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Metabolic Aspects of Adenosine Functions in the Brain.

Frontiers in pharmacology

Garcia-Gil M, Camici M, Allegrini S, Pesi R, Tozzi MG.
PMID: 34054547
Front Pharmacol. 2021 May 14;12:672182. doi: 10.3389/fphar.2021.672182. eCollection 2021.

Adenosine, acting both through G-protein coupled adenosine receptors and intracellularly, plays a complex role in multiple physiological and pathophysiological processes by modulating neuronal plasticity, astrocytic activity, learning and memory, motor function, feeding, control of sleep and aging. Adenosine is...

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Garcia-Gil M, Camici M, Allegrini S, et al. Metabolic Aspects of Adenosine Functions in the Brain. Front Pharmacol. 2021;12:672182doi: 10.3389/fphar.2021.672182.
Garcia-Gil, M., Camici, M., Allegrini, S., Pesi, R., & Tozzi, M. G. (2021). Metabolic Aspects of Adenosine Functions in the Brain. Frontiers in pharmacology, 12672182. https://doi.org/10.3389/fphar.2021.672182
Garcia-Gil, Mercedes, et al. "Metabolic Aspects of Adenosine Functions in the Brain." Frontiers in pharmacology vol. 12 (2021): 672182. doi: https://doi.org/10.3389/fphar.2021.672182
Garcia-Gil M, Camici M, Allegrini S, Pesi R, Tozzi MG. Metabolic Aspects of Adenosine Functions in the Brain. Front Pharmacol. 2021 May 14;12:672182. doi: 10.3389/fphar.2021.672182. eCollection 2021. PMID: 34054547; PMCID: PMC8160517.
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Adenosine Kinase Expression Determines DNA Methylation in Cancer Cell Lines.

ACS pharmacology & translational science

Wahba AE, Fedele D, Gebril H, AlHarfoush E, Toti KS, Jacobson KA, Boison D.
PMID: 33860193
ACS Pharmacol Transl Sci. 2021 Feb 16;4(2):680-686. doi: 10.1021/acsptsci.1c00008. eCollection 2021 Apr 09.

DNA methylation has a major role in cancer, and its inhibitors are used therapeutically. DNA methylation depends on methyl group flux through the transmethylation pathway, which forms adenosine. We hypothesized that an adenosine kinase isoform with nuclear expression (ADK-L)...

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Wahba AE, Fedele D, Gebril H, et al. Adenosine Kinase Expression Determines DNA Methylation in Cancer Cell Lines. ACS Pharmacol Transl Sci. 2021;4(2):680-686doi: 10.1021/acsptsci.1c00008.
Wahba, A. E., Fedele, D., Gebril, H., AlHarfoush, E., Toti, K. S., Jacobson, K. A., & Boison, D. (2021). Adenosine Kinase Expression Determines DNA Methylation in Cancer Cell Lines. ACS pharmacology & translational science, 4(2), 680-686. https://doi.org/10.1021/acsptsci.1c00008
Wahba, Amir E, et al. "Adenosine Kinase Expression Determines DNA Methylation in Cancer Cell Lines." ACS pharmacology & translational science vol. 4,2 (2021): 680-686. doi: https://doi.org/10.1021/acsptsci.1c00008
Wahba AE, Fedele D, Gebril H, AlHarfoush E, Toti KS, Jacobson KA, Boison D. Adenosine Kinase Expression Determines DNA Methylation in Cancer Cell Lines. ACS Pharmacol Transl Sci. 2021 Feb 16;4(2):680-686. doi: 10.1021/acsptsci.1c00008. eCollection 2021 Apr 09. PMID: 33860193; PMCID: PMC8033756.
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Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury.

Brain communications

Gebril HM, Rose RM, Gesese R, Emond MP, Huo Y, Aronica E, Boison D.
PMID: 32322821
Brain Commun. 2020;2(1):fcaa017. doi: 10.1093/braincomms/fcaa017. Epub 2020 Feb 20.

Traumatic brain injury (TBI) is a major public health concern and remains a leading cause of disability and socio-economic burden. To date, there is no proven therapy that promotes brain repair following an injury to the brain. In this...

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Gebril HM, Rose RM, Gesese R, et al. Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury. Brain Commun. 2020;2(1):fcaa017doi: 10.1093/braincomms/fcaa017.
Gebril, H. M., Rose, R. M., Gesese, R., Emond, M. P., Huo, Y., Aronica, E., & Boison, D. (2020). Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury. Brain communications, 2(1), fcaa017. https://doi.org/10.1093/braincomms/fcaa017
Gebril, Hoda M, et al. "Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury." Brain communications vol. 2,1 (2020): fcaa017. doi: https://doi.org/10.1093/braincomms/fcaa017
Gebril HM, Rose RM, Gesese R, Emond MP, Huo Y, Aronica E, Boison D. Adenosine kinase inhibition promotes proliferation of neural stem cells after traumatic brain injury. Brain Commun. 2020;2(1):fcaa017. doi: 10.1093/braincomms/fcaa017. Epub 2020 Feb 20. PMID: 32322821; PMCID: PMC7158236.
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Clinical utility of methionine restriction in adenosine kinase deficiency.

JIMD reports

Almuhsen N, Guay SP, Lefrancois M, Gauvin C, Al Bahlani AQ, Ahmed N, Saint-Martin C, Gagnon T, Waters P, Braverman N, Buhas D.
PMID: 34485018
JIMD Rep. 2021 Jul 27;61(1):52-59. doi: 10.1002/jmd2.12238. eCollection 2021 Sep.

Adenosine kinase (ADK) deficiency is a rare autosomal recessive inborn error of metabolism involving the methionine and purine metabolic pathways. Prior reports show that most patients present in infancy with jaundice, hypotonia, developmental delay, and mild dysmorphic features. Characteristic...

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Almuhsen N, Guay SP, Lefrancois M, et al. Clinical utility of methionine restriction in adenosine kinase deficiency. JIMD Rep. 2021;61(1):52-59doi: 10.1002/jmd2.12238.
Almuhsen, N., Guay, S. P., Lefrancois, M., Gauvin, C., Al Bahlani, A. Q., Ahmed, N., Saint-Martin, C., Gagnon, T., Waters, P., Braverman, N., & Buhas, D. (2021). Clinical utility of methionine restriction in adenosine kinase deficiency. JIMD reports, 61(1), 52-59. https://doi.org/10.1002/jmd2.12238
Almuhsen, Najmah, et al. "Clinical utility of methionine restriction in adenosine kinase deficiency." JIMD reports vol. 61,1 (2021): 52-59. doi: https://doi.org/10.1002/jmd2.12238
Almuhsen N, Guay SP, Lefrancois M, Gauvin C, Al Bahlani AQ, Ahmed N, Saint-Martin C, Gagnon T, Waters P, Braverman N, Buhas D. Clinical utility of methionine restriction in adenosine kinase deficiency. JIMD Rep. 2021 Jul 27;61(1):52-59. doi: 10.1002/jmd2.12238. eCollection 2021 Sep. PMID: 34485018; PMCID: PMC8411109.
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Clearance of rapid adenosine release is regulated by nucleoside transporters and metabolism.

Pharmacology research & perspectives

Nguyen MD, Ross AE, Ryals M, Lee ST, Venton BJ.
PMID: 27022463
Pharmacol Res Perspect. 2015 Nov 16;3(6):e00189. doi: 10.1002/prp2.189. eCollection 2015 Dec.

Adenosine is a neuromodulator that regulates neurotransmission in the brain and central nervous system. Recently, spontaneous adenosine release that is cleared in 3-4 sec was discovered in mouse spinal cord slices and anesthetized rat brains. Here, we examined the...

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Nguyen MD, Ross AE, Ryals M, et al. Clearance of rapid adenosine release is regulated by nucleoside transporters and metabolism. Pharmacol Res Perspect. 2015;3(6):e00189doi: 10.1002/prp2.189.
Nguyen, M. D., Ross, A. E., Ryals, M., Lee, S. T., & Venton, B. J. (2015). Clearance of rapid adenosine release is regulated by nucleoside transporters and metabolism. Pharmacology research & perspectives, 3(6), e00189. https://doi.org/10.1002/prp2.189
Nguyen, Michael D, et al. "Clearance of rapid adenosine release is regulated by nucleoside transporters and metabolism." Pharmacology research & perspectives vol. 3,6 (2015): e00189. doi: https://doi.org/10.1002/prp2.189
Nguyen MD, Ross AE, Ryals M, Lee ST, Venton BJ. Clearance of rapid adenosine release is regulated by nucleoside transporters and metabolism. Pharmacol Res Perspect. 2015 Nov 16;3(6):e00189. doi: 10.1002/prp2.189. eCollection 2015 Dec. PMID: 27022463; PMCID: PMC4777247.
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Corrigendum: Adenosine Kinase Inhibition Protects against Cranial Radiation-Induced Cognitive Dysfunction.

Frontiers in molecular neuroscience

Acharya MM, Baulch JE, Lusardi TA, Allen BD, Chmielewski NN, Baddour AAD, Limoli CL, Boison D.
PMID: 28698714
Front Mol Neurosci. 2017 Jul 10;10:218. doi: 10.3389/fnmol.2017.00218. eCollection 2017.

[This corrects the article on p. 42 in vol. 9, PMID: 27375429.].

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Acharya MM, Baulch JE, Lusardi TA, et al. Corrigendum: Adenosine Kinase Inhibition Protects against Cranial Radiation-Induced Cognitive Dysfunction. Front Mol Neurosci. 2017;10:218doi: 10.3389/fnmol.2017.00218.
Acharya, M. M., Baulch, J. E., Lusardi, T. A., Allen, B. D., Chmielewski, N. N., Baddour, A. A. D., Limoli, C. L., & Boison, D. (2017). Corrigendum: Adenosine Kinase Inhibition Protects against Cranial Radiation-Induced Cognitive Dysfunction. Frontiers in molecular neuroscience, 10218. https://doi.org/10.3389/fnmol.2017.00218
Acharya, Munjal M, et al. "Corrigendum: Adenosine Kinase Inhibition Protects against Cranial Radiation-Induced Cognitive Dysfunction." Frontiers in molecular neuroscience vol. 10 (2017): 218. doi: https://doi.org/10.3389/fnmol.2017.00218
Acharya MM, Baulch JE, Lusardi TA, Allen BD, Chmielewski NN, Baddour AAD, Limoli CL, Boison D. Corrigendum: Adenosine Kinase Inhibition Protects against Cranial Radiation-Induced Cognitive Dysfunction. Front Mol Neurosci. 2017 Jul 10;10:218. doi: 10.3389/fnmol.2017.00218. eCollection 2017. PMID: 28698714; PMCID: PMC5502282.
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Adenosine kinase is a new therapeutic target to prevent ischemic neuronal death.

The open drug discovery journal

Boison D, Shen HY.
PMID: 24089624
Open Drug Discov J. 2010 Jan 01;2(3):108-118.

The brain has evolved several endogenous mechanisms to protect itself from the deleterious consequences of stroke. One of those endogenous neuroprotective systems is centered on the purine ribonucleoside adenosine, which exerts potent neuroprotective functions within the brain. One major...

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Boison D, Shen HY. Adenosine kinase is a new therapeutic target to prevent ischemic neuronal death. Open Drug Discov J. 2010;2(3):108-118
Boison, D., & Shen, H. Y. (2010). Adenosine kinase is a new therapeutic target to prevent ischemic neuronal death. The open drug discovery journal, 2(3), 108-118.
Boison, Detlev, and Shen, Hai-Ying. "Adenosine kinase is a new therapeutic target to prevent ischemic neuronal death." The open drug discovery journal vol. 2,3 (2010): 108-118.
Boison D, Shen HY. Adenosine kinase is a new therapeutic target to prevent ischemic neuronal death. Open Drug Discov J. 2010 Jan 01;2(3):108-118. PMID: 24089624; PMCID: PMC3786597.
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Phosphorylation of cytokinin by adenosine kinase from wheat germ.

Plant physiology

Chen CM, Eckert RL.
PMID: 16659870
Plant Physiol. 1977 Mar;59(3):443-7. doi: 10.1104/pp.59.3.443.

Adenosine kinase was partially purified from wheat germ. This enzyme preparation, which was devoid of adenine phosphoribosyltransferase and nearly free of adenosine deaminase but contained adenylate kinase, rapidly phosphorylated adenosine and a cytokinin, N(6)-(delta(2)-isopentenyl)adenosine. Electrophoretic analysis indicated that only...

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Chen CM, Eckert RL. Phosphorylation of cytokinin by adenosine kinase from wheat germ. Plant Physiol. 1977;59(3):443-7doi: 10.1104/pp.59.3.443.
Chen, C. M., & Eckert, R. L. (1977). Phosphorylation of cytokinin by adenosine kinase from wheat germ. Plant physiology, 59(3), 443-7. https://doi.org/10.1104/pp.59.3.443
Chen, C M, and Eckert, R L. "Phosphorylation of cytokinin by adenosine kinase from wheat germ." Plant physiology vol. 59,3 (1977): 443-7. doi: https://doi.org/10.1104/pp.59.3.443
Chen CM, Eckert RL. Phosphorylation of cytokinin by adenosine kinase from wheat germ. Plant Physiol. 1977 Mar;59(3):443-7. doi: 10.1104/pp.59.3.443. PMID: 16659870; PMCID: PMC542421.
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Adenosine dysfunction in astrogliosis: cause for seizure generation?.

Neuron glia biology

Li T, Quan Lan J, Fredholm BB, Simon RP, Boison D.
PMID: 18634566
Neuron Glia Biol. 2007 Nov;3(4):353-66. doi: 10.1017/S1740925X0800015X.

Epilepsy is characterized by both neuronal and astroglial dysfunction. The endogenous anticonvulsant adenosine, the level of which is largely controlled by astrocytes, might provide a crucial link between astrocyte and neuron dysfunction in epilepsy. Here we have studied astrogliosis,...

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Li T, Quan Lan J, Fredholm BB, et al. Adenosine dysfunction in astrogliosis: cause for seizure generation?. Neuron Glia Biol. 2007;3(4):353-66doi: 10.1017/S1740925X0800015X.
Li, T., Quan Lan, J., Fredholm, B. B., Simon, R. P., & Boison, D. (2007). Adenosine dysfunction in astrogliosis: cause for seizure generation?. Neuron glia biology, 3(4), 353-66. https://doi.org/10.1017/S1740925X0800015X
Li, Tianfu, et al. "Adenosine dysfunction in astrogliosis: cause for seizure generation?." Neuron glia biology vol. 3,4 (2007): 353-66. doi: https://doi.org/10.1017/S1740925X0800015X
Li T, Quan Lan J, Fredholm BB, Simon RP, Boison D. Adenosine dysfunction in astrogliosis: cause for seizure generation?. Neuron Glia Biol. 2007 Nov;3(4):353-66. doi: 10.1017/S1740925X0800015X. PMID: 18634566; PMCID: PMC2561997.
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Adenosine neuromodulation and traumatic brain injury.

Current neuropharmacology

Lusardi TA.
PMID: 20190964
Curr Neuropharmacol. 2009 Sep;7(3):228-37. doi: 10.2174/157015909789152137.

Adenosine is a ubiquitous signaling molecule, with widespread activity across all organ systems. There is evidence that adenosine regulation is a significant factor in traumatic brain injury (TBI) onset, recovery, and outcome, and a growing body of experimental work...

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Lusardi TA. Adenosine neuromodulation and traumatic brain injury. Curr Neuropharmacol. 2009;7(3):228-37doi: 10.2174/157015909789152137.
Lusardi, T. A. (2009). Adenosine neuromodulation and traumatic brain injury. Current neuropharmacology, 7(3), 228-37. https://doi.org/10.2174/157015909789152137
Lusardi, T A. "Adenosine neuromodulation and traumatic brain injury." Current neuropharmacology vol. 7,3 (2009): 228-37. doi: https://doi.org/10.2174/157015909789152137
Lusardi TA. Adenosine neuromodulation and traumatic brain injury. Curr Neuropharmacol. 2009 Sep;7(3):228-37. doi: 10.2174/157015909789152137. PMID: 20190964; PMCID: PMC2769006.
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Nucleotide-metabolism and chromosome alterations in human-malignant melanoma xenografts.

International journal of oncology

Bardot V, Luccioni C, Dutrillaux A, Blancho D, Beaumatin J, Dutrillaux B.
PMID: 21552873
Int J Oncol. 1995 Sep;7(3):547-54.

The karyotypes of human melanomas exhibit multiple chromosome alterations. Recurrent deletions of 9p, 10q and 14q arms, which carry genes encoding for enzymes of purine metabolism, were also found in human gliomas, another neuroectodermal tumor previously studied for both...

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Bardot V, Luccioni C, Dutrillaux A, et al. Nucleotide-metabolism and chromosome alterations in human-malignant melanoma xenografts. Int J Oncol. 1995;7(3):547-54
Bardot, V., Luccioni, C., Dutrillaux, A., Blancho, D., Beaumatin, J., & Dutrillaux, B. (1995). Nucleotide-metabolism and chromosome alterations in human-malignant melanoma xenografts. International journal of oncology, 7(3), 547-54.
Bardot, V, et al. "Nucleotide-metabolism and chromosome alterations in human-malignant melanoma xenografts." International journal of oncology vol. 7,3 (1995): 547-54.
Bardot V, Luccioni C, Dutrillaux A, Blancho D, Beaumatin J, Dutrillaux B. Nucleotide-metabolism and chromosome alterations in human-malignant melanoma xenografts. Int J Oncol. 1995 Sep;7(3):547-54. PMID: 21552873.
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Preventing ATP Degradation by ASO-Mediated Knockdown of CD39 and CD73 Results in A2aR-Independent Rescue of T Cell Proliferation.

Molecular therapy. Nucleic acids

Festag J, Thelemann T, Schell M, Raith S, Michel S, Jaschinski F, Klar R.
PMID: 32739778
Mol Ther Nucleic Acids. 2020 Sep 04;21:656-669. doi: 10.1016/j.omtn.2020.06.020. Epub 2020 Jun 27.

The adenosine axis contributes to the suppression of antitumor immune responses. The ectonucleotidase CD39 degrades extracellular adenosine triphosphate (ATP) to adenosine monophosphate (AMP), which is degraded to adenosine by CD73. Adenosine binds to, e.g., the A2a receptor (A2aR), which...

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Festag J, Thelemann T, Schell M, et al. Preventing ATP Degradation by ASO-Mediated Knockdown of CD39 and CD73 Results in A2aR-Independent Rescue of T Cell Proliferation. Mol Ther Nucleic Acids. 2020;21:656-669doi: 10.1016/j.omtn.2020.06.020.
Festag, J., Thelemann, T., Schell, M., Raith, S., Michel, S., Jaschinski, F., & Klar, R. (2020). Preventing ATP Degradation by ASO-Mediated Knockdown of CD39 and CD73 Results in A2aR-Independent Rescue of T Cell Proliferation. Molecular therapy. Nucleic acids, 21656-669. https://doi.org/10.1016/j.omtn.2020.06.020
Festag, Julia, et al. "Preventing ATP Degradation by ASO-Mediated Knockdown of CD39 and CD73 Results in A2aR-Independent Rescue of T Cell Proliferation." Molecular therapy. Nucleic acids vol. 21 (2020): 656-669. doi: https://doi.org/10.1016/j.omtn.2020.06.020
Festag J, Thelemann T, Schell M, Raith S, Michel S, Jaschinski F, Klar R. Preventing ATP Degradation by ASO-Mediated Knockdown of CD39 and CD73 Results in A2aR-Independent Rescue of T Cell Proliferation. Mol Ther Nucleic Acids. 2020 Sep 04;21:656-669. doi: 10.1016/j.omtn.2020.06.020. Epub 2020 Jun 27. PMID: 32739778; PMCID: PMC7393471.
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Showing 13 to 24 of 60 entries