Relevant bibliographies by topics / R6-2 skeletal muscle

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  1. Journal articles
  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'R6-2 skeletal muscle'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "R6-2 skeletal muscle"

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Miranda, Daniel R., Monica Wong, Shannon H. Romer, et al. "Progressive Cl− channel defects reveal disrupted skeletal muscle maturation in R6/2 Huntington’s mice." Journal of General Physiology 149, no. 1 (2016): 55–74. http://dx.doi.org/10.1085/jgp.201611603.

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Huntington’s disease (HD) patients suffer from progressive and debilitating motor dysfunction. Previously, we discovered reduced skeletal muscle chloride channel (ClC-1) currents, inwardly rectifying potassium (Kir) channel currents, and membrane capacitance in R6/2 transgenic HD mice. The ClC-1 loss-of-function correlated with increased aberrant mRNA processing and decreased levels of full-length ClC-1 mRNA (Clcn1 gene). Physiologically, the resulting muscle hyperexcitability may help explain involuntary contractions of HD. In this study, the onset and progression of these defects are investi
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Miranda, Daniel R., Eric Reed, Abdulrahman Jama, et al. "Mechanisms of altered skeletal muscle action potentials in the R6/2 mouse model of Huntington’s disease." American Journal of Physiology-Cell Physiology 319, no. 1 (2020): C218—C232. http://dx.doi.org/10.1152/ajpcell.00153.2020.

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Huntington’s disease (HD) patients suffer from progressive and debilitating motor dysfunction for which only palliative treatment is currently available. Previously, we discovered reduced skeletal muscle Cl− channel (ClC-1) and inwardly rectifying K+ channel (Kir) currents in R6/2 HD transgenic mice. To further investigate the role of ClC-1 and Kir currents in HD skeletal muscle pathology, we measured the effect of reduced ClC-1 and Kir currents on action potential (AP) repetitive firing in R6/2 mice using a two-electrode current clamp. We found that R6/2 APs had a significantly lower peak amp
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Braubach, Peter, Murat Orynbayev, Zoita Andronache, et al. "Altered Ca2+ signaling in skeletal muscle fibers of the R6/2 mouse, a model of Huntington’s disease." Journal of General Physiology 144, no. 5 (2014): 393–413. http://dx.doi.org/10.1085/jgp.201411255.

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Huntington’s disease (HD) is caused by an expanded CAG trinucleotide repeat within the gene encoding the protein huntingtin. The resulting elongated glutamine (poly-Q) sequence of mutant huntingtin (mhtt) affects both central neurons and skeletal muscle. Recent reports suggest that ryanodine receptor–based Ca2+ signaling, which is crucial for skeletal muscle excitation–contraction coupling (ECC), is changed by mhtt in HD neurons. Consequently, we searched for alterations of ECC in muscle fibers of the R6/2 mouse, a mouse model of HD. We performed fluorometric recordings of action potentials (A
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Hayashi, Yoshihiro, Takaaki Ikata, Hiroaki Takai, Shinjiro Takata, Takayuki Sogabe, and Keiko Koga. "Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation." Journal of Applied Physiology 82, no. 3 (1997): 732–37. http://dx.doi.org/10.1152/jappl.1997.82.3.732.

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Hayashi, Yoshihiro, Takaaki Ikata, Hiroaki Takai, Shinjiro Takata, Takayuki Sogabe, and Keiko Koga. Time course of recovery from nerve injury in skeletal muscle: energy state and local circulation. J. Appl. Physiol. 82(3): 732–737, 1997.—This study examined the time course of recovery from nerve injury on energy state assessed by phosphorus-31 magnetic resonance spectroscopy and local circulation dynamics by fluorine-19 magnetic resonance spectroscopy in skeletal muscles of rats. The hindlimb muscles that had undergone unilateral sciatic nerve compression for 2 wk (CN) were compared with sham-
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Magnusson-Lind, Anna, Marcus Davidsson, Edina Silajdžić, et al. "Skeletal Muscle Atrophy in R6/2 Mice – Altered Circulating Skeletal Muscle Markers and Gene Expression Profile Changes." Journal of Huntington's Disease 3, no. 1 (2014): 13–24. http://dx.doi.org/10.3233/jhd-130075.

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She, Pengxiang, Zhiyou Zhang, Deanna Marchionini, et al. "Molecular characterization of skeletal muscle atrophy in the R6/2 mouse model of Huntington's disease." American Journal of Physiology-Endocrinology and Metabolism 301, no. 1 (2011): E49—E61. http://dx.doi.org/10.1152/ajpendo.00630.2010.

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Huntington's disease (HD), a neurodegenerative disorder caused by mutant huntingtin, is characterized by a catabolic phenotype. To determine the mechanisms underlying muscle wasting, we examined key signal transduction pathways governing muscle protein metabolism, apoptosis, and autophagy in R6/2 mice, a well-characterized transgenic model of HD. R6/2 mice exhibited increased adiposity, elevated energy expenditure, and decreased body weight and lean mass without altered food intake. Severe skeletal muscle wasting accounted for a majority of the weight loss. Protein synthesis was unexpectedly i
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Braubach, P., Z. Andronache, A. Riecker, et al. "A21 Altered calcium kinetics in skeletal muscle fibres of the R6/2 mouse model of HD." Journal of Neurology, Neurosurgery & Psychiatry 81, Suppl 1 (2010): A7.1—A7. http://dx.doi.org/10.1136/jnnp.2010.222570.21.

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Kojer, Kerstin, Tanja Hering, Chantal Bazenet, et al. "Huntingtin Aggregates and Mitochondrial Pathology in Skeletal Muscle but not Heart of Late-Stage R6/2 Mice." Journal of Huntington's Disease 8, no. 2 (2019): 145–59. http://dx.doi.org/10.3233/jhd-180324.

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Hering, T., K. Kojer, N. Birth, et al. "D03 Mitochondrial Biogenesis, And Respiratory Chain Assembly And Function, In Skeletal Muscle Of The R6/2 Mouse Model And Human Huntington's Disease." Journal of Neurology, Neurosurgery & Psychiatry 85, Suppl 1 (2014): A32. http://dx.doi.org/10.1136/jnnp-2014-309032.95.

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Wackler, P., T. Lenk, T. Hering, M. Orth, GB Landwehrmeyer, and KS Lindenberg. "B21 Decreased expression and reduced translocation to the sarcolemma of the insulin-sensitive glucose transporter GLUT4 in skeletal muscle of R6/2 MICE." Journal of Neurology, Neurosurgery & Psychiatry 83, Suppl 1 (2012): A12.1—A12. http://dx.doi.org/10.1136/jnnp-2012-303524.37.

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Dissertations / Theses on the topic "R6-2 skeletal muscle"

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Reed, Eric Joshua. "Fast Voltage-Gated Sodium Channel Currents and Action Potential Firing in R6/2 Skeletal Muscle." Wright State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=wright1546463750930042.

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Burke, Steven Russell Alan. "Assessment of In Vivo Muscle Force in the R6/2 Mouse Model of Huntington's Disease Using Newly Designed Force Rig." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1610360658382723.

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Conference papers on the topic "R6-2 skeletal muscle"

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Lindenberg, Katrin S., Eva Buck, G. Bernhard Landwehrmeyer, and Enrico Calzia. "A34 Mitochondrial respiration is limited by atp-production in the skeletal muscle of the R6/2 hd mouse model." In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.32.

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You might also be interested in the extended bibliographies on the topic 'R6-2 skeletal muscle' for particular source types:
Journal articles
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