
  • Therefore, in two closely related epithelial cell lines TGF beta 1 activates two different signal transduction pathways, one ras-dependent and one ras-independent, and modulates the activities of a set of MBP kinases [17].
  • In conclusion, our study of two families with conjugal MS has shown a dominant T-cell response against the same MBP peptide within the family both in MS-affected parents and unaffected children, and this T-cell response seems to be independent of the HLA class II phenotypes of the family members [18].
  • These results indicate that although average electrostatic forces are the primary determinant of the interaction of MBP with actin, phosphorylation may have an additional effect due to a site-specific electrostatic effect or to a conformational change [19].
  • In each of the patients with other HLA-DR haplotypes (DR2-), as well as in three DR2+ non-MS donors, the T cell response to MBP appeared to be considerably more heterogeneous [20].

Anatomical context of MBP

  • In tissue from three other chronic cases, viral antiserum stained fewer oligodendrocytes and the differences in MAG and MBP staining were much less striking [2].
  • A total of 638 short-term T-cell lines were established and characterized for MBP-specific proliferative and cytotoxic activity, fine specificity, and human leukocyte antigen (HLA) restriction [21].
  • At all ages examined, the MBP immunohistochemical method revealed more myelin than LFB or MAG staining [22].
  • To determine whether MAG might be involved in an autoimmune reaction in MS, we screened peripheral blood lymphocytes from MS patients and normal subjects for their sensitization to human MBP and MAG antigen using a [3H]thymidine incorporation assay [23].
  • Phosphorylation decreased the ability of MBP to polymerize actin and to bundle actin filaments but had no effect on the dissociation constant of the MBP-actin complex or on the ability of Ca2+-calmodulin to dissociate the complex [19].

Associations of MBP with chemical compounds

  • However, DEVD-CHO treatment failed to inhibit FTY720-induced activation of JNK and the 36-kDa MBP kinase [24].
  • The effect was much greater than that reported earlier for another charge isomer of MBP, C8, in which six arginines were deiminated to citrulline, resulting in a reduction of net positive charge of 6 [19].
  • Based on the inhibition of MBP degradation in the presence of EGTA and the analysis of the degradation products obtained following incubation of myelin with mAbs to GalC and MOG (8-18C5), the neutral protease involved in this antibody-induced degradation of MBP could be calcium-activated neutral protease [25].
  • Our studies also showed a dramatic increase in MBP phosphotransferase activity occurred by 4 days PF that arose from a third kinase that phosphorylated MBP solely on serine residues [26].
  • Like Mapk, this protein phosphorylated MBP mostly on threonine residues, but it failed to phosphorylate a peptide (APRTPGGRR) based upon the Thr-97 MAP kinase phosphorylation site in MBP [26].
  • Our study reveals a link between MBP, glatiramer acetate, and the alpha(M)beta(2) integrin, and suggests a new model for MS pathogenesis based on the recognition of unfolded MBP by the alpha(M)beta(2) integrin [27].

Physical interactions of MBP

  • Taken together, these results suggest that antibodies to GalC and MOG can play a major role in destabilizing myelin through MBP breakdown mediated by neutral proteases and thus have an important role to play in the pathogenesis of MS [25].
  • Peptides 147-154aa of La/SSB and 139-146aa of the MBP were attached on tetrameric sequential oligopeptide carriers and used for immunizations of New Zealand White rabbits [28].
  • Furthermore, MBP binds to the ERK2 x ATP complex at least 1500-fold more tightly than does ERKtide (K(d(ERKtide)) >/= 1.5 mM) [29].
  • This electron microscopical study has identified that, in vitro, the less cationic Marburg MBP isomer forms a more extended protein-lipid complex than MBP from healthy or chronic MS-afflicted individuals [30].
  • Surface plasmon resonance measurements confirmed that MBP bound more tightly to Dutch/Iowa CAA double mutant Abeta than to wild-type Abeta [31].

Enzymatic interactions of MBP


Co-localisations of MBP

  • Native LDL, epitopes of MDA-LDL, peptides of myelin basic protein and neutral lipid oil red O (ORO) staining were found to be co-localized within foamy macrophages in early and actively demyelinating MS plaques [37].
  • Immunoreactivity for IL-4 and RANTES co-localized with MBP in maturing colony eosinophils on day 23 of culture in semisolid media, as judged by CLSM [38].

Regulatory relationships of MBP

  • The results suggest that PLP and MAG are expressed later than MBP but follow similar spatial gradients [39].
  • Demyelinating antibodies to myelin oligodendrocyte glycoprotein and galactocerebroside induce degradation of myelin basic protein in isolated human myelin [25].
  • Anti-idiotypic T cells induced by the 8mer TCR peptide were predominantly CD8+ cytotoxic T cells and exhibited cytotoxic activity against autologous MBP-specific T cells expressing the CDR3 sequence [40].
  • METHODS: Two hundred sixty-nine unrelated patients with definite MS and 385 unrelated healthy control subjects from Italy and Russia were genotyped for the MBP VNTR region and for the human leukocyte antigen (HLA) class II DRB1 gene [41].
  • The obtained anti-idiotypic T cells recognizing the 15mer TCR peptide were found to express the CD4 phenotype, produce predominantly IL-10 and inhibit the proliferation of autologous T cells recognizing the immunodominant peptide of MBP [40].

Other interactions of MBP

  • CTLs specific for MBP 110-118 and MAG 556-564 could recognize endogenously processed antigens presented by HLA-A2 [42].
  • When challenged with either MBP or a bacterial superantigen, the clones expressed similar levels of the proinflammatory cytokine IFN gamma [43].
  • It is interesting that MBP-reactive T cells from MS patients expressing the disease-associated HLA-DRB1*15 allele produced increased quantities of TNF alpha, a cytokine suggested to play an important role in inflammation and demyelination [43].
  • When TGF beta 1 acts as a mitogen for U9 cells, it increases the activity of MBP kinases of 57, 105, and 130 kDa within 10 min of the addition without detectably activating ras proteins [17].
  • Myelin basic protein methylated by PRMT5 contained monomethylated and dimethylated arginine residues [44].

Analytical, diagnostic and therapeutic context of MBP


  1. A humanized model for multiple sclerosis using HLA-DR2 and a human T-cell receptor. Madsen, L.S., Andersson, E.C., Jansson, L., krogsgaard, M., Andersen, C.B., Engberg, J., Strominger, J.L., Svejgaard, A., Hjorth, J.P., Holmdahl, R., Wucherpfennig, K.W., Fugger, L. Nat. Genet. (1999) [Pubmed]
  2. Distribution of papovavirus, myelin-associated glycoprotein, and myelin basic protein in progressive multifocal leukoencephalopathy lesions. Itoyama, Y., Webster, H.D., Sternberger, N.H., Richardson, E.P., Walker, D.L., Quarles, R.H., Padgett, B.L. Ann. Neurol. (1982) [Pubmed]
  3. Anti-myelin basic protein and anti-proteolipid protein specific forms of multiple sclerosis. Warren, K.G., Catz, I., Johnson, E., Mielke, B. Ann. Neurol. (1994) [Pubmed]
  4. Organ-specific autoantigens induce transforming growth factor-beta mRNA expression in mononuclear cells in multiple sclerosis and myasthenia gravis. Link, J., Fredrikson, S., Söderström, M., Olsson, T., Höjeberg, B., Ljungdahl, A., Link, H. Ann. Neurol. (1994) [Pubmed]
  5. The involvement of specific anti myelin basic protein antibody-forming cells in multiple sclerosis immunopathology. Gerritse, K., Deen, C., Fasbender, M., Ravid, R., Boersma, W., Claassen, E. J. Neuroimmunol. (1994) [Pubmed]
  6. Intrathecal synthesis of anti-myelin basic protein IgG in HIV-1+ patients. Maimone, D., Annunziata, P., Cioni, C., Leonardi, A., Guazzi, G.C. Acta neurologica Scandinavica. (1994) [Pubmed]
  7. Cross-reactive idiotypy in cerebrospinal fluid immunoglobulins in multiple sclerosis. LaGanke, C.C., Freeman, D.W., Whitaker, J.N. Ann. Neurol. (2000) [Pubmed]
  8. Myelin basic protein antibodies in catatonic schizophrenia. Rimón, R., Ahokas, A., Ruutiainen, J., Halonen, P. The Journal of clinical psychiatry. (1986) [Pubmed]
  9. Molecular mimicry in T cell-mediated autoimmunity: viral peptides activate human T cell clones specific for myelin basic protein. Wucherpfennig, K.W., Strominger, J.L. Cell (1995) [Pubmed]
  10. Ras is essential for nerve growth factor- and phorbol ester-induced tyrosine phosphorylation of MAP kinases. Thomas, S.M., DeMarco, M., D'Arcangelo, G., Halegoua, S., Brugge, J.S. Cell (1992) [Pubmed]
  11. Myelin basic protein as an encephalitogen in encephalomyelitis and polyneuritis following rabies vaccination. Hemachudha, T., Griffin, D.E., Giffels, J.J., Johnson, R.T., Moser, A.B., Phanuphak, P. N. Engl. J. Med. (1987) [Pubmed]
  12. Interleukin-1 activates p54 mitogen-activated protein (MAP) kinase/stress-activated protein kinase by a pathway that is independent of p21ras, Raf-1, and MAP kinase kinase. Bird, T.A., Kyriakis, J.M., Tyshler, L., Gayle, M., Milne, A., Virca, G.D. J. Biol. Chem. (1994) [Pubmed]
  13. Cryoelectron microscopy of protein-lipid complexes of human myelin basic protein charge isomers differing in degree of citrullination. Beniac, D.R., Wood, D.D., Palaniyar, N., Ottensmeyer, F.P., Moscarello, M.A., Harauz, G. J. Struct. Biol. (2000) [Pubmed]
  14. Longitudinal study of myelin basic protein-specific T-cell receptors during the course of multiple sclerosis. Lovett-Racke, A.E., Martin, R., McFarland, H.F., Racke, M.K., Utz, U. J. Neuroimmunol. (1997) [Pubmed]
  15. Enhanced T cell responsiveness to citrulline-containing myelin basic protein in multiple sclerosis patients. Tranquill, L.R., Cao, L., Ling, N.C., Kalbacher, H., Martin, R.M., Whitaker, J.N. Mult. Scler. (2000) [Pubmed]
  16. Antibodies against the myelin oligodendrocyte glycoprotein and the myelin basic protein in multiple sclerosis and other neurological diseases: a comparative study. Reindl, M., Linington, C., Brehm, U., Egg, R., Dilitz, E., Deisenhammer, F., Poewe, W., Berger, T. Brain (1999) [Pubmed]
  17. Two different signal transduction pathways can be activated by transforming growth factor beta 1 in epithelial cells. Yan, Z., Winawer, S., Friedman, E. J. Biol. Chem. (1994) [Pubmed]
  18. Conjugal multiple sclerosis: immunogenetic characterization and analysis of T- and B-cell reactivity to myelin proteins. Fredrikson, S., Michelsberg, J., Hillert, J., Wang, Z., Sun, J.B., Olerup, O., Olsson, T., Link, H. Neurology (1992) [Pubmed]
  19. Effect of phosphorylation of myelin basic protein by MAPK on its interactions with actin and actin binding to a lipid membrane in vitro. Boggs, J.M., Rangaraj, G., Gao, W., Heng, Y.M. Biochemistry (2006) [Pubmed]
  20. Predominant and stable T cell responses to regions of myelin basic protein can be detected in individual patients with multiple sclerosis. Salvetti, M., Ristori, G., D'Amato, M., Buttinelli, C., Falcone, M., Fieschi, C., Wekerle, H., Pozzilli, C. Eur. J. Immunol. (1993) [Pubmed]
  21. Myelin basic protein-specific T-cell responses in identical twins discordant or concordant for multiple sclerosis. Martin, R., Voskuhl, R., Flerlage, M., McFarlin, D.E., McFarland, H.F. Ann. Neurol. (1993) [Pubmed]
  22. Immunohistochemical detection of myelin basic protein is a sensitive marker of myelination in second trimester human fetal spinal cord. Bodhireddy, S.R., Lyman, W.D., Rashbaum, W.K., Weidenheim, K.M. J. Neuropathol. Exp. Neurol. (1994) [Pubmed]
  23. The T-lymphocyte response against myelin-associated glycoprotein and myelin basic protein in patients with multiple sclerosis. Zhang, Y., Burger, D., Saruhan, G., Jeannet, M., Steck, A.J. Neurology (1993) [Pubmed]
  24. Differential activation of c-Jun NH2-terminal kinase and p38 pathways during FTY720-induced apoptosis of T lymphocytes that is suppressed by the extracellular signal-regulated kinase pathway. Matsuda, S., Minowa, A., Suzuki, S., Koyasu, S. J. Immunol. (1999) [Pubmed]
  25. Demyelinating antibodies to myelin oligodendrocyte glycoprotein and galactocerebroside induce degradation of myelin basic protein in isolated human myelin. Menon, K.K., Piddlesden, S.J., Bernard, C.C. J. Neurochem. (1997) [Pubmed]
  26. Characterization of fertilization-modulated myelin basic protein kinases from sea star: regulation of Mapk. Lefebvre, D.L., Charest, D.L., Yee, A., Crawford, B.J., Pelech, S.L. J. Cell. Biochem. (1999) [Pubmed]
  27. Structural insight into the function of myelin basic protein as a ligand for integrin alpha M beta 2. Stapulionis, R., Oliveira, C.L., Gjelstrup, M.C., Pedersen, J.S., Hokland, M.E., Hoffmann, S.V., Poulsen, K., Jacobsen, C., Vorup-Jensen, T. J. Immunol. (2008) [Pubmed]
  28. Linear epitopes of two different autoantigens-La/SSB and myelin basic protein--with a high degree of molecular similarity, cause different humoral immune responses. Terzoglou, A.G., Routsias, J.G., Sakarellos, C., Sakarellos-Daitsiotis, M., Moutsopoulos, H.M., Tzioufas, A.G. J. Autoimmun. (2003) [Pubmed]
  29. Catalytic reaction pathway for the mitogen-activated protein kinase ERK2. Prowse, C.N., Hagopian, J.C., Cobb, M.H., Ahn, N.G., Lew, J. Biochemistry (2000) [Pubmed]
  30. Marburg's variant of multiple sclerosis correlates with a less compact structure of myelin basic protein. Beniac, D.R., Wood, D.D., Palaniyar, N., Ottensmeyer, F.P., Moscarello, M.A., Harauz, G. Mol. Cell Biol. Res. Commun. (1999) [Pubmed]
  31. Inhibition of Familial Cerebral Amyloid Angiopathy Mutant Amyloid beta-Protein Fibril Assembly by Myelin Basic Protein. Hoos, M.D., Ahmed, M., Smith, S.O., Van Nostrand, W.E. J. Biol. Chem. (2007) [Pubmed]
  32. MST4, a new Ste20-related kinase that mediates cell growth and transformation via modulating ERK pathway. Lin, J.L., Chen, H.C., Fang, H.I., Robinson, D., Kung, H.J., Shih, H.M. Oncogene (2001) [Pubmed]
  33. PRMT5 (Janus kinase-binding protein 1) catalyzes the formation of symmetric dimethylarginine residues in proteins. Branscombe, T.L., Frankel, A., Lee, J.H., Cook, J.R., Yang , Z., Pestka, S., Clarke, S. J. Biol. Chem. (2001) [Pubmed]
  34. LOK is a novel mouse STE20-like protein kinase that is expressed predominantly in lymphocytes. Kuramochi, S., Moriguchi, T., Kuida, K., Endo, J., Semba, K., Nishida, E., Karasuyama, H. J. Biol. Chem. (1997) [Pubmed]
  35. Phosphatidylinositol 3-kinase-dependent activation of protein kinase C-zeta in bacterial lipopolysaccharide-treated human monocytes. Herrera-Velit, P., Knutson, K.L., Reiner, N.E. J. Biol. Chem. (1997) [Pubmed]
  36. Metal-dependent hydrolysis of myelin basic protein by IgGs from the sera of patients with multiple sclerosis. Polosukhina, D.I., Kanyshkova, T.G., Doronin, B.M., Tyshkevich, O.B., Buneva, V.N., Boiko, A.N., Gusev, E.I., Nevinsky, G.A., Favorova, O.O. Immunol. Lett. (2006) [Pubmed]
  37. Low density lipoprotein uptake by macrophages in multiple sclerosis plaques: implications for pathogenesis. Newcombe, J., Li, H., Cuzner, M.L. Neuropathol. Appl. Neurobiol. (1994) [Pubmed]
  38. Interleukin-4 and RANTES expression in maturing eosinophils derived from human cord blood CD34+ progenitors. Velazquez, J.R., Lacy, P., Mahmudi-Azer, S., Bablitz, B., Milne, C.D., Denburg, J.A., Moqbel, R. Immunology (2000) [Pubmed]
  39. Temporal and spatial expression of major myelin proteins in the human fetal spinal cord during the second trimester. Weidenheim, K.M., Bodhireddy, S.R., Rashbaum, W.K., Lyman, W.D. J. Neuropathol. Exp. Neurol. (1996) [Pubmed]
  40. Human anti-idiotypic T cells induced by TCR peptides corresponding to a common CDR3 sequence motif in myelin basic protein-reactive T cells. Zang, Y.C., Hong, J., Rivera, V.M., Killian, J., Zhang, J.Z. Int. Immunol. (2003) [Pubmed]
  41. Myelin basic protein gene is associated with MS in DR4- and DR5-positive Italians and Russians. Guerini, F.R., Ferrante, P., Losciale, L., Caputo, D., Lombardi, M.L., Pirozzi, G., Luongo, V., Sudomoina, M.A., Andreewski, T.V., Alekseenkov, A.D., Boiko, A.N., Gusev, E.I., Favorova, O.O. Neurology (2003) [Pubmed]
  42. Autoreactive CD8+ T-cell responses to human myelin protein-derived peptides. Tsuchida, T., Parker, K.C., Turner, R.V., McFarland, H.F., Coligan, J.E., Biddison, W.E. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  43. Cytokine profile of myelin basic protein-reactive T cells in multiple sclerosis and healthy individuals. Hermans, G., Stinissen, P., Hauben, L., Van den Berg-Loonen, E., Raus, J., Zhang, J. Ann. Neurol. (1997) [Pubmed]
  44. Prmt5, which forms distinct homo-oligomers, is a member of the protein-arginine methyltransferase family. Rho, J., Choi, S., Seong, Y.R., Cho, W.K., Kim, S.H., Im, D.S. J. Biol. Chem. (2001) [Pubmed]
  45. Differential macrophage/microglia activation in neocortical EAE lesions in the marmoset monkey. Merkler, D., Böscke, R., Schmelting, B., Czéh, B., Fuchs, E., Brück, W., Stadelmann, C. Brain Pathol. (2006) [Pubmed]
  46. A role for CXCL12 (SDF-1alpha) in the pathogenesis of multiple sclerosis: regulation of CXCL12 expression in astrocytes by soluble myelin basic protein. Calderon, T.M., Eugenin, E.A., Lopez, L., Kumar, S.S., Hesselgesser, J., Raine, C.S., Berman, J.W. J. Neuroimmunol. (2006) [Pubmed]
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