David Beeson

Summary

Affiliation: University of Oxford
Country: UK

Publications

  1. ncbi request reprint Dok-7 mutations underlie a neuromuscular junction synaptopathy
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK
    Science 313:1975-8. 2006
  2. ncbi request reprint Congenital myasthenic syndromes and the formation of the neuromuscular junction
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
    Ann N Y Acad Sci 1132:99-103. 2008
  3. ncbi request reprint Structural abnormalities of the AChR caused by mutations underlying congenital myasthenic syndromes
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Headington, Oxford OX3 9DS, United Kingdom
    Ann N Y Acad Sci 998:114-24. 2003
  4. ncbi request reprint Clinical features of congenital myasthenic syndrome due to mutations in DPAGT1
    Sarah Finlayson
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
    J Neurol Neurosurg Psychiatry 84:1119-25. 2013
  5. ncbi request reprint Clinical features of the DOK7 neuromuscular junction synaptopathy
    Jacqueline Palace
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK
    Brain 130:1507-15. 2007
  6. pmc IgG1 antibodies to acetylcholine receptors in 'seronegative' myasthenia gravis
    Maria Isabel Leite
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK
    Brain 131:1940-52. 2008
  7. ncbi request reprint Diverse molecular mechanisms involved in AChR deficiency due to rapsyn mutations
    Judy Cossins
    Neurosciences Group, Weatherall Institute of Molecular Medicine, Churchill Hospital, Oxford, UK
    Brain 129:2773-83. 2006
  8. ncbi request reprint The spectrum of mutations that underlie the neuromuscular junction synaptopathy in DOK7 congenital myasthenic syndrome
    Judith Cossins
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK
    Hum Mol Genet 21:3765-75. 2012
  9. ncbi request reprint Non-radioactive serological diagnosis of myasthenia gravis and clinical features of patients from Tianjin, China
    Li Yang
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, England, UK
    J Neurol Sci 301:71-6. 2011
  10. ncbi request reprint Myasthenia gravis seronegative for acetylcholine receptor antibodies
    Angela Vincent
    Neurosciences Group, Weatherall Institute of Molecular Medicine and Department of Clinical Neurology, John Radcliffe Hospital, Oxford, United Kingdom
    Ann N Y Acad Sci 1132:84-92. 2008

Collaborators

Detail Information

Publications55

  1. ncbi request reprint Dok-7 mutations underlie a neuromuscular junction synaptopathy
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DS, UK
    Science 313:1975-8. 2006
    ..We showed that recessive inheritance of mutations in Dok-7, which result in a defective structure of the neuromuscular junction, is a cause of CMS with proximal muscle weakness...
  2. ncbi request reprint Congenital myasthenic syndromes and the formation of the neuromuscular junction
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
    Ann N Y Acad Sci 1132:99-103. 2008
    ....
  3. ncbi request reprint Structural abnormalities of the AChR caused by mutations underlying congenital myasthenic syndromes
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Headington, Oxford OX3 9DS, United Kingdom
    Ann N Y Acad Sci 998:114-24. 2003
    ..It was found that mutations within muscle AChRs are the most common cause of CMS. The majority are located within the epsilon-subunit gene and result in AChR deficiency...
  4. ncbi request reprint Clinical features of congenital myasthenic syndrome due to mutations in DPAGT1
    Sarah Finlayson
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK
    J Neurol Neurosurg Psychiatry 84:1119-25. 2013
    ..While many other CMS-associated proteins have discrete roles localised to the neuromuscular junction, DPAGT1 is ubiquitously expressed, modifying many proteins, and as such is an unexpected cause of isolated neuromuscular involvement...
  5. ncbi request reprint Clinical features of the DOK7 neuromuscular junction synaptopathy
    Jacqueline Palace
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK
    Brain 130:1507-15. 2007
    ..CMS due to DOK7 mutations are common within our UK cohort and is likely to be under-diagnosed; recognition of the phenotype will help clinical diagnosis, targeted genetic screening and appropriate management...
  6. pmc IgG1 antibodies to acetylcholine receptors in 'seronegative' myasthenia gravis
    Maria Isabel Leite
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK
    Brain 131:1940-52. 2008
    ..These observations throw new light on different forms of MG paving the way for improved diagnosis and management, and the approaches used have applicability to other antibody-mediated conditions...
  7. ncbi request reprint Diverse molecular mechanisms involved in AChR deficiency due to rapsyn mutations
    Judy Cossins
    Neurosciences Group, Weatherall Institute of Molecular Medicine, Churchill Hospital, Oxford, UK
    Brain 129:2773-83. 2006
    ..The disease severity of patients harbouring the compound allelic mutations was greater than that of patients with homozygous rapsyn mutation N88K, suggesting that the second mutant allele may largely determine severity...
  8. ncbi request reprint The spectrum of mutations that underlie the neuromuscular junction synaptopathy in DOK7 congenital myasthenic syndrome
    Judith Cossins
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK
    Hum Mol Genet 21:3765-75. 2012
    ..The DOK7 gene is highly polymorphic, and within these many variants, we define a spectrum of mutations that can underlie DOK7 CMS that will inform in managing this disorder...
  9. ncbi request reprint Non-radioactive serological diagnosis of myasthenia gravis and clinical features of patients from Tianjin, China
    Li Yang
    Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, England, UK
    J Neurol Sci 301:71-6. 2011
    ..To establish non-radioactive assays for detection of antibodies (Abs) to the acetylcholine receptor (AChR) and to muscle specific kinase (MuSK). To show that the assays can be used in Tianjin for testing patients with MG...
  10. ncbi request reprint Myasthenia gravis seronegative for acetylcholine receptor antibodies
    Angela Vincent
    Neurosciences Group, Weatherall Institute of Molecular Medicine and Department of Clinical Neurology, John Radcliffe Hospital, Oxford, United Kingdom
    Ann N Y Acad Sci 1132:84-92. 2008
    ..Overall, these results suggest that complement-activation may be an important pathogenic mechanism even in patients without conventional AChR antibodies...
  11. ncbi request reprint Antibodies in myasthenia gravis and related disorders
    Angela Vincent
    Neurosciences Group, Department of Clinical Neurology, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
    Ann N Y Acad Sci 998:324-35. 2003
    ..These antibodies are not found in AChR antibody-positive MG and are predominantly IgG4. MuSK antibody positivity appears to be associated with more severe bulbar disease that can be difficult to treat effectively...
  12. ncbi request reprint Antibodies identified by cell-based assays in myasthenia gravis and associated diseases
    Angela Vincent
    Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, United Kingdom
    Ann N Y Acad Sci 1274:92-8. 2012
    ..The cell-based method is time consuming but has many advantages and may provide a gold standard for the future in the detection of pathogenic autoantibodies in patients with immune-mediated diseases...
  13. ncbi request reprint Inhibition of acetylcholine receptor function by seronegative myasthenia gravis non-IgG factor correlates with desensitisation
    Ian Spreadbury
    Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom
    J Neuroimmunol 162:149-56. 2005
    ..The results suggest that, rather than acting indirectly as previously proposed, the SNMG factor may bind directly to an allosteric site that induces or enhances AChR desensitisation...
  14. ncbi request reprint A novel congenital myasthenic syndrome due to decreased acetylcholine receptor ion-channel conductance
    Richard Webster
    Neurosciences Group, Weatherall Institute of Molecular Medicine, Headley Way, Oxford OX3 9DS, UK
    Brain 135:1070-80. 2012
    ..F266 deletion mutation revealed by the coinheritance of the low-expressor mutation p.εP282R...
  15. ncbi request reprint Effect of sera from AChR-antibody negative myasthenia gravis patients on AChR and MuSK in cell cultures
    Maria Elena Farrugia
    Neurosciences Group, Weatherall Institute of Molecular Medicine, Department of Clinical Neurology, University of Oxford, UK
    J Neuroimmunol 185:136-44. 2007
    ..Thus, although these results have, disappointingly, demonstrated little effect of MuSK antibodies on AChR expression, they do imply that SNMG antibodies act on AChR-associated pathways...
  16. ncbi request reprint Spontaneous production of anti-IFN-alpha and anti-IL-12 autoantibodies by thymoma cells from myasthenia gravis patients suggests autoimmunization in the tumor
    Hiroyuki Shiono
    Neuroscience Group, Weatherall Institute for Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK
    Int Immunol 15:903-13. 2003
    ..With these molecules, it should be easier to identify provoking cell type(s) that may give novel additional clues to autoimmunization against T-cell epitopes from the more complex AChR...
  17. ncbi request reprint Lack of association between acetylcholine receptor epsilon polymorphisms and early-onset myasthenia gravis
    Domenico Marco Bonifati
    Neurosciences Group, Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, United Kingdom
    Muscle Nerve 29:436-9. 2004
    ..These data provide no evidence that heteroallelic mutations or polymorphisms in the AChR epsilon subunit are involved in the development of autoimmune early-onset MG but raise issues for future studies...
  18. doi request reprint Identification of DPAGT1 as a new gene in which mutations cause a congenital myasthenic syndrome
    Katsiaryna Belaya
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom
    Ann N Y Acad Sci 1275:29-35. 2012
    ..This finding demonstrates that impairment of the N-linked glycosylation pathway can lead to the development of CMS...
  19. ncbi request reprint The search for new antigenic targets in myasthenia gravis
    Judith Cossins
    Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom
    Ann N Y Acad Sci 1275:123-8. 2012
    ..These assays, combined with use of myotube cultures to explore the effects of the antibodies, enable us to begin to identify new antigenic targets and test antibody pathogenicity in vitro...
  20. pmc Congenital myasthenic syndromes due to mutations in ALG2 and ALG14
    Judith Cossins
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Oxford OX3 9DS, UK
    Brain 136:944-56. 2013
    ..Our findings suggest that treatment with cholinesterase inhibitors may improve muscle function in many of the congenital disorders of glycosylation...
  21. ncbi request reprint Myasthenia gravis in a woman with congenital AChR deficiency due to epsilon-subunit mutations
    Rebecca Croxen
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Oxford, United Kingdom
    Neurology 58:1563-5. 2002
    ..The younger sister developed MG at 34 years. This unusual case raises the possibility that genetic defects of the AChR might be a factor in the etiology of autoimmune MG...
  22. ncbi request reprint Preferential expression of AChR epsilon-subunit in thymomas from patients with myasthenia gravis
    Calman A MacLennan
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford OX3 9DS, UK
    J Neuroimmunol 201:28-32. 2008
    ..The greater abundance of mRNA for AChR epsilon-subunit than for other subunits suggests that the AChR epsilon-subunit may play a distinctive role in autosensitization in MG-associated thymomas, particularly those of type A or AB...
  23. doi request reprint Mutations in GFPT1 that underlie limb-girdle congenital myasthenic syndrome result in reduced cell-surface expression of muscle AChR
    Katarzyna Zoltowska
    Nuffield Department of Clinical Neurosciences, University of Oxford, OX3 9DS Oxford, UK
    Hum Mol Genet 22:2905-13. 2013
    ..Similarity between CMS due to GFPT1 mutations and CMS due to DPAGT1 mutations would suggest that reduced endplate AChR due to defective N-linked glycosylation is a primary disease mechanism in this disorder. ..
  24. ncbi request reprint Hairpin DNAzymes: a new tool for efficient cellular gene silencing
    Amr Abdelgany
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, The John Radcliffe Hospital, Oxford OX3 9DS, UK
    J Gene Med 9:727-38. 2007
    ..Chemical modifications can be introduced into the binding arms to increase stability but these may alter catalytic activity and in some cases increase cell toxicity...
  25. ncbi request reprint Mutations in congenital myasthenic syndromes reveal an epsilon subunit C-terminal cysteine, C470, crucial for maturation and surface expression of adult AChR
    John Ealing
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Oxford OX3 9DS, UK
    Hum Mol Genet 11:3087-96. 2002
    ....
  26. ncbi request reprint Detection and characterization of MuSK antibodies in seronegative myasthenia gravis
    John McConville
    Weatherall Institute of Molecular Medicine and Department of Clinical Neurology, Oxford, UK
    Ann Neurol 55:580-4. 2004
    ..They bind to the extracellular Ig-like domains of soluble or native MuSK. Surprisingly they are predominantly in the IgG4 subclass. MuSK-antibody associated MG may be different in etiological and pathological mechanisms...
  27. ncbi request reprint Allele-specific silencing of a pathogenic mutant acetylcholine receptor subunit by RNA interference
    Amr Abdelgany
    Neurosciences Group, Weatherall Institute of Molecular Medicine, University of Oxford, UK
    Hum Mol Genet 12:2637-44. 2003
    ....
  28. ncbi request reprint 126th International Workshop: congenital myasthenic syndromes, 24-26 September 2004, Naarden, the Netherlands
    David Beeson
    Neurosciences Group, Weatherall Institute of Molecular Medicine, The John Radcliff, Oxford, UK
    Neuromuscul Disord 15:498-512. 2005
  29. ncbi request reprint A mouse model of AChR deficiency syndrome with a phenotype reflecting the human condition
    Judy Cossins
    Neuroscience Group, Weatherall Institute of Molecular Medicine, The John Radcliffe, Oxford, UK
    Hum Mol Genet 13:2947-57. 2004
    ....
  30. pmc Mutations in DPAGT1 cause a limb-girdle congenital myasthenic syndrome with tubular aggregates
    Katsiaryna Belaya
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, UK
    Am J Hum Genet 91:193-201. 2012
    ....
  31. ncbi request reprint Clinical features in a series of fast channel congenital myasthenia syndrome
    Jacqueline Palace
    Department of Neurology, John Radcliffe Hospital, Oxford, UK
    Neuromuscul Disord 22:112-7. 2012
    ..Referral to a specialist paediatric respiratory centre and regular resuscitation training for parents are recommended...
  32. ncbi request reprint Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin
    Rebecca H Clark
    Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford, OX1 3PT, UK
    Science 329:458-61. 2010
    ..These findings suggest that drugs targeted against neuronal, rather than muscle, KATP channels are needed to treat the motor deficits and that such drugs require high blood-brain barrier permeability...
  33. pmc MuSK myasthenia gravis IgG4 disrupts the interaction of LRP4 with MuSK but both IgG4 and IgG1-3 can disperse preformed agrin-independent AChR clusters
    Inga Koneczny
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom
    PLoS ONE 8:e80695. 2013
    ....
  34. ncbi request reprint Slow channel congenital myasthenic syndrome responsive to a combination of fluoxetine and salbutamol
    Sarah Finlayson
    Neuroscience Group, Weatherall Institute of Molecular Medicine, The John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK
    Muscle Nerve 47:279-82. 2013
    ..Slow channel congenital myasthenic syndrome is a dominant disorder characterized by prolonged acetylcholine receptor ion-channel activation...
  35. ncbi request reprint Aquaporin-4 antibodies in neuromyelitis optica and longitudinally extensive transverse myelitis
    Patrick Waters
    Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, England
    Arch Neurol 65:913-9. 2008
    ..There is increasing recognition of antibody-mediated immunotherapy-responsive neurologic diseases and a need for appropriate immunoassays...
  36. ncbi request reprint The agrin/muscle-specific kinase pathway: new targets for autoimmune and genetic disorders at the neuromuscular junction
    Yohan Liyanage
    Neurosciences Group, Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford OX3 9DS, UK
    Muscle Nerve 25:4-16. 2002
    ..We then review the development of the NMJ, focusing on the important roles of nerve-derived agrin and MuSK in clustering of AChRs and other essential components of the NMJ...
  37. ncbi request reprint Fast-channel congenital myasthenic syndrome with a novel acetylcholine receptor mutation at the α-ε subunit interface
    Richard Webster
    Neurosciences Group, Nuffield Department of Clinical Neurosciences, University of Oxford, John Radcliffe Hospital, Headley Way, Oxford, UK
    Neuromuscul Disord 24:143-7. 2014
    ..Fast channel syndromes are frequently characterised by severe myasthenic weakness with apnoeic crises; knowledge of the underlying mutation and its functional consequences can be vital for appropriate therapy and patient management. ..
  38. doi request reprint Synaptic dysfunction in congenital myasthenic syndromes
    David Beeson
    Weatherall Institute of Molecular Medicine, The John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
    Ann N Y Acad Sci 1275:63-9. 2012
    ..The study of these disorders is proving highly informative for understanding the diverse molecular mechanisms that can underlie synaptic dysfunction...
  39. ncbi request reprint Antibodies to acetylcholine receptor in parous women with myasthenia: evidence for immunization by fetal antigen
    Ian Matthews
    Neurosciences Group, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom
    Lab Invest 82:1407-17. 2002
    ....
  40. ncbi request reprint Ribozymes and siRNA for the treatment of diseases of the nervous system
    Matthew J Wood
    Department of Human Anatomy and Genetics, Oxford University, South Parks Road, Oxford, OX1 3QX, UK
    Curr Opin Mol Ther 5:383-8. 2003
    ..This review will assess the potential of these RNA-based therapeutic strategies and the challenges ahead in their application to the treatment of neurological disease...
  41. pmc N-methyl-D-aspartate antibody encephalitis: temporal progression of clinical and paraclinical observations in a predominantly non-paraneoplastic disorder of both sexes
    Sarosh R Irani
    Department of Clinical Neurology, L6 West Wing, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DU, UK
    Brain 133:1655-67. 2010
    ..Four patients, who only had temporal lobe epilepsy without oligoclonal bands, may represent restriction to the first stage...
  42. ncbi request reprint How common is childhood myasthenia? The UK incidence and prevalence of autoimmune and congenital myasthenia
    Jeremy Ross Parr
    Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK Department of Paediatrics, University of Oxford, Oxford, UK
    Arch Dis Child 99:539-42. 2014
    ..Specifically, we aimed to identify the detected incidence of autoimmune myasthenia and the detected prevalence of genetically confirmed congenital myasthenic syndrome (CMS) in children...
  43. ncbi request reprint The congenital myasthenic syndromes
    Jackie Palace
    Department of Clinical Neurology, Level 3, West Wing, John Radcliffe Hospital, Headley Way, Headington OX3 9DU, UK
    J Neuroimmunol 201:2-5. 2008
    ..Although each syndrome results from defective synaptic transmission at the neuromuscular junction, the patients show a variable set of phenotypes. Here, we provide a brief clinical review...
  44. ncbi request reprint Therapeutic gene silencing in the nervous system
    Matthew J A Wood
    Department of Human Anatomy and Genetics, Oxford University, Oxford, UK
    Hum Mol Genet 12:R279-84. 2003
    ....
  45. pmc Mutation analysis of CHRNA1, CHRNB1, CHRND, and RAPSN genes in multiple pterygium syndrome/fetal akinesia patients
    Julie Vogt
    Department of Medical and Molecular Genetics and WellChild Paediatric Research Centre, Division of Reproductive and Child Health, University of Birmingham, Birmingham B15 2TT, UK
    Am J Hum Genet 82:222-7. 2008
    ..Functional studies were consistent with the hypothesis that whereas incomplete loss of rapsyn function may cause congenital myasthenia, more severe loss of function can result in a lethal fetal akinesia phenotype...
  46. ncbi request reprint Mutations causing DOK7 congenital myasthenia ablate functional motifs in Dok-7
    Johko Hamuro
    Department of Cell Regulation, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo ku, Yushima, Tokyo 113 8510, Japan
    J Biol Chem 283:5518-24. 2008
    ..Ablation or disruption of these functional elements in Dok-7 probably underlies the neuromuscular junction synaptopathy observed in DOK7 CMS...
  47. ncbi request reprint An IRF8-binding promoter variant and AIRE control CHRNA1 promiscuous expression in thymus
    Matthieu Giraud
    INSERM, U580, 75015 Paris, France
    Nature 448:934-7. 2007
    ....
  48. ncbi request reprint CHRND mutation causes a congenital myasthenic syndrome by impairing co-clustering of the acetylcholine receptor with rapsyn
    Juliane S Muller
    Department of Neurology, Friedrich Baur Institute, Ludwig Maximilians University, Munich, Germany
    Brain 129:2784-93. 2006
    ..Introduction of the same mutation in the epsilon subunit had no effect on AChR clustering indicating a special role of the delta subunit in AChR-rapsyn interactions...
  49. ncbi request reprint Phenotypical spectrum of DOK7 mutations in congenital myasthenic syndromes
    Juliane S Muller
    Friedrich Baur Institute, Department of Neurology, Ludwig Maximilians University, Munich, Germany
    Brain 130:1497-506. 2007
    ....
  50. ncbi request reprint Isolation of potent human Fab fragments against a novel highly immunogenic region on human muscle acetylcholine receptor which protect the receptor from myasthenic autoantibodies
    Efrosini Fostieri
    Department of Biochemistry, Hellenic Pasteur Institute, Athens, Greece
    Eur J Immunol 35:632-43. 2005
    ..Furthermore, this Fab protected surface AChR in cell cultures against MG autoantibody-induced antigenic modulation, suggesting a potential therapeutic use in MG, especially in combination with a human anti-MIR Fab...
  51. ncbi request reprint Rhabdomyosarcoma lysis by T cells expressing a human autoantibody-based chimeric receptor targeting the fetal acetylcholine receptor
    Stefan Gattenlohner
    Institute of Pathology, University of Wuerzburg, Wuerzburg, Germany
    Cancer Res 66:24-8. 2006
    ....
  52. pmc Mutation history of the roma/gypsies
    Bharti Morar
    Laboratory of Molecular Genetics, Western Australian Institute for Medical Research and UWA Centre for Medical Research, University of Western Australia, Perth, Australia
    Am J Hum Genet 75:596-609. 2004
    ....