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Showing 1 to 12 of 221 entries
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Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay.

Skeletal muscle

Bergen HR, Farr JN, Vanderboom PM, Atkinson EJ, White TA, Singh RJ, Khosla S, LeBrasseur NK.
PMID: 26180626
Skelet Muscle. 2015 Jul 15;5:21. doi: 10.1186/s13395-015-0047-5. eCollection 2015.

BACKGROUND: Myostatin is a protein synthesized and secreted by skeletal muscle that negatively regulates muscle mass. The extent to which circulating myostatin levels change in the context of aging is controversial, largely due to methodological barriers.METHODS: We developed a...

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Bergen HR, Farr JN, Vanderboom PM, et al. Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay. Skelet Muscle. 2015;5:21doi: 10.1186/s13395-015-0047-5.
Bergen, H. R., Farr, J. N., Vanderboom, P. M., Atkinson, E. J., White, T. A., Singh, R. J., Khosla, S., & LeBrasseur, N. K. (2015). Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay. Skeletal muscle, 521. https://doi.org/10.1186/s13395-015-0047-5
Bergen, H Robert, et al. "Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay." Skeletal muscle vol. 5 (2015): 21. doi: https://doi.org/10.1186/s13395-015-0047-5
Bergen HR, Farr JN, Vanderboom PM, Atkinson EJ, White TA, Singh RJ, Khosla S, LeBrasseur NK. Myostatin as a mediator of sarcopenia versus homeostatic regulator of muscle mass: insights using a new mass spectrometry-based assay. Skelet Muscle. 2015 Jul 15;5:21. doi: 10.1186/s13395-015-0047-5. eCollection 2015. PMID: 26180626; PMCID: PMC4502935.
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Developmental myosins: expression patterns and functional significance.

Skeletal muscle

Schiaffino S, Rossi AC, Smerdu V, Leinwand LA, Reggiani C.
PMID: 26180627
Skelet Muscle. 2015 Jul 15;5:22. doi: 10.1186/s13395-015-0046-6. eCollection 2015.

Developing skeletal muscles express unique myosin isoforms, including embryonic and neonatal myosin heavy chains, coded by the myosin heavy chain 3 (MYH3) and MYH8 genes, respectively, and myosin light chain 1 embryonic/atrial, encoded by the myosin light chain 4...

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Schiaffino S, Rossi AC, Smerdu V, et al. Developmental myosins: expression patterns and functional significance. Skelet Muscle. 2015;5:22doi: 10.1186/s13395-015-0046-6.
Schiaffino, S., Rossi, A. C., Smerdu, V., Leinwand, L. A., & Reggiani, C. (2015). Developmental myosins: expression patterns and functional significance. Skeletal muscle, 522. https://doi.org/10.1186/s13395-015-0046-6
Schiaffino, Stefano, et al. "Developmental myosins: expression patterns and functional significance." Skeletal muscle vol. 5 (2015): 22. doi: https://doi.org/10.1186/s13395-015-0046-6
Schiaffino S, Rossi AC, Smerdu V, Leinwand LA, Reggiani C. Developmental myosins: expression patterns and functional significance. Skelet Muscle. 2015 Jul 15;5:22. doi: 10.1186/s13395-015-0046-6. eCollection 2015. PMID: 26180627; PMCID: PMC4502549.
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Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ.

Skeletal muscle

Lamarche É, Lala-Tabbert N, Gunanayagam A, St-Louis C, Wiper-Bergeron N.
PMID: 25878769
Skelet Muscle. 2015 Mar 18;5:8. doi: 10.1186/s13395-015-0032-z. eCollection 2015.

BACKGROUND: The effects of transforming growth factor-beta (TGFβ) are mediated by the transcription factors Smad2 and Smad3. During adult skeletal myogenesis, TGFβ signaling inhibits the differentiation of myoblasts, and this can be reversed by treatment with retinoic acid (RA)....

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Lamarche É, Lala-Tabbert N, Gunanayagam A, et al. Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ. Skelet Muscle. 2015;5:8doi: 10.1186/s13395-015-0032-z.
Lamarche, �. �., Lala-Tabbert, N., Gunanayagam, A., St-Louis, C., & Wiper-Bergeron, N. (2015). Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ. Skeletal muscle, 58. https://doi.org/10.1186/s13395-015-0032-z
Lamarche, Émilie, et al. "Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ." Skeletal muscle vol. 5 (2015): 8. doi: https://doi.org/10.1186/s13395-015-0032-z
Lamarche É, Lala-Tabbert N, Gunanayagam A, St-Louis C, Wiper-Bergeron N. Retinoic acid promotes myogenesis in myoblasts by antagonizing transforming growth factor-beta signaling via C/EBPβ. Skelet Muscle. 2015 Mar 18;5:8. doi: 10.1186/s13395-015-0032-z. eCollection 2015. PMID: 25878769; PMCID: PMC4397812.
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Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice.

Skeletal muscle

Latres E, Pangilinan J, Miloscio L, Bauerlein R, Na E, Potocky TB, Huang Y, Eckersdorff M, Rafique A, Mastaitis J, Lin C, Murphy AJ, Yancopoulos GD, Gromada J, Stitt T.
PMID: 26457176
Skelet Muscle. 2015 Oct 09;5:34. doi: 10.1186/s13395-015-0060-8. eCollection 2015.

BACKGROUND: Loss of skeletal muscle mass and function in humans is associated with significant morbidity and mortality. The role of myostatin as a key negative regulator of skeletal muscle mass and function has supported the concept that inactivation of...

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Latres E, Pangilinan J, Miloscio L, et al. Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice. Skelet Muscle. 2015;5:34doi: 10.1186/s13395-015-0060-8.
Latres, E., Pangilinan, J., Miloscio, L., Bauerlein, R., Na, E., Potocky, T. B., Huang, Y., Eckersdorff, M., Rafique, A., Mastaitis, J., Lin, C., Murphy, A. J., Yancopoulos, G. D., Gromada, J., & Stitt, T. (2015). Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice. Skeletal muscle, 534. https://doi.org/10.1186/s13395-015-0060-8
Latres, Esther, et al. "Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice." Skeletal muscle vol. 5 (2015): 34. doi: https://doi.org/10.1186/s13395-015-0060-8
Latres E, Pangilinan J, Miloscio L, Bauerlein R, Na E, Potocky TB, Huang Y, Eckersdorff M, Rafique A, Mastaitis J, Lin C, Murphy AJ, Yancopoulos GD, Gromada J, Stitt T. Myostatin blockade with a fully human monoclonal antibody induces muscle hypertrophy and reverses muscle atrophy in young and aged mice. Skelet Muscle. 2015 Oct 09;5:34. doi: 10.1186/s13395-015-0060-8. eCollection 2015. PMID: 26457176; PMCID: PMC4600334.
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Pax7 is back.

Skeletal muscle

Brack AS.
PMID: 25546147
Skelet Muscle. 2014 Dec 14;4(1):24. doi: 10.1186/s13395-014-0024-4. eCollection 2014.

Two recent studies have reinvigorated the conversation regarding the role of Pax7 in adult satellite. Studies by Gunther et al (Cell Stem Cell 13:590-601, 2013) and Von Maltzhen et al (Proc Natl Acad Sci U S A 110:16474-16479) show...

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Brack AS. Pax7 is back. Skelet Muscle. 2014;4(1):24doi: 10.1186/s13395-014-0024-4.
Brack, A. S. (2014). Pax7 is back. Skeletal muscle, 4(1), 24. https://doi.org/10.1186/s13395-014-0024-4
Brack, Andrew S. "Pax7 is back." Skeletal muscle vol. 4,1 (2014): 24. doi: https://doi.org/10.1186/s13395-014-0024-4
Brack AS. Pax7 is back. Skelet Muscle. 2014 Dec 14;4(1):24. doi: 10.1186/s13395-014-0024-4. eCollection 2014. PMID: 25546147; PMCID: PMC4276024.
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BMP-9 expression in human traumatic heterotopic ossification: a case report.

Skeletal muscle

Grenier G, Leblanc E, Faucheux N, Lauzier D, Kloen P, Hamdy RC.
PMID: 24330639
Skelet Muscle. 2013 Dec 16;3(1):29. doi: 10.1186/2044-5040-3-29.

BACKGROUND: Heterotopic ossification (HO) is defined as the abnormal formation of mature bone in soft tissue, notably skeletal muscle. The morbidity of HO in polytraumatized patients impacts the functional outcome, impairs rehabilitation, and increases costs due to subsequent surgical...

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Grenier G, Leblanc E, Faucheux N, et al. BMP-9 expression in human traumatic heterotopic ossification: a case report. Skelet Muscle. 2013;3(1):29doi: 10.1186/2044-5040-3-29.
Grenier, G., Leblanc, E., Faucheux, N., Lauzier, D., Kloen, P., & Hamdy, R. C. (2013). BMP-9 expression in human traumatic heterotopic ossification: a case report. Skeletal muscle, 3(1), 29. https://doi.org/10.1186/2044-5040-3-29
Grenier, Guillaume, et al. "BMP-9 expression in human traumatic heterotopic ossification: a case report." Skeletal muscle vol. 3,1 (2013): 29. doi: https://doi.org/10.1186/2044-5040-3-29
Grenier G, Leblanc E, Faucheux N, Lauzier D, Kloen P, Hamdy RC. BMP-9 expression in human traumatic heterotopic ossification: a case report. Skelet Muscle. 2013 Dec 16;3(1):29. doi: 10.1186/2044-5040-3-29. PMID: 24330639; PMCID: PMC3878643.
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C-terminal residues of skeletal muscle calsequestrin are essential for calcium binding and for skeletal ryanodine receptor inhibition.

Skeletal muscle

Beard NA, Dulhunty AF.
PMID: 25861445
Skelet Muscle. 2015 Feb 22;5:6. doi: 10.1186/s13395-015-0029-7. eCollection 2015.

BACKGROUND: Skeletal muscle function depends on calcium signaling proteins in the sarcoplasmic reticulum (SR), including the calcium-binding protein calsequestrin (CSQ), the ryanodine receptor (RyR) calcium release channel, and skeletal triadin 95 kDa (trisk95) and junctin, proteins that bind to...

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Beard NA, Dulhunty AF. C-terminal residues of skeletal muscle calsequestrin are essential for calcium binding and for skeletal ryanodine receptor inhibition. Skelet Muscle. 2015;5:6doi: 10.1186/s13395-015-0029-7.
Beard, N. A., & Dulhunty, A. F. (2015). C-terminal residues of skeletal muscle calsequestrin are essential for calcium binding and for skeletal ryanodine receptor inhibition. Skeletal muscle, 56. https://doi.org/10.1186/s13395-015-0029-7
Beard, Nicole A, and Dulhunty, Angela F. "C-terminal residues of skeletal muscle calsequestrin are essential for calcium binding and for skeletal ryanodine receptor inhibition." Skeletal muscle vol. 5 (2015): 6. doi: https://doi.org/10.1186/s13395-015-0029-7
Beard NA, Dulhunty AF. C-terminal residues of skeletal muscle calsequestrin are essential for calcium binding and for skeletal ryanodine receptor inhibition. Skelet Muscle. 2015 Feb 22;5:6. doi: 10.1186/s13395-015-0029-7. eCollection 2015. PMID: 25861445; PMCID: PMC4389316.
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Involvement of adiponectin in the pathogenesis of dystrophinopathy.

Skeletal muscle

Abou-Samra M, Lecompte S, Schakman O, Noel L, Many MC, Gailly P, Brichard SM.
PMID: 26257862
Skelet Muscle. 2015 Aug 07;5:25. doi: 10.1186/s13395-015-0051-9. eCollection 2015.

BACKGROUND: The hormone adiponectin (ApN) is decreased in the metabolic syndrome, where it plays a key pathogenic role. ApN also exerts some anti-inflammatory effects on skeletal muscles in mice exposed to acute or chronic inflammation. Here, we investigate whether...

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Abou-Samra M, Lecompte S, Schakman O, et al. Involvement of adiponectin in the pathogenesis of dystrophinopathy. Skelet Muscle. 2015;5:25doi: 10.1186/s13395-015-0051-9.
Abou-Samra, M., Lecompte, S., Schakman, O., Noel, L., Many, M. C., Gailly, P., & Brichard, S. M. (2015). Involvement of adiponectin in the pathogenesis of dystrophinopathy. Skeletal muscle, 525. https://doi.org/10.1186/s13395-015-0051-9
Abou-Samra, Michel, et al. "Involvement of adiponectin in the pathogenesis of dystrophinopathy." Skeletal muscle vol. 5 (2015): 25. doi: https://doi.org/10.1186/s13395-015-0051-9
Abou-Samra M, Lecompte S, Schakman O, Noel L, Many MC, Gailly P, Brichard SM. Involvement of adiponectin in the pathogenesis of dystrophinopathy. Skelet Muscle. 2015 Aug 07;5:25. doi: 10.1186/s13395-015-0051-9. eCollection 2015. PMID: 26257862; PMCID: PMC4528853.
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In vitro stability of therapeutically relevant, internally truncated dystrophins.

Skeletal muscle

McCourt JL, Rhett KK, Jaeger MA, Belanto JJ, Talsness DM, Ervasti JM.
PMID: 25954502
Skelet Muscle. 2015 Apr 28;5:13. doi: 10.1186/s13395-015-0040-z. eCollection 2015.

BACKGROUND: The X-linked recessive disease Duchenne muscular dystrophy (DMD) is caused by mutations in the gene encoding the protein dystrophin. Despite its large size, dystrophin is a highly stable protein, demonstrating cooperative unfolding during thermal denaturation as monitored by...

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McCourt JL, Rhett KK, Jaeger MA, et al. In vitro stability of therapeutically relevant, internally truncated dystrophins. Skelet Muscle. 2015;5:13doi: 10.1186/s13395-015-0040-z.
McCourt, J. L., Rhett, K. K., Jaeger, M. A., Belanto, J. J., Talsness, D. M., & Ervasti, J. M. (2015). In vitro stability of therapeutically relevant, internally truncated dystrophins. Skeletal muscle, 513. https://doi.org/10.1186/s13395-015-0040-z
McCourt, Jackie L, et al. "In vitro stability of therapeutically relevant, internally truncated dystrophins." Skeletal muscle vol. 5 (2015): 13. doi: https://doi.org/10.1186/s13395-015-0040-z
McCourt JL, Rhett KK, Jaeger MA, Belanto JJ, Talsness DM, Ervasti JM. In vitro stability of therapeutically relevant, internally truncated dystrophins. Skelet Muscle. 2015 Apr 28;5:13. doi: 10.1186/s13395-015-0040-z. eCollection 2015. PMID: 25954502; PMCID: PMC4424174.
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The effect of the muscle environment on the regenerative capacity of human skeletal muscle stem cells.

Skeletal muscle

Meng J, Bencze M, Asfahani R, Muntoni F, Morgan JE.
PMID: 25949786
Skelet Muscle. 2015 Apr 28;5:11. doi: 10.1186/s13395-015-0036-8. eCollection 2015.

BACKGROUND: Muscle stem cell transplantation is a possible treatment for muscular dystrophy. In addition to the intrinsic properties of the stem cells, the local and systemic environment plays an important role in determining the fate of the grafted cells....

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Meng J, Bencze M, Asfahani R, et al. The effect of the muscle environment on the regenerative capacity of human skeletal muscle stem cells. Skelet Muscle. 2015;5:11doi: 10.1186/s13395-015-0036-8.
Meng, J., Bencze, M., Asfahani, R., Muntoni, F., & Morgan, J. E. (2015). The effect of the muscle environment on the regenerative capacity of human skeletal muscle stem cells. Skeletal muscle, 511. https://doi.org/10.1186/s13395-015-0036-8
Meng, Jinhong, et al. "The effect of the muscle environment on the regenerative capacity of human skeletal muscle stem cells." Skeletal muscle vol. 5 (2015): 11. doi: https://doi.org/10.1186/s13395-015-0036-8
Meng J, Bencze M, Asfahani R, Muntoni F, Morgan JE. The effect of the muscle environment on the regenerative capacity of human skeletal muscle stem cells. Skelet Muscle. 2015 Apr 28;5:11. doi: 10.1186/s13395-015-0036-8. eCollection 2015. PMID: 25949786; PMCID: PMC4422426.
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Differential myofiber-type transduction preference of adeno-associated virus serotypes 6 and 9.

Skeletal muscle

Riaz M, Raz Y, Moloney EB, van Putten M, Krom YD, van der Maarel SM, Verhaagen J, Raz V.
PMID: 26561520
Skelet Muscle. 2015 Nov 10;5:37. doi: 10.1186/s13395-015-0064-4. eCollection 2015.

BACKGROUND: Gene therapy strategies are promising therapeutic options for monogenic muscular dystrophies, with several currently underways. The adeno-associated viral (AAV) vector is among the most effective gene delivery systems. However, transduction efficiency in skeletal muscles varies between AAV serotypes,...

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Riaz M, Raz Y, Moloney EB, et al. Differential myofiber-type transduction preference of adeno-associated virus serotypes 6 and 9. Skelet Muscle. 2015;5:37doi: 10.1186/s13395-015-0064-4.
Riaz, M., Raz, Y., Moloney, E. B., van Putten, M., Krom, Y. D., van der Maarel, S. M., Verhaagen, J., & Raz, V. (2015). Differential myofiber-type transduction preference of adeno-associated virus serotypes 6 and 9. Skeletal muscle, 537. https://doi.org/10.1186/s13395-015-0064-4
Riaz, Muhammad, et al. "Differential myofiber-type transduction preference of adeno-associated virus serotypes 6 and 9." Skeletal muscle vol. 5 (2015): 37. doi: https://doi.org/10.1186/s13395-015-0064-4
Riaz M, Raz Y, Moloney EB, van Putten M, Krom YD, van der Maarel SM, Verhaagen J, Raz V. Differential myofiber-type transduction preference of adeno-associated virus serotypes 6 and 9. Skelet Muscle. 2015 Nov 10;5:37. doi: 10.1186/s13395-015-0064-4. eCollection 2015. PMID: 26561520; PMCID: PMC4641337.
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Elusive sources of variability of dystrophin rescue by exon skipping.

Skeletal muscle

Vila MC, Klimek MB, Novak JS, Rayavarapu S, Uaesoontrachoon K, Boehler JF, Fiorillo AA, Hogarth MW, Zhang A, Shaughnessy C, Gordish-Dressman H, Burki U, Straub V, Lu QL, Partridge TA, Brown KJ, Hathout Y, van den Anker J, Hoffman EP, Nagaraju K.
PMID: 26634117
Skelet Muscle. 2015 Dec 01;5:44. doi: 10.1186/s13395-015-0070-6. eCollection 2015.

BACKGROUND: Systemic delivery of anti-sense oligonucleotides to Duchenne muscular dystrophy (DMD) patients to induce de novo dystrophin protein expression in muscle (exon skipping) is a promising therapy. Treatment with Phosphorodiamidate morpholino oligomers (PMO) lead to shorter de novo dystrophin...

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Vila MC, Klimek MB, Novak JS, et al. Elusive sources of variability of dystrophin rescue by exon skipping. Skelet Muscle. 2015;5:44doi: 10.1186/s13395-015-0070-6.
Vila, M. C., Klimek, M. B., Novak, J. S., Rayavarapu, S., Uaesoontrachoon, K., Boehler, J. F., Fiorillo, A. A., Hogarth, M. W., Zhang, A., Shaughnessy, C., Gordish-Dressman, H., Burki, U., Straub, V., Lu, Q. L., Partridge, T. A., Brown, K. J., Hathout, Y., van den Anker, J., Hoffman, E. P., & Nagaraju, K. (2015). Elusive sources of variability of dystrophin rescue by exon skipping. Skeletal muscle, 544. https://doi.org/10.1186/s13395-015-0070-6
Vila, Maria Candida, et al. "Elusive sources of variability of dystrophin rescue by exon skipping." Skeletal muscle vol. 5 (2015): 44. doi: https://doi.org/10.1186/s13395-015-0070-6
Vila MC, Klimek MB, Novak JS, Rayavarapu S, Uaesoontrachoon K, Boehler JF, Fiorillo AA, Hogarth MW, Zhang A, Shaughnessy C, Gordish-Dressman H, Burki U, Straub V, Lu QL, Partridge TA, Brown KJ, Hathout Y, van den Anker J, Hoffman EP, Nagaraju K. Elusive sources of variability of dystrophin rescue by exon skipping. Skelet Muscle. 2015 Dec 01;5:44. doi: 10.1186/s13395-015-0070-6. eCollection 2015. PMID: 26634117; PMCID: PMC4667482.
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Showing 1 to 12 of 221 entries