Journal articles on the topic 'FM19G11'

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1

Marcuzzo, Stefania, Davide Isaia, Silvia Bonanno, Claudia Malacarne, Paola Cavalcante, Antonella Zacheo, Valentino Laquintana, et al. "FM19G11-Loaded Gold Nanoparticles Enhance the Proliferation and Self-Renewal of Ependymal Stem Progenitor Cells Derived from ALS Mice." Cells 8, no. 3 (March 23, 2019): 279. http://dx.doi.org/10.3390/cells8030279.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease affecting motor neurons. In ALS mice, neurodegeneration is associated with the proliferative restorative attempts of ependymal stem progenitor cells (epSPCs) that normally lie in a quiescent in the spinal cord. Thus, modulation of the proliferation of epSPCs may represent a potential strategy to counteract neurodegeneration. Recent studies demonstrated that FM19G11, a hypoxia-inducible factor modulator, induces epSPC self-renewal and proliferation. The aim of the study was to investigate whether FM19G11-loaded gold nanoparticles (NPs) can affect self-renewal and proliferation processes in epSPCs isolated from G93A-SOD1 mice at disease onset. We discovered elevated levels of SOX2, OCT4, AKT1, and AKT3, key genes associated with pluripotency, self-renewal, and proliferation, in G93A-SOD1 epSPCs at the transcriptional and protein levels after treatment with FM19G11-loaded NPs. We also observed an increase in the levels of the mitochondrial uncoupling protein (UCP) gene in treated cells. FM19G11-loaded NPs treatment also affected the expression of the cell cycle-related microRNA (miR)-19a, along with its target gene PTEN, in G93A-SOD1 epSPCs. Overall our findings establish the significant impact of FM19G11-loaded NPs on the cellular pathways involved in self-renewal and proliferation in G93A-SOD1 epSPCs, thus providing an impetus to the design of novel tailored approaches to delay ALS disease progression.
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2

Moreno-Manzano, Victoria, Francisco J. Rodríguez-Jiménez, Jose L. Aceña-Bonilla, Santos Fustero-Lardíes, Slaven Erceg, Joaquin Dopazo, David Montaner, Miodrag Stojkovic, and Jose M. Sánchez-Puelles. "FM19G11, a New Hypoxia-inducible Factor (HIF) Modulator, Affects Stem Cell Differentiation Status." Journal of Biological Chemistry 285, no. 2 (November 6, 2009): 1333–42. http://dx.doi.org/10.1074/jbc.m109.008326.

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3

You, Chao-guo, Han-song Sheng, Chao-ran Xie, Nu Zhang, and Xue-sheng Zheng. "FM19G11 inhibits O6 -methylguanine DNA-methyltransferase expression under both hypoxic and normoxic conditions." Cancer Medicine 7, no. 7 (May 15, 2018): 3292–300. http://dx.doi.org/10.1002/cam4.1551.

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4

Valdes-Sánchez, Teresa, Francisco Javier Rodriguez-Jimenez, Dunia M. García-Cruz, Jorge L. Escobar-Ivirico, Ana Alastrue-Agudo, Slaven Erceg, Manuel Monleón, and Victoria Moreno-Manzano. "Methacrylate-endcapped caprolactone and FM19G11 provide a proper niche for spinal cord-derived neural cells." Journal of Tissue Engineering and Regenerative Medicine 9, no. 6 (March 27, 2013): 734–39. http://dx.doi.org/10.1002/term.1735.

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5

Ruzaeva, V. A., A. V. Morgun, E. D. Khilazheva, N. V. Kuvacheva, E. A. Pozhilenkova, E. B. Boitsova, G. P. Martynova, T. E. Taranushenko, and A. B. Salmina. "Development of blood-brain barrier under the modulation of HIF activity in astroglial and neuronal cells in vitro." Biomeditsinskaya Khimiya 62, no. 6 (2016): 664–69. http://dx.doi.org/10.18097/pbmc20166206664.

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Barriergenesis is the process of maturation of the primary vascular network of the brain responsible for the establishment of the blood-brain barrier. It represents a combination of factors that, on the one hand, contribute to the process of migration and tubulogenesis of endothelial cells (angiogenesis), on the other hand, contribute to the formation of new connections between endothelial cells and other elements of the neurovascular unit. Astrocytes play a key role in barriergenesis, however, mechanisms of their action are still poorly examined. We have studied the effects of HIF-1 modulators acting on the cells of non-endothelial origin (neurons and astrocytes) on the development of the blood-brain barrier in vitro. Application of FM19G11 regulating expression of HIF-1 activity and GSI-1 suppressing gamma-secretase and/or proteasomal activity resulted in the elevated expression of thrombospondins and matrix metalloproteinases in the developing blood-brain barrier. However, it caused the opposite effect on VEGF expression thus promoting barrier maturation in vitro.
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6

Rodríguez-Jiménez, Francisco Javier, Victoria Moreno-Manzano, Pablo Mateos-Gregorio, Inmaculada Royo, Slaven Erceg, José Ramón Murguia, and Jose María Sánchez-Puelles. "FM19G11: A new modulator of HIF that links mTOR activation with the DNA damage checkpoint pathways." Cell Cycle 9, no. 14 (July 15, 2010): 2875–85. http://dx.doi.org/10.4161/cc.9.14.12250.

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7

Alastrue-Agudo, Ana, Francisco Rodriguez-Jimenez, Eric Mocholi, Francesca De Giorgio, Slaven Erceg, and Victoria Moreno-Manzano. "FM19G11 and Ependymal Progenitor/Stem Cell Combinatory Treatment Enhances Neuronal Preservation and Oligodendrogenesis after Severe Spinal Cord Injury." International Journal of Molecular Sciences 19, no. 1 (January 9, 2018): 200. http://dx.doi.org/10.3390/ijms19010200.

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8

Rodríguez-Jiménez, Francisco Javier, Ana Alastrue-Agudo, Slaven Erceg, Miodrag Stojkovic, and Victoria Moreno-Manzano. "FM19G11 Favors Spinal Cord Injury Regeneration and Stem Cell Self-Renewal by Mitochondrial Uncoupling and Glucose Metabolism Induction." STEM CELLS 30, no. 10 (September 20, 2012): 2221–33. http://dx.doi.org/10.1002/stem.1189.

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9

El Assar, M., J. M. Sánchez-Puelles, I. Royo, E. López-Hernández, A. Sánchez-Ferrer, J. L. Aceña, L. Rodríguez-Mañas, and J. Angulo. "FM19G11 reverses endothelial dysfunction in rat and human arteries through stimulation of the PI3K/Akt/eNOS pathway, independently of mTOR/HIF-1α activation." British Journal of Pharmacology 172, no. 5 (January 12, 2015): 1277–91. http://dx.doi.org/10.1111/bph.12993.

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10

Endo, Kyoko, Hiroaki Kito, Ryo Tanaka, Junko Kajikuri, Satoshi Tanaka, Elghareeb E. Elboray, Takayoshi Suzuki, and Susumu Ohya. "Possible Contribution of Inflammation-Associated Hypoxia to Increased K2P5.1 K+ Channel Expression in CD4+ T Cells of the Mouse Model for Inflammatory Bowel Disease." International Journal of Molecular Sciences 21, no. 1 (December 19, 2019): 38. http://dx.doi.org/10.3390/ijms21010038.

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Previous studies have reported the up-regulation of the two-pore domain K+ channel K2P5.1 in the CD4+ T cells of patients with multiple sclerosis (MS) and rheumatoid arthritis (RA), as well as in a mouse model of inflammatory bowel disease (IBD). However, the mechanisms underlying this up-regulation remain unclear. Inflammation-associated hypoxia is involved in the pathogenesis of autoimmune diseases, such as IBD, MS, and RA, and T cells are exposed to a hypoxic environment during their recruitment from inflamed tissues to secondary lymphoid tissues. We herein investigated whether inflammation-associated hypoxia is attributable to the increased expression and activity of K2P5.1 in the splenic CD4+ T cells of chemically-induced IBD model mice. Significant increases in hypoxia-inducible factor (HIF)-1α transcripts and proteins were found in the splenic CD4+ T cells of the IBD model. In the activated splenic CD4+ T cells, hypoxia (1.5% O2) increased K2P5.1 expression and activity, whereas a treatment with the HIF inhibitor FM19G11 but not the selective HIF-2 inhibitor exerted the opposite effect. Hypoxia-exposed K2P5.1 up-regulation was also detected in stimulated thymocytes and the mouse T-cell line. The class III histone deacetylase sirtuin-1 (SIRT1) is a downstream molecule of HIF-1α signaling. We examined the effects of the SIRT1 inhibitor NCO-01 on K2P5.1 transcription in activated CD4+ T cells, and we found no significant effects on the K2P5.1 transcription. No acute compensatory responses of K2P3.1–K2P5.1 up-regulation were found in the CD4+ T cells of the IBD model and the hypoxia-exposed T cells. Collectively, these results suggest a mechanism for K2P5.1 up-regulation via HIF-1 in the CD4+ T cells of the IBD model.
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11

Good, Chris, and Brian E. Raines. "Continuum many tent map inverse limits with homeomorphic postcritical ω-limit sets." Fundamenta Mathematicae 191, no. 1 (2006): 1–21. http://dx.doi.org/10.4064/fm191-1-1.

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12

Maszczyk, Tomasz. "One-dimensional infinitesimal-birational duality through differential operators." Fundamenta Mathematicae 191, no. 1 (2006): 23–43. http://dx.doi.org/10.4064/fm191-1-2.

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13

Zoble, Stuart. "Stationary reflection and the universal Baire property." Fundamenta Mathematicae 191, no. 1 (2006): 45–56. http://dx.doi.org/10.4064/fm191-1-3.

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14

Apter, Arthur W. "How many normal measures can \alephω+ 1carry?" Fundamenta Mathematicae 191, no. 1 (2006): 57–66. http://dx.doi.org/10.4064/fm191-1-4.

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15

Dow, Alan, and Oleg Pavlov. "More about spaces with a small diagonal." Fundamenta Mathematicae 191, no. 1 (2006): 67–80. http://dx.doi.org/10.4064/fm191-1-5.

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16

Miller, Benjamin D. "Coordinatewise decomposition, Borel cohomology, and invariant measures." Fundamenta Mathematicae 191, no. 1 (2006): 81–94. http://dx.doi.org/10.4064/fm191-1-6.

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17

Laskowski, M. C., and S. Shelah. "Decompositions of saturated models of stable theories." Fundamenta Mathematicae 191, no. 2 (2006): 95–124. http://dx.doi.org/10.4064/fm191-2-1.

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18

Štimac, Sonja. "Structure of inverse limit spaces of tent maps with finite critical orbit." Fundamenta Mathematicae 191, no. 2 (2006): 125–50. http://dx.doi.org/10.4064/fm191-2-2.

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19

Montalbán, Antonio. "Equimorphism invariants for scattered linear orderings." Fundamenta Mathematicae 191, no. 2 (2006): 151–73. http://dx.doi.org/10.4064/fm191-2-3.

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20

Raymond, Jean Saint. "Quasi-bounded trees and analytic inductions." Fundamenta Mathematicae 191, no. 2 (2006): 175–85. http://dx.doi.org/10.4064/fm191-2-4.

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21

Ohta, Haruto, and Kaori Yamazaki. "Extension of point-finite partitions of unity." Fundamenta Mathematicae 191, no. 3 (2006): 187–99. http://dx.doi.org/10.4064/fm191-3-1.

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22

Newelski, Ludomir, and Marcin Petrykowski. "Weak generic types and coverings of groups I." Fundamenta Mathematicae 191, no. 3 (2006): 201–25. http://dx.doi.org/10.4064/fm191-3-2.

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23

Ivanov, A. A. "Strongly determined types and G-compactness." Fundamenta Mathematicae 191, no. 3 (2006): 227–47. http://dx.doi.org/10.4064/fm191-3-3.

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24

Fehér, László M., and Balázs Kőműves. "On second order Thom–Boardman singularities." Fundamenta Mathematicae 191, no. 3 (2006): 249–64. http://dx.doi.org/10.4064/fm191-3-4.

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25

Balibrea, Francisco, Juan Luis García Guirao, Marek Lampart, and Jaume Llibre. "Dynamics of a Lotka–Volterra map." Fundamenta Mathematicae 191, no. 3 (2006): 265–79. http://dx.doi.org/10.4064/fm191-3-5.

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26

Bartoszynski, Tomek, Paul Larson, and Saharon Shelah. "Closed sets which consistently have few translations covering the line." Fundamenta Mathematicae 237, no. 2 (2017): 101–25. http://dx.doi.org/10.4064/fm191-8-2016.

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