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An Actin Filament Population Defined by the Tropomyosin Tpm3.1 Regulates Glucose Uptake.

Traffic (Copenhagen, Denmark)

Kee AJ, Yang L, Lucas CA, Greenberg MJ, Martel N, Leong GM, Hughes WE, Cooney GJ, James DE, Ostap EM, Han W, Gunning PW, Hardeman EC.
PMID: 26688443
Traffic. 2016 Jan;17(1):80-1. doi: 10.1111/tra.12342.

No abstract available.

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Kee AJ, Yang L, Lucas CA, et al. An Actin Filament Population Defined by the Tropomyosin Tpm3.1 Regulates Glucose Uptake. Traffic. 2016;17(1):80-1doi: 10.1111/tra.12342.
Kee, A. J., Yang, L., Lucas, C. A., Greenberg, M. J., Martel, N., Leong, G. M., Hughes, W. E., Cooney, G. J., James, D. E., Ostap, E. M., Han, W., Gunning, P. W., & Hardeman, E. C. (2016). An Actin Filament Population Defined by the Tropomyosin Tpm3.1 Regulates Glucose Uptake. Traffic (Copenhagen, Denmark), 17(1), 80-1. https://doi.org/10.1111/tra.12342
Kee, Anthony J, et al. "An Actin Filament Population Defined by the Tropomyosin Tpm3.1 Regulates Glucose Uptake." Traffic (Copenhagen, Denmark) vol. 17,1 (2016): 80-1. doi: https://doi.org/10.1111/tra.12342
Kee AJ, Yang L, Lucas CA, Greenberg MJ, Martel N, Leong GM, Hughes WE, Cooney GJ, James DE, Ostap EM, Han W, Gunning PW, Hardeman EC. An Actin Filament Population Defined by the Tropomyosin Tpm3.1 Regulates Glucose Uptake. Traffic. 2016 Jan;17(1):80-1. doi: 10.1111/tra.12342. PMID: 26688443; PMCID: PMC6886021.
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Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling.

Frontiers in physiology

Sewanan LR, Moore JR, Lehman W, Campbell SG.
PMID: 27833562
Front Physiol. 2016 Oct 26;7:473. doi: 10.3389/fphys.2016.00473. eCollection 2016.

Point mutations to the human gene TPM1 have been implicated in the development of both hypertrophic and dilated cardiomyopathies. Such observations have led to studies investigating the link between single residue changes and the biophysical behavior of the tropomyosin...

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Sewanan LR, Moore JR, Lehman W, et al. Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling. Front Physiol. 2016;7:473doi: 10.3389/fphys.2016.00473.
Sewanan, L. R., Moore, J. R., Lehman, W., & Campbell, S. G. (2016). Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling. Frontiers in physiology, 7473. https://doi.org/10.3389/fphys.2016.00473
Sewanan, Lorenzo R, et al. "Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling." Frontiers in physiology vol. 7 (2016): 473. doi: https://doi.org/10.3389/fphys.2016.00473
Sewanan LR, Moore JR, Lehman W, Campbell SG. Predicting Effects of Tropomyosin Mutations on Cardiac Muscle Contraction through Myofilament Modeling. Front Physiol. 2016 Oct 26;7:473. doi: 10.3389/fphys.2016.00473. eCollection 2016. PMID: 27833562; PMCID: PMC5081029.
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Myristic acid hitchhiking on sigma-1 receptor to fend off neurodegeneration.

Receptors & clinical investigation

Ciesielski J, Su TP, Tsai SY.
PMID: 27077074
Receptors Clin Investig. 2016;3(1). doi: 10.14800/rci.1114.

Neurodegenerative diseases are linked to tauopathy as a result of cyclin dependent kinase 5 (cdk5) binding to its p25 activator instead of its p35 activator and becoming over-activated. The overactive complex stimulates the hyperphosphorylation of tau proteins, leading to...

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Ciesielski J, Su TP, Tsai SY. Myristic acid hitchhiking on sigma-1 receptor to fend off neurodegeneration. Receptors Clin Investig. 2016;3(1)doi: 10.14800/rci.1114.
Ciesielski, J., Su, T. P., & Tsai, S. Y. (2016). Myristic acid hitchhiking on sigma-1 receptor to fend off neurodegeneration. Receptors & clinical investigation, 3(1), . https://doi.org/10.14800/rci.1114
Ciesielski, Jenna, et al. "Myristic acid hitchhiking on sigma-1 receptor to fend off neurodegeneration." Receptors & clinical investigation vol. 3,1 (2016). doi: https://doi.org/10.14800/rci.1114
Ciesielski J, Su TP, Tsai SY. Myristic acid hitchhiking on sigma-1 receptor to fend off neurodegeneration. Receptors Clin Investig. 2016;3(1). doi: 10.14800/rci.1114. PMID: 27077074; PMCID: PMC4827442.
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Myogenesis in the sea urchin embryo: the molecular fingerprint of the myoblast precursors.

EvoDevo

Andrikou C, Iovene E, Rizzo F, Oliveri P, Arnone MI.
PMID: 24295205
Evodevo. 2013 Dec 02;4(1):33. doi: 10.1186/2041-9139-4-33.

BACKGROUND: In sea urchin larvae the circumesophageal fibers form a prominent muscle system of mesodermal origin. Although the morphology and later development of this muscle system has been well-described, little is known about the molecular signature of these cells...

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Andrikou C, Iovene E, Rizzo F, et al. Myogenesis in the sea urchin embryo: the molecular fingerprint of the myoblast precursors. Evodevo. 2013;4(1):33doi: 10.1186/2041-9139-4-33.
Andrikou, C., Iovene, E., Rizzo, F., Oliveri, P., & Arnone, M. I. (2013). Myogenesis in the sea urchin embryo: the molecular fingerprint of the myoblast precursors. EvoDevo, 4(1), 33. https://doi.org/10.1186/2041-9139-4-33
Andrikou, Carmen, et al. "Myogenesis in the sea urchin embryo: the molecular fingerprint of the myoblast precursors." EvoDevo vol. 4,1 (2013): 33. doi: https://doi.org/10.1186/2041-9139-4-33
Andrikou C, Iovene E, Rizzo F, Oliveri P, Arnone MI. Myogenesis in the sea urchin embryo: the molecular fingerprint of the myoblast precursors. Evodevo. 2013 Dec 02;4(1):33. doi: 10.1186/2041-9139-4-33. PMID: 24295205; PMCID: PMC4175510.
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Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts.

Regenerative medicine research

Zajdel RW, McLean MD, Dube S, Dube DK.
PMID: 25984327
Regen Med Res. 2013 Dec 04;1(1):8. doi: 10.1186/2050-490X-1-8. eCollection 2013 Dec.

The anatomy, function and embryonic development of the heart have been of interest to clinicians and researchers alike for centuries. A beating heart is one of the key criteria in defining life or death in humans. An understanding of...

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Zajdel RW, McLean MD, Dube S, et al. Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts. Regen Med Res. 2013;1(1):8doi: 10.1186/2050-490X-1-8.
Zajdel, R. W., McLean, M. D., Dube, S., & Dube, D. K. (2013). Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts. Regenerative medicine research, 1(1), 8. https://doi.org/10.1186/2050-490X-1-8
Zajdel, Robert W, et al. "Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts." Regenerative medicine research vol. 1,1 (2013): 8. doi: https://doi.org/10.1186/2050-490X-1-8
Zajdel RW, McLean MD, Dube S, Dube DK. Expression of tropomyosin in relation to myofibrillogenesis in axolotl hearts. Regen Med Res. 2013 Dec 04;1(1):8. doi: 10.1186/2050-490X-1-8. eCollection 2013 Dec. PMID: 25984327; PMCID: PMC4431041.
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Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model.

Frontiers in physiology

Woodward M, Previs MJ, Mader TJ, Debold EP.
PMID: 26236240
Front Physiol. 2015 Jul 16;6:199. doi: 10.3389/fphys.2015.00199. eCollection 2015.

Cardiac arrest is a prevalent condition with a poor prognosis, attributable in part to persistent myocardial dysfunction following resuscitation. The molecular basis of this dysfunction remains unclear. We induced cardiac arrest in a porcine model of acute sudden death...

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Woodward M, Previs MJ, Mader TJ, et al. Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model. Front Physiol. 2015;6:199doi: 10.3389/fphys.2015.00199.
Woodward, M., Previs, M. J., Mader, T. J., & Debold, E. P. (2015). Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model. Frontiers in physiology, 6199. https://doi.org/10.3389/fphys.2015.00199
Woodward, Mike, et al. "Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model." Frontiers in physiology vol. 6 (2015): 199. doi: https://doi.org/10.3389/fphys.2015.00199
Woodward M, Previs MJ, Mader TJ, Debold EP. Modifications of myofilament protein phosphorylation and function in response to cardiac arrest induced in a swine model. Front Physiol. 2015 Jul 16;6:199. doi: 10.3389/fphys.2015.00199. eCollection 2015. PMID: 26236240; PMCID: PMC4503891.
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Systems Pharmacology of the NGF Signaling Through p75 and TrkA Receptors.

CPT: pharmacometrics & systems pharmacology

Toni T, Dua P, van der Graaf PH.
PMID: 25470184
CPT Pharmacometrics Syst Pharmacol. 2014 Dec 03;3:e150. doi: 10.1038/psp.2014.48.

The nerve growth factor (NGF) pathway has been shown to play a key role in pain treatment. Recently, a systems pharmacology model has been proposed that can aid in the identification and validation of drug targets in the NGF...

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Toni T, Dua P, van der Graaf PH. Systems Pharmacology of the NGF Signaling Through p75 and TrkA Receptors. CPT Pharmacometrics Syst Pharmacol. 2014;3:e150doi: 10.1038/psp.2014.48.
Toni, T., Dua, P., & van der Graaf, P. H. (2014). Systems Pharmacology of the NGF Signaling Through p75 and TrkA Receptors. CPT: pharmacometrics & systems pharmacology, 3e150. https://doi.org/10.1038/psp.2014.48
Toni, T, et al. "Systems Pharmacology of the NGF Signaling Through p75 and TrkA Receptors." CPT: pharmacometrics & systems pharmacology vol. 3 (2014): e150. doi: https://doi.org/10.1038/psp.2014.48
Toni T, Dua P, van der Graaf PH. Systems Pharmacology of the NGF Signaling Through p75 and TrkA Receptors. CPT Pharmacometrics Syst Pharmacol. 2014 Dec 03;3:e150. doi: 10.1038/psp.2014.48. PMID: 25470184; PMCID: PMC4288001.
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Molecular characterization of myoplasmin-C1: a cytoskeletal component localized in the myoplasm of the ascidian egg.

Development genes and evolution

Nishikata T, Wada M.
PMID: 24173399
Dev Genes Evol. 1996 Jun;206(1):72-9. doi: 10.1007/s004270050032.

Myoplasmin-C1 is a polypeptide detected by a monoclonal antibody, which is localized in the myoplasm of ascidian eggs. Since microinjection of the antibody blocks larval muscle development, myoplasmin-C1 may play a role in muscle cell differentiation (Nishikata et al....

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Nishikata T, Wada M. Molecular characterization of myoplasmin-C1: a cytoskeletal component localized in the myoplasm of the ascidian egg. Dev Genes Evol. 1996;206(1):72-9doi: 10.1007/s004270050032.
Nishikata, T., & Wada, M. (1996). Molecular characterization of myoplasmin-C1: a cytoskeletal component localized in the myoplasm of the ascidian egg. Development genes and evolution, 206(1), 72-9. https://doi.org/10.1007/s004270050032
Nishikata, T, and Wada, M. "Molecular characterization of myoplasmin-C1: a cytoskeletal component localized in the myoplasm of the ascidian egg." Development genes and evolution vol. 206,1 (1996): 72-9. doi: https://doi.org/10.1007/s004270050032
Nishikata T, Wada M. Molecular characterization of myoplasmin-C1: a cytoskeletal component localized in the myoplasm of the ascidian egg. Dev Genes Evol. 1996 Jun;206(1):72-9. doi: 10.1007/s004270050032. PMID: 24173399.
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(R)-2-Phenylpyrrolidine Substituted Imidazopyridazines: A New Class of Potent and Selective Pan-TRK Inhibitors.

ACS medicinal chemistry letters

Choi HS, Rucker PV, Wang Z, Fan Y, Albaugh P, Chopiuk G, Gessier F, Sun F, Adrian F, Liu G, Hood T, Li N, Jia Y, Che J, McCormack S, Li A, Li J, Steffy A, Culazzo A, Tompkins C, Phung V, Kreusch A, Lu M, Hu B, Chaudhary A, Prashad M, Tuntland T, Liu B, Harris J, Seidel HM, Loren J, Molteni V.
PMID: 26005534
ACS Med Chem Lett. 2015 Mar 16;6(5):562-7. doi: 10.1021/acsmedchemlett.5b00050. eCollection 2015 May 14.

Deregulated kinase activities of tropomyosin receptor kinase (TRK) family members have been shown to be associated with tumorigenesis and poor prognosis in a variety of cancer types. In particular, several chromosomal rearrangements involving TRKA have been reported in colorectal,...

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Choi HS, Rucker PV, Wang Z, et al. (R)-2-Phenylpyrrolidine Substituted Imidazopyridazines: A New Class of Potent and Selective Pan-TRK Inhibitors. ACS Med Chem Lett. 2015;6(5):562-7doi: 10.1021/acsmedchemlett.5b00050.
Choi, H. S., Rucker, P. V., Wang, Z., Fan, Y., Albaugh, P., Chopiuk, G., Gessier, F., Sun, F., Adrian, F., Liu, G., Hood, T., Li, N., Jia, Y., Che, J., McCormack, S., Li, A., Li, J., Steffy, A., Culazzo, A., Tompkins, C., Phung, V., Kreusch, A., Lu, M., Hu, B., Chaudhary, A., Prashad, M., Tuntland, T., Liu, B., Harris, J., Seidel, H. M., Loren, J., & Molteni, V. (2015). (R)-2-Phenylpyrrolidine Substituted Imidazopyridazines: A New Class of Potent and Selective Pan-TRK Inhibitors. ACS medicinal chemistry letters, 6(5), 562-7. https://doi.org/10.1021/acsmedchemlett.5b00050
Choi, Ha-Soon, et al. "(R)-2-Phenylpyrrolidine Substituted Imidazopyridazines: A New Class of Potent and Selective Pan-TRK Inhibitors." ACS medicinal chemistry letters vol. 6,5 (2015): 562-7. doi: https://doi.org/10.1021/acsmedchemlett.5b00050
Choi HS, Rucker PV, Wang Z, Fan Y, Albaugh P, Chopiuk G, Gessier F, Sun F, Adrian F, Liu G, Hood T, Li N, Jia Y, Che J, McCormack S, Li A, Li J, Steffy A, Culazzo A, Tompkins C, Phung V, Kreusch A, Lu M, Hu B, Chaudhary A, Prashad M, Tuntland T, Liu B, Harris J, Seidel HM, Loren J, Molteni V. (R)-2-Phenylpyrrolidine Substituted Imidazopyridazines: A New Class of Potent and Selective Pan-TRK Inhibitors. ACS Med Chem Lett. 2015 Mar 16;6(5):562-7. doi: 10.1021/acsmedchemlett.5b00050. eCollection 2015 May 14. PMID: 26005534; PMCID: PMC4434478.
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NTRK2 expression levels are reduced in laser captured pyramidal neurons from the anterior cingulate cortex in males with autism spectrum disorder.

Molecular autism

Chandley MJ, Crawford JD, Szebeni A, Szebeni K, Ordway GA.
PMID: 26000162
Mol Autism. 2015 May 16;6:28. doi: 10.1186/s13229-015-0023-2. eCollection 2015.

BACKGROUND: The anterior cingulate cortex (ACC) is a brain area involved in modulating behavior associated with social interaction, disruption of which is a core feature of autism spectrum disorder (ASD). Functional brain imaging studies demonstrate abnormalities of the ACC...

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Chandley MJ, Crawford JD, Szebeni A, et al. NTRK2 expression levels are reduced in laser captured pyramidal neurons from the anterior cingulate cortex in males with autism spectrum disorder. Mol Autism. 2015;6:28doi: 10.1186/s13229-015-0023-2.
Chandley, M. J., Crawford, J. D., Szebeni, A., Szebeni, K., & Ordway, G. A. (2015). NTRK2 expression levels are reduced in laser captured pyramidal neurons from the anterior cingulate cortex in males with autism spectrum disorder. Molecular autism, 628. https://doi.org/10.1186/s13229-015-0023-2
Chandley, Michelle J, et al. "NTRK2 expression levels are reduced in laser captured pyramidal neurons from the anterior cingulate cortex in males with autism spectrum disorder." Molecular autism vol. 6 (2015): 28. doi: https://doi.org/10.1186/s13229-015-0023-2
Chandley MJ, Crawford JD, Szebeni A, Szebeni K, Ordway GA. NTRK2 expression levels are reduced in laser captured pyramidal neurons from the anterior cingulate cortex in males with autism spectrum disorder. Mol Autism. 2015 May 16;6:28. doi: 10.1186/s13229-015-0023-2. eCollection 2015. PMID: 26000162; PMCID: PMC4440594.
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Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance.

Molecular metabolism

Ozek C, Zimmer DJ, De Jonghe BC, Kalb RG, Bence KK.
PMID: 26629410
Mol Metab. 2015 Aug 18;4(11):867-80. doi: 10.1016/j.molmet.2015.08.002. eCollection 2015 Nov.

OBJECTIVE: Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB), play a paramount role in the central regulation of energy balance. Despite the substantial body of genetic evidence implicating BDNF- or TrkB-deficiency in human obesity, the...

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Ozek C, Zimmer DJ, De Jonghe BC, et al. Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance. Mol Metab. 2015;4(11):867-80doi: 10.1016/j.molmet.2015.08.002.
Ozek, C., Zimmer, D. J., De Jonghe, B. C., Kalb, R. G., & Bence, K. K. (2015). Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance. Molecular metabolism, 4(11), 867-80. https://doi.org/10.1016/j.molmet.2015.08.002
Ozek, Ceren, et al. "Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance." Molecular metabolism vol. 4,11 (2015): 867-80. doi: https://doi.org/10.1016/j.molmet.2015.08.002
Ozek C, Zimmer DJ, De Jonghe BC, Kalb RG, Bence KK. Ablation of intact hypothalamic and/or hindbrain TrkB signaling leads to perturbations in energy balance. Mol Metab. 2015 Aug 18;4(11):867-80. doi: 10.1016/j.molmet.2015.08.002. eCollection 2015 Nov. PMID: 26629410; PMCID: PMC4632115.
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Trk Neurotrophin Receptor Activators.

Drug news & perspectives

Pollack SJ, Harper SJ.
PMID: 12677222
Drug News Perspect. 2002 Jun;15(5):268-277. doi: 10.1358/dnp.2002.15.5.840039.

The neurotrophins are a small group of proteins whose binding at the tropomyosin related kinase (Trk) and p75 neurotrophin receptor transmembrane receptors triggers a cascade of signaling events that give rise to neurotrophic responses in neuronal cells and in...

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Pollack SJ, Harper SJ. Trk Neurotrophin Receptor Activators. Drug News Perspect. 2002;15(5):268-277doi: 10.1358/dnp.2002.15.5.840039.
Pollack, S. J., & Harper, S. J. (2002). Trk Neurotrophin Receptor Activators. Drug news & perspectives, 15(5), 268-277. https://doi.org/10.1358/dnp.2002.15.5.840039
Pollack, Scott J., and Harper, Sarah J.. "Trk Neurotrophin Receptor Activators." Drug news & perspectives vol. 15,5 (2002): 268-277. doi: https://doi.org/10.1358/dnp.2002.15.5.840039
Pollack SJ, Harper SJ. Trk Neurotrophin Receptor Activators. Drug News Perspect. 2002 Jun;15(5):268-277. doi: 10.1358/dnp.2002.15.5.840039. PMID: 12677222.
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Showing 1 to 12 of 599 entries