Beta-synemin expression in cardiotoxin-injected rat skeletal muscle

Mizuno, Yuji; Guyon, Jeffrey R.; Ishii, Akiko; Hoshino, Satoshi; Ohkoshi, Norio; Tamaoka, Akira; Okamoto, Koichi; Kunkel, Louis M.

doi:10.1186/1471-2474-8-40

Cited by 2 publications

(3 citation statements)

References 26 publications

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“…12 As such, it is possible that ␣-and ␤-synemin could specifically interact with ␣-dystrobrevin-1 in neurons of the midbrain and pons. This was tested using in situ hybridization experiments with an ␣-dystrobrevin-1-specific probe (321 bp; position 2068 -2388 of GenBank Accession No.…”

Section: Discussionmentioning

confidence: 99%

“…same time in regenerating adult muscle (day 7 following cardiotoxin injection), whereas ␣-dystrobrevin-2 is observed as early as day 1 post-injection. 12 ␣-Dystrobrevin-1 and ␤-synemin expression levels are similar between control and dystrophin-deficient (mdx) mouse skeletal muscle, whereas ␣-dystrobrevin-2 expression is greatly decreased in mdx mice. 14 Taken together, these data suggest that ␤-synemin participates in the stabilization of muscle by linking the myofibrillar Z-lines with the membrane-associated ␣-dystrobrevin-1 protein at the costameres.…”

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confidence: 97%

“…For example, it has been shown that ␣-dystrobrevin-1 (rather than ␣-dystrobrevin-2) preferentially co-immunoprecipitates with ␤-synemin in rat skeletal muscle. 12 ␤-Synemin and ␣-dystrobrevin-1 are expressed at the same developmental time (in mice, 5 days post-birth), whereas ␣-dystrobrevin-2 is detectable before birth. same time in regenerating adult muscle (day 7 following cardiotoxin injection), whereas ␣-dystrobrevin-2 is observed as early as day 1 post-injection.…”

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confidence: 98%

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Expression of synemin in the mouse spinal cord

et al. 2009

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beta-Synemin was previously identified as an alpha-dystrobrevin-interacting protein in muscle. To better understand its function in neural tissue, in situ and immunohistochemical analyses were performed to identify where the synemin isoforms are expressed in the spinal cord of C57BL/6 and dystrophin-deficient (mdx) C57BL/10 mice. These analyses show that synemin transcript and its encoded protein colocalize in the anterior horn cells and that no differences in synemin expression were found in nerve tissue from C57BL/6 or mdx mice. The expression of synemin mRNA and protein predominantly in the anterior horn cells suggests that synemin performs an essential function in those cells. Because synemin is more highly expressed in the midbrain and pons, its function in neurological cells was further pursued by identifying coexpressed proteins in cells from those regions of the brain. These results show that neurons that express synemin also express tryptophan hydroxylase-1, a marker of serotoninergic nerve fibers. Muscle Nerve, 2009.

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Section: Discussionmentioning

confidence: 99%

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confidence: 97%

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confidence: 98%

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Expression of synemin in the mouse spinal cord

et al. 2009

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Dysbindin, Syncoilin, and β-Synemin mRNA Levels in Dystrophic Muscles

Wakayama

Matsuzaki

Yamashita

et al. 2010

International Journal of Neuroscience

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Progressive muscular dystrophies are genetic diseases with various modes of transmission. Duchenne muscular dystrophy (DMD) is caused by the defect of dystrophin, and Fukuyama congenital muscular dystrophy (FCMD) is caused by an abnormal fukutin gene leading to the glycosylation defect of alpha-dystroglycan. Dystrobrevin is one member of the dystrophin glycoprotein complex and its binding partners include dysbindin, syncoilin, and beta-synemin (desmuslin). Dysbindin is reported to be upregulated at the protein level in mdx mouse muscles, and syncoilin protein is also reported to be upregulated in biopsied muscles with neuromuscular disorders. In the present study we measured mRNA levels of dysbindin, syncoilin, and beta-synemin in biopsied muscles with DMD and FCMD. Upregulation of human dysbindin mRNA was observed in DMD muscles in comparison with normal muscles (p < .05). The differences in human syncoilin and beta-synemin mRNA ratios between DMD and normal muscles were not statistically significant, although upregulation tendency of human syncoilin mRNA was noted in DMD muscles (.05 < p < .1). Furthermore, the differences of human dysbindin, syncoilin, and beta-synemin mRNA ratios between FCMD and normal muscles were not statistically significant. These data provide insight into the pathophysiology of these muscular dystrophies.

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Beta-synemin expression in cardiotoxin-injected rat skeletal muscle

Cited by 2 publications

References 26 publications

Expression of synemin in the mouse spinal cord

Expression of synemin in the mouse spinal cord

Dysbindin, Syncoilin, and β-Synemin mRNA Levels in Dystrophic Muscles

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