Use of anti‐neurofilament antibody to identify paired‐helical filaments in inclusion‐body myositis

Askanas, Valerie; Alvarez, Renate B.; Mirabella, Massimiliano; Engel, W. King

doi:10.1002/ana.410390318

Cited by 49 publications

(29 citation statements)

References 7 publications

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“…We next examined the relationship between the Elk-1-positive deposits and those of SMI-31, a marker of IBM filaments. 8 The distribution and configuration of the Elk-1-positive deposits were the same as those of SMI-31 (see figure 4, lower row) in vacuolated fibers. Although SMI-31 also stained axons of IM nerves, as described previously, 21 anti-Elk-1 did not.…”

Section: Results Localization Of Mapks and Elk-1 In S-ibmsupporting

confidence: 53%

“…It can also react with other proteins such as microtubule-associated protein (MAP) tau and MAP-2. 29 Because SMI-31 stains IBM filaments, 8 ERK and its target Elk-1 may be associated with the filaments or might be components of the filaments. Electron microscopic studies indicated that IBM filaments are largely cytoplasmic, and only occasional nuclei contain those filaments.…”

Section: Extracellular Signalregulated Kinase (Erk) and Elk-1 Immunolmentioning

confidence: 99%

“…Because protein kinases play pivotal roles in regulating intracellular signal transduction and transcription, 6,7 studies of protein kinases in IBM may help to clarify the changes of protein expression in this disease. Accumulation of phosphorylated protein, which is immunoreactive for an antibody directed against phosphorylated neurofilament proteins (SMI-31) in vacuolated fibers in IBM, 8 could indicate abnormal intracellular signal transduction. 9 Extracellular signal-regulated kinase (ERK) belongs to the mitogen-activated protein kinase (MAPK) family, and plays a central role in transducing extracellular signals to the nucleus.…”

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confidence: 99%

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Inclusion body myositis

Nakano¹,

Shinde²,

Kawashima³

et al. 2001

Neurology

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Article abstract-Objective: To assess abnormal intracellular signal transduction in inclusion body myositis (IBM). Background: Mitogen-activated protein kinases (MAPKs) play pivotal roles in intracellular signal transduction and regulate cell growth and differentiation. Upon their activation, MAPKs translocate from the cytoplasm into the nucleus. Design/methods: The authors investigated the localization of several forms of the MAPK family-extracellular signalregulated kinase (ERK), c-Jun N-terminal protein kinase (JNK), and p38 MAPK (p38)-in 10 patients with sporadic IBM and in 52 control subjects. The relationship between the localization of immunopositive deposits and nuclei was tested with bis-benzimide. Results: Vacuolated fibers in IBM displayed very strong focal immunoreactivity of ERK, but not of JNK or p38. The ERK-positive deposits in these vacuolated fibers colocalized with the nuclear substrate of ERK, Elk-1. ERK-and Elk-1-positive deposits were located frequently on the surface of the nuclei in vacuolated fibers in IBM. Similar findings to those of sporadic IBM were observed in three patients with distal myopathy with rimmed vacuoles, but not in eight normal or the other 41 disease controls. Conclusion: There is evidence for impaired molecular transport to the nucleus from the cytoplasm in the vacuolated fibers in IBM. This could be due to cytoplasmic aggregation of ERK and Elk-1 or to abnormal nuclear pore machinery involved in the transport of ERK and its substrate upon ERK activation.

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Section: Results Localization Of Mapks and Elk-1 In S-ibmsupporting

confidence: 53%

Section: Extracellular Signalregulated Kinase (Erk) and Elk-1 Immunolmentioning

confidence: 99%

mentioning

confidence: 99%

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Inclusion body myositis

Nakano¹,

Shinde²,

Kawashima³

et al. 2001

Neurology

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“…11 All IBM biopsies showed muscle fibers with vacuoles on Engel trichrome staining 12 and 15-to 21-nm paired helical filaments (PHFs) by electron microscopy and by SMI-31 immunoreactivity. 13 In addition, all s-IBM patients had, in 60 to 80% of their vacuolated muscle fibers, Congo Red positivity using fluorescence enhancement. 14 …”

Section: Muscle Biopsiesmentioning

confidence: 98%

Endoplasmic Reticulum Stress and Unfolded Protein Response in Inclusion Body Myositis Muscle

Vattemi

Engel

McFerrin

et al. 2004

The American Journal of Pathology

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171

175

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“…Several proteins found in amyloid plaques typical of AD accumulate in s-IBM muscle fibres, including apolipoprotein E (ApoE), α 1 -antichymotrypsin (α 1 -ACT), prion protein, hyperphosphorylated tau, presenilin 1, ubiquitin, β-amyloid (Aβ) and β-amyloid precursor protein [8, 9]. Moreover, tubulofilaments found in s-IBM resemble AD neurofibrillary tangles [10]. These points questioned the analogies in degenerative processes between AD and s-IBM [6].…”

Section: Introductionmentioning

confidence: 99%

Apolipoprotein E and Alpha-1-Antichymotrypsin Polymorphisms in Sporadic Inclusion Body Myositis

Goßrau

Gestrich²,

Koch³

et al. 2004

Eur Neurol

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Sporadic inclusion body myositis (s-IBM) is a progressive muscle disease of unknown aetiology. Characteristically, intracellular amyloid deposits are detectable, including β-amyloid precursor protein, phosphorylated tau, α₁-antichymotrypsin (α₁-ACT) and apolipoprotein E (ApoE). Polymorphisms and mutations of the encoding genes have been identified in a variety of neurodegenerative diseases including Alzheimer’s disease (AD). Beside other factors, polymorphisms may lead to protein accumulation in both diseases. In particular, polymorphisms within the ApoE and α₁-ACT gene have been implicated in the aetiology of AD and s-IBM. We analysed ApoE and α₁-ACT gene polymorphisms in 35 s-IBM patients. We could not identify any statistical significant correlation between distinct ApoE and α₁-ACT genotypes and the risk of developing s-IBM. Additionally, ApoE and α₁-ACT genotypes seem not to influence the onset age of s-IBM. A combination of different α₁-ACT and ApoE genotypes appears not to enhance the risk of developing s-IBM. Therefore, allelic variations of α₁-ACT and ApoE are unlikely to be genetic key factors in the aetiology of s-IBM.

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Use of anti‐neurofilament antibody to identify paired‐helical filaments in inclusion‐body myositis

Cited by 49 publications

References 7 publications

Inclusion body myositis

Inclusion body myositis

Endoplasmic Reticulum Stress and Unfolded Protein Response in Inclusion Body Myositis Muscle

Apolipoprotein E and Alpha-1-Antichymotrypsin Polymorphisms in Sporadic Inclusion Body Myositis

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