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Showing 1 to 12 of 37 entries
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Activity of D-amino acid oxidase is widespread in the human central nervous system.

Frontiers in synaptic neuroscience

Sasabe J, Suzuki M, Imanishi N, Aiso S.
PMID: 24959138
Front Synaptic Neurosci. 2014 Jun 10;6:14. doi: 10.3389/fnsyn.2014.00014. eCollection 2014.

It has been proposed that D-amino acid oxidase (DAO) plays an essential role in degrading D-serine, an endogenous coagonist of N-methyl-D-aspartate (NMDA) glutamate receptors. DAO shows genetic association with amyotrophic lateral sclerosis (ALS) and schizophrenia, in whose pathophysiology aberrant...

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Sasabe J, Suzuki M, Imanishi N, et al. Activity of D-amino acid oxidase is widespread in the human central nervous system. Front Synaptic Neurosci. 2014;6:14doi: 10.3389/fnsyn.2014.00014.
Sasabe, J., Suzuki, M., Imanishi, N., & Aiso, S. (2014). Activity of D-amino acid oxidase is widespread in the human central nervous system. Frontiers in synaptic neuroscience, 614. https://doi.org/10.3389/fnsyn.2014.00014
Sasabe, Jumpei, et al. "Activity of D-amino acid oxidase is widespread in the human central nervous system." Frontiers in synaptic neuroscience vol. 6 (2014): 14. doi: https://doi.org/10.3389/fnsyn.2014.00014
Sasabe J, Suzuki M, Imanishi N, Aiso S. Activity of D-amino acid oxidase is widespread in the human central nervous system. Front Synaptic Neurosci. 2014 Jun 10;6:14. doi: 10.3389/fnsyn.2014.00014. eCollection 2014. PMID: 24959138; PMCID: PMC4050652.
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Potential therapeutic role of glutamate transporter 1 for the treatment of alcohol dependence.

OA alcohol

Sari Y.
PMID: 24409344
OA Alcohol. 2013;1(1):6. doi: 10.13172/2053-0285-1-1-574.

INTRODUCTION: Evidence has demonstrated that deficits in glutamate transmission impair neurocircuits involved in drug abuse or drug-seeking behaviour and affect many aspects of neuroplasticity associated with alcohol and drug addiction. Alcohol-seeking behaviour is promoted by increased glutamate transmission in...

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Sari Y. Potential therapeutic role of glutamate transporter 1 for the treatment of alcohol dependence. OA Alcohol. 2013;1(1):6doi: 10.13172/2053-0285-1-1-574.
Sari, Y. (2013). Potential therapeutic role of glutamate transporter 1 for the treatment of alcohol dependence. OA alcohol, 1(1), 6. https://doi.org/10.13172/2053-0285-1-1-574
Sari, Y. "Potential therapeutic role of glutamate transporter 1 for the treatment of alcohol dependence." OA alcohol vol. 1,1 (2013): 6. doi: https://doi.org/10.13172/2053-0285-1-1-574
Sari Y. Potential therapeutic role of glutamate transporter 1 for the treatment of alcohol dependence. OA Alcohol. 2013;1(1):6. doi: 10.13172/2053-0285-1-1-574. PMID: 24409344; PMCID: PMC3883353.
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Differential .

Frontiers in cellular neuroscience

Jia YF, Choi Y, Ayers-Ringler JR, Biernacka JM, Geske JR, Lindberg DR, McElroy SL, Frye MA, Choi DS, Veldic M.
PMID: 28785205
Front Cell Neurosci. 2017 Jul 21;11:217. doi: 10.3389/fncel.2017.00217. eCollection 2017.

While downregulation of excitatory amino acid transporter 2 (EAAT2), the main transporter removing glutamate from the synapse, has been recognized in bipolar disorder (BD), the underlying mechanisms of downregulation have not been elucidated. BD is influenced by environmental factors,...

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Jia YF, Choi Y, Ayers-Ringler JR, et al. Differential . Front Cell Neurosci. 2017;11:217doi: 10.3389/fncel.2017.00217.
Jia, Y. F., Choi, Y., Ayers-Ringler, J. R., Biernacka, J. M., Geske, J. R., Lindberg, D. R., McElroy, S. L., Frye, M. A., Choi, D. S., & Veldic, M. (2017). Differential . Frontiers in cellular neuroscience, 11217. https://doi.org/10.3389/fncel.2017.00217
Jia, Yun-Fang, et al. "Differential ." Frontiers in cellular neuroscience vol. 11 (2017): 217. doi: https://doi.org/10.3389/fncel.2017.00217
Jia YF, Choi Y, Ayers-Ringler JR, Biernacka JM, Geske JR, Lindberg DR, McElroy SL, Frye MA, Choi DS, Veldic M. Differential . Front Cell Neurosci. 2017 Jul 21;11:217. doi: 10.3389/fncel.2017.00217. eCollection 2017. PMID: 28785205; PMCID: PMC5520464.
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Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population.

Neuropsychiatric disease and treatment

Merk W, Kucia K, Mędrala T, Kowalczyk M, Owczarek A, Kowalski J.
PMID: 31118638
Neuropsychiatr Dis Treat. 2019 Apr 24;15:989-1000. doi: 10.2147/NDT.S194924. eCollection 2019.

No abstract available.

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Merk W, Kucia K, Mędrala T, et al. Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population. Neuropsychiatr Dis Treat. 2019;15:989-1000doi: 10.2147/NDT.S194924.
Merk, W., Kucia, K., Mędrala, T., Kowalczyk, M., Owczarek, A., & Kowalski, J. (2019). Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population. Neuropsychiatric disease and treatment, 15989-1000. https://doi.org/10.2147/NDT.S194924
Merk, Wojciech, et al. "Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population." Neuropsychiatric disease and treatment vol. 15 (2019): 989-1000. doi: https://doi.org/10.2147/NDT.S194924
Merk W, Kucia K, Mędrala T, Kowalczyk M, Owczarek A, Kowalski J. Association study of the excitatory amino acid transporter 2 (EAAT2) and glycine transporter 1 (GlyT1) gene polymorphism with schizophrenia in a Polish population. Neuropsychiatr Dis Treat. 2019 Apr 24;15:989-1000. doi: 10.2147/NDT.S194924. eCollection 2019. PMID: 31118638; PMCID: PMC6499478.
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Glutamate Transport and Preterm Brain Injury.

Frontiers in physiology

Pregnolato S, Chakkarapani E, Isles AR, Luyt K.
PMID: 31068830
Front Physiol. 2019 Apr 24;10:417. doi: 10.3389/fphys.2019.00417. eCollection 2019.

Preterm birth complications are the leading cause of child death worldwide and a top global health priority. Among the survivors, the risk of life-long disabilities is high, including cerebral palsy and impairment of movement, cognition, and behavior. Understanding the...

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Pregnolato S, Chakkarapani E, Isles AR, et al. Glutamate Transport and Preterm Brain Injury. Front Physiol. 2019;10:417doi: 10.3389/fphys.2019.00417.
Pregnolato, S., Chakkarapani, E., Isles, A. R., & Luyt, K. (2019). Glutamate Transport and Preterm Brain Injury. Frontiers in physiology, 10417. https://doi.org/10.3389/fphys.2019.00417
Pregnolato, Silvia, et al. "Glutamate Transport and Preterm Brain Injury." Frontiers in physiology vol. 10 (2019): 417. doi: https://doi.org/10.3389/fphys.2019.00417
Pregnolato S, Chakkarapani E, Isles AR, Luyt K. Glutamate Transport and Preterm Brain Injury. Front Physiol. 2019 Apr 24;10:417. doi: 10.3389/fphys.2019.00417. eCollection 2019. PMID: 31068830; PMCID: PMC6491644.
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Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity.

The Journal of biological chemistry

Pajarillo E, Digman A, Nyarko-Danquah I, Son DS, Soliman KFA, Aschner M, Lee E.
PMID: 34756885
J Biol Chem. 2021 Oct 29;297(6):101372. doi: 10.1016/j.jbc.2021.101372. Epub 2021 Oct 29.

Chronic exposure to high levels of manganese (Mn) leads to manganism, a neurological disorder with similar symptoms to those inherent to Parkinson's disease. However, the underlying mechanisms of this pathological condition have yet to be established. Since the human...

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Pajarillo E, Digman A, Nyarko-Danquah I, et al. Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. J Biol Chem. 2021;297(6):101372doi: 10.1016/j.jbc.2021.101372.
Pajarillo, E., Digman, A., Nyarko-Danquah, I., Son, D. S., Soliman, K. F. A., Aschner, M., & Lee, E. (2021). Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. The Journal of biological chemistry, 297(6), 101372. https://doi.org/10.1016/j.jbc.2021.101372
Pajarillo, Edward, et al. "Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity." The Journal of biological chemistry vol. 297,6 (2021): 101372. doi: https://doi.org/10.1016/j.jbc.2021.101372
Pajarillo E, Digman A, Nyarko-Danquah I, Son DS, Soliman KFA, Aschner M, Lee E. Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. J Biol Chem. 2021 Oct 29;297(6):101372. doi: 10.1016/j.jbc.2021.101372. Epub 2021 Oct 29. PMID: 34756885; PMCID: PMC8626589.
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Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders.

Frontiers in neurology

Cisneros IE, Ghorpade A, Borgmann K.
PMID: 33324330
Front Neurol. 2020 Nov 25;11:593146. doi: 10.3389/fneur.2020.593146. eCollection 2020.

Methamphetamine (METH) use, referred to as methamphetamine use disorder (MUD), results in neurocognitive decline, a characteristic shared with HIV-associated neurocognitive disorders (HAND). MUD exacerbates HAND partly through glutamate dysregulation. Astrocyte excitatory amino acid transporter (EAAT)-2 is responsible for >90%...

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Cisneros IE, Ghorpade A, Borgmann K. Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders. Front Neurol. 2020;11:593146doi: 10.3389/fneur.2020.593146.
Cisneros, I. E., Ghorpade, A., & Borgmann, K. (2020). Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders. Frontiers in neurology, 11593146. https://doi.org/10.3389/fneur.2020.593146
Cisneros, Irma E, et al. "Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders." Frontiers in neurology vol. 11 (2020): 593146. doi: https://doi.org/10.3389/fneur.2020.593146
Cisneros IE, Ghorpade A, Borgmann K. Methamphetamine Activates Trace Amine Associated Receptor 1 to Regulate Astrocyte Excitatory Amino Acid Transporter-2 via Differential CREB Phosphorylation During HIV-Associated Neurocognitive Disorders. Front Neurol. 2020 Nov 25;11:593146. doi: 10.3389/fneur.2020.593146. eCollection 2020. PMID: 33324330; PMCID: PMC7724046.
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5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model.

Frontiers in cellular neuroscience

Zhou X, Li G, Zhang S, Wu J.
PMID: 31130845
Front Cell Neurosci. 2019 May 03;13:167. doi: 10.3389/fncel.2019.00167. eCollection 2019.

Serotonin receptors are potential neuroprotective agents in degenerative diseases of the central nervous system. The protective effects of serotonin receptor (5-HT1A) agonists on the survival and function of retinal ganglion cells (RGCs) by regulating the release of the presynaptic...

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Zhou X, Li G, Zhang S, et al. 5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model. Front Cell Neurosci. 2019;13:167doi: 10.3389/fncel.2019.00167.
Zhou, X., Li, G., Zhang, S., & Wu, J. (2019). 5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model. Frontiers in cellular neuroscience, 13167. https://doi.org/10.3389/fncel.2019.00167
Zhou, Xujiao, et al. "5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model." Frontiers in cellular neuroscience vol. 13 (2019): 167. doi: https://doi.org/10.3389/fncel.2019.00167
Zhou X, Li G, Zhang S, Wu J. 5-HT1A Receptor Agonist Promotes Retinal Ganglion Cell Function by Inhibiting OFF-Type Presynaptic Glutamatergic Activity in a Chronic Glaucoma Model. Front Cell Neurosci. 2019 May 03;13:167. doi: 10.3389/fncel.2019.00167. eCollection 2019. PMID: 31130845; PMCID: PMC6509153.
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Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity.

The Journal of biological chemistry

Pajarillo E, Digman A, Nyarko-Danquah I, Son DS, Soliman KFA, Aschner M, Lee E.
PMID: 34756885
J Biol Chem. 2021 Dec;297(6):101372. doi: 10.1016/j.jbc.2021.101372. Epub 2021 Oct 29.

Chronic exposure to high levels of manganese (Mn) leads to manganism, a neurological disorder with similar symptoms to those inherent to Parkinson's disease. However, the underlying mechanisms of this pathological condition have yet to be established. Since the human...

Cite
Pajarillo E, Digman A, Nyarko-Danquah I, et al. Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. J Biol Chem. 2021;297(6):101372doi: 10.1016/j.jbc.2021.101372.
Pajarillo, E., Digman, A., Nyarko-Danquah, I., Son, D. S., Soliman, K. F. A., Aschner, M., & Lee, E. (2021). Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. The Journal of biological chemistry, 297(6), 101372. https://doi.org/10.1016/j.jbc.2021.101372
Pajarillo, Edward, et al. "Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity." The Journal of biological chemistry vol. 297,6 (2021): 101372. doi: https://doi.org/10.1016/j.jbc.2021.101372
Pajarillo E, Digman A, Nyarko-Danquah I, Son DS, Soliman KFA, Aschner M, Lee E. Astrocytic transcription factor REST upregulates glutamate transporter EAAT2, protecting dopaminergic neurons from manganese-induced excitotoxicity. J Biol Chem. 2021 Dec;297(6):101372. doi: 10.1016/j.jbc.2021.101372. Epub 2021 Oct 29. PMID: 34756885; PMCID: PMC8626589.
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Chandamarutha Chenduram, an Indian traditional Siddha preparation attenuated the neuronal degeneration in ischemic mice through ameliorating cytokines and oxy-radicals mediated EAAT-2 dysfunction.

Journal of ethnopharmacology

Justin A, Thomas P, Narasimha Rao G, Jeyabalan JB, Narendar C, Ponnusankar S, Selvaraj J, R H.
PMID: 34774684
J Ethnopharmacol. 2022 Feb 10;284:114827. doi: 10.1016/j.jep.2021.114827. Epub 2021 Nov 10.

ETHNOPHARMACOLOGICAL RELEVANCE: Chandamarutha Chenduram (CC), an Indian traditional Siddha preparation officially recorded in the Siddha formulary of India and its composition are widely used in the Siddha practice of neurological disorders like stroke/paralysis in India. However, the scientific validation...

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Justin A, Thomas P, Narasimha Rao G, et al. Chandamarutha Chenduram, an Indian traditional Siddha preparation attenuated the neuronal degeneration in ischemic mice through ameliorating cytokines and oxy-radicals mediated EAAT-2 dysfunction. J Ethnopharmacol. 2021;284:114827doi: 10.1016/j.jep.2021.114827.
Justin, A., Thomas, P., Narasimha Rao, G., Jeyabalan, J. B., Narendar, C., Ponnusankar, S., Selvaraj, J., & R, H. (2022). Chandamarutha Chenduram, an Indian traditional Siddha preparation attenuated the neuronal degeneration in ischemic mice through ameliorating cytokines and oxy-radicals mediated EAAT-2 dysfunction. Journal of ethnopharmacology, 284114827. https://doi.org/10.1016/j.jep.2021.114827
Justin, Antony, et al. "Chandamarutha Chenduram, an Indian traditional Siddha preparation attenuated the neuronal degeneration in ischemic mice through ameliorating cytokines and oxy-radicals mediated EAAT-2 dysfunction." Journal of ethnopharmacology vol. 284 (2022): 114827. doi: https://doi.org/10.1016/j.jep.2021.114827
Justin A, Thomas P, Narasimha Rao G, Jeyabalan JB, Narendar C, Ponnusankar S, Selvaraj J, R H. Chandamarutha Chenduram, an Indian traditional Siddha preparation attenuated the neuronal degeneration in ischemic mice through ameliorating cytokines and oxy-radicals mediated EAAT-2 dysfunction. J Ethnopharmacol. 2022 Feb 10;284:114827. doi: 10.1016/j.jep.2021.114827. Epub 2021 Nov 10. PMID: 34774684.
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No evidence for genetic association between glutamate transporter EAAT2 and Devic's neuromyelitis optica in caucasians and afro-caribbeans.

Multiple sclerosis and related disorders

Hanoux V, Coulbault L, Derache N, Cabre P, De Seze J, Marignier R, Rudolf G, Emmanuelle Dugué A, Allouche S, Defer G.
PMID: 25877978
Mult Scler Relat Disord. 2014 Jan;3(1):89-93. doi: 10.1016/j.msard.2013.06.012. Epub 2013 Jul 18.

Devic's neuromyelitis optica (NMO) is a severe inflammatory and autoimmune disease producing demyelinating lesions. Recent data suggest that a complex genetic component could be involved. While impairment of glutamate homeostasis has emerged as a contributing etiological factor in NMO,...

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Hanoux V, Coulbault L, Derache N, et al. No evidence for genetic association between glutamate transporter EAAT2 and Devic's neuromyelitis optica in caucasians and afro-caribbeans. Mult Scler Relat Disord. 2013;3(1):89-93doi: 10.1016/j.msard.2013.06.012.
Hanoux, V., Coulbault, L., Derache, N., Cabre, P., De Seze, J., Marignier, R., Rudolf, G., Emmanuelle Dugué, A., Allouche, S., Defer, G. (2014). No evidence for genetic association between glutamate transporter EAAT2 and Devic's neuromyelitis optica in caucasians and afro-caribbeans. Multiple sclerosis and related disorders, 3(1), 89-93. https://doi.org/10.1016/j.msard.2013.06.012
Hanoux, Vincent, et al. "No evidence for genetic association between glutamate transporter EAAT2 and Devic's neuromyelitis optica in caucasians and afro-caribbeans." Multiple sclerosis and related disorders vol. 3,1 (2014): 89-93. doi: https://doi.org/10.1016/j.msard.2013.06.012
Hanoux V, Coulbault L, Derache N, Cabre P, De Seze J, Marignier R, Rudolf G, Emmanuelle Dugué A, Allouche S, Defer G. No evidence for genetic association between glutamate transporter EAAT2 and Devic's neuromyelitis optica in caucasians and afro-caribbeans. Mult Scler Relat Disord. 2014 Jan;3(1):89-93. doi: 10.1016/j.msard.2013.06.012. Epub 2013 Jul 18. PMID: 25877978.
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Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes.

Toxicology letters

Rizor A, Pajarillo E, Son DS, Aschner M, Lee E.
PMID: 34800614
Toxicol Lett. 2022 Feb 01;355:41-46. doi: 10.1016/j.toxlet.2021.11.007. Epub 2021 Nov 17.

Impairment of the astrocytic glutamate transporter excitatory amino acid transporter 2 (EAAT2) is associated with neurological disorders such as Parkinson's disease (PD), Alzheimer's disease (AD), and manganism, a neurological disorder caused by overexposure to manganese (Mn) which shares the...

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Rizor A, Pajarillo E, Son DS, et al. Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes. Toxicol Lett. 2021;355:41-46doi: 10.1016/j.toxlet.2021.11.007.
Rizor, A., Pajarillo, E., Son, D. S., Aschner, M., & Lee, E. (2022). Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes. Toxicology letters, 35541-46. https://doi.org/10.1016/j.toxlet.2021.11.007
Rizor, Asha, et al. "Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes." Toxicology letters vol. 355 (2022): 41-46. doi: https://doi.org/10.1016/j.toxlet.2021.11.007
Rizor A, Pajarillo E, Son DS, Aschner M, Lee E. Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes. Toxicol Lett. 2022 Feb 01;355:41-46. doi: 10.1016/j.toxlet.2021.11.007. Epub 2021 Nov 17. PMID: 34800614; PMCID: PMC8713424.
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Showing 1 to 12 of 37 entries