Disease relevance of Myositis, Inclusion Body

• Apolipoprotein E alleles in sporadic inclusion-body myositis and hereditary inclusion-body myopathy [1].
• We report a patient with a slow-channel congenital myasthenic syndrome who carries a novel slow-channel mutation in the epsilon subunit of the acetylcholine receptor and has tubulofilamentous inclusion bodies, in skeletal muscle of the type observed in hereditary and sporadic inclusion body myositis [2].

High impact information on Myositis, Inclusion Body

• Presence of BACE1 and BACE2 in muscle fibres of patients with sporadic inclusion-body myositis [3].
• Methionine homozygosity at prion gene codon 129 may predispose to sporadic inclusion-body myositis [4].
• Increased amounts of prion protein expression and deposition have been described in pathological muscle fibers of two human muscle disorders, called sporadic inclusion-body myositis (s-IBM) and hereditary inclusion-body myopathy, but it is unknown whether accumulated prion protein reflects normal PrPc or PrP(Sc) [5].
• In this study, we performed both ex vivo and in situ analyses using muscle biopsies obtained from an HTLV-1-infected patient with HAM/TSP and sporadic inclusion body myositis [6].
• OBJECTIVE: To investigate whether the combination of intravenous immunoglobulin (IVIg) with prednisone improves muscle strength and alters endomysial inflammation in patients with sporadic inclusion body myositis (s-IBM) [7].

Biological context of Myositis, Inclusion Body

• In Caucasians, sporadic inclusion body myositis has been associated with the MHC ancestral haplotypes; HLA-A1, B8, DR3 (8.1AH) and HLA-B35, DR1 (35.2AH) [8].

Anatomical context of Myositis, Inclusion Body

• Homocysteine-induced endoplasmic reticulum protein (Herp) is up-regulated in sporadic inclusion-body myositis and in endoplasmic reticulum stress-induced cultured human muscle fibers [9].

Gene context of Myositis, Inclusion Body

• OBJECTIVE: To investigate alterations in protein kinases and phosphatases that regulate the activity of mitogen activated protein kinase (MAPK) in sporadic inclusion body myositis (IBM) [10].
• Apolipoprotein E and alpha-1-antichymotrypsin polymorphisms in sporadic inclusion body myositis [11].
• The muscle mitogen-activated protein kinase is altered in sporadic inclusion body myositis [12].
• Myostatin is increased and complexes with amyloid-beta within sporadic inclusion-body myositis muscle fibers [13].
• This is the first description of a haplotypic MHC association with sporadic inclusion body myositis in Japanese patients [8].

References