Research Topics
Genomes and Genes | Mohammad SalajeghehSummaryAffiliation: Massachusetts General Hospital Country: USA Publications
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Detail Information
Publications
Autoantibodies against a 43 KDa muscle protein in inclusion body myositisMohammad Salajegheh
Department of Neurology, Brigham and Women s Hospital, Boston, Massachusetts, United States of America
PLoS ONE 6:e20266. 2011..Though widely believed to have no significant humoral autoimmunity, we sought to identify novel autoantibodies with high specificity for this disease...
Sarcoplasmic redistribution of nuclear TDP-43 in inclusion body myositisMohammad Salajegheh
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital, and Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
Muscle Nerve 40:19-31. 2009..TDP-43 could be one of many nucleic acid binding proteins that are abnormally present in IBM sarcoplasm. They could potentially interfere with the normal function of extranuclear RNAs that maintain myofiber protein production...
Permissive environment for B-cell maturation in myositis muscle in the absence of B-cell folliclesMohammad Salajegheh
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts 02115, USA
Muscle Nerve 42:576-83. 2010..An atypical lymphoid histology, lacking concentrated collections of germinal-center-like B-cell follicles, is capable of antigen-stimulated clonal maturation of antibody-producing plasma cells...
Interferon-stimulated gene 15 (ISG15) conjugates proteins in dermatomyositis muscle with perifascicular atrophyMohammad Salajegheh
Children s Hospital Informatics Program, Division of Neuromuscular Disease, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Ann Neurol 67:53-63. 2010..We investigated interferon-stimulated gene 15 (ISG15), a poorly understood ubiquitin-like modifier, and its enzymatic pathway in dermatomyositis (DM), an autoimmune disease primarily involving muscle and skin...
Nature of "Tau" immunoreactivity in normal myonuclei and inclusion body myositisMohammad Salajegheh
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Muscle Nerve 40:520-8. 2009..Normal myonuclei contain neurofilament H or other unidentified 200 kDa proteins with similar phosphorylated motifs accounting for SMI-31 immunoreactivity...
Human plasmacytoid dendritic cell accumulation amplifies their type 1 interferon productionAnne P Liao
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital, Boston, MA, USA
Clin Immunol 136:130-8. 2010..The role of the IFNAR-dependent mechanism of interferon production by human pDCs is greater than previously suggested. IFNAR blockade has potential for diminishing type 1 interferon production by all human cells...
Interferon β is associated with type 1 interferon-inducible gene expression in dermatomyositisAnne P Liao
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital and Children s Hospital Informatics Program, Harvard Medical School, 75 Francis Street, Boston, MA 02115, USA
Ann Rheum Dis 70:831-6. 2011..To determine whether type 1 interferon (IFN) proteins in blood are associated with downstream type 1 IFN-inducible gene expression in blood from patients with myositis...
Etiology of limb girdle muscular dystrophy 1D/1E determined by laser capture microdissection proteomicsSteven A Greenberg
Department of Neurology, Division of Neuromuscular Disease, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Ann Neurol 71:141-5. 2012..Sequencing in this patient and family members identified the genetic basis of the previously reported 6q23 linked LGMD1D/1E to be due to an intron splice donor site mutation (IVS3+3A>G) of the desmin gene located on chromosome 2q35...
A local antigen-driven humoral response is present in the inflammatory myopathiesElizabeth M Bradshaw
Department of Neurology, Laboratory of Molecular Immunology, Center for Neurologic Diseases and Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
J Immunol 178:547-56. 2007..These findings highlight the need for a revision of the current paradigm of exclusively T cell-mediated intramuscular Ag-specific autoimmunity in inclusion body myositis and polymyositis...
Targeted mutation of mouse skeletal muscle sodium channel produces myotonia and potassium-sensitive weaknessLawrence J Hayward
Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA
J Clin Invest 118:1437-49. 2008....
Upregulation of thrombospondin-1(TSP-1) and its binding partners, CD36 and CD47, in sporadic inclusion body myositisMohammad Salajegheh
The Division of Neuromuscular Disease, Department of Neurology, Brigham and Women s Hospital, 75 Francis Street, Tower 5D, Boston, MA 02115, USA
J Neuroimmunol 187:166-74. 2007..The TSP-complex is another inflammatory mediator associated with chronic inflammation in IBM that may perpetuate the immune responses to local antigens in response to TNF-alpha...
