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Artículos de revistas sobre el tema "158N oligodendroglial cell line"

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Publicado: 25 de mayo de 2024
Última modificación: 31 de julio de 2025

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1

ROSE, LYNN M., SUSANNE L. JACKEVICIUS, and EDWARD A. CLARK. "Expression of Leukocyte Antigens on an Oligodendroglial Cell Line." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (1988): 455–58. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27132.x.

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2

Schuster, Norbert, Herdis Bender, Anja Philippi, et al. "TGF-? induces cell death in the oligodendroglial cell line OLI-neu." Glia 40, no. 1 (2002): 95–108. http://dx.doi.org/10.1002/glia.10110.

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3

Fukushima, Nana, Yuki Miyamoto, and Junji Yamauchi. "Knockdown of Rab9 Recovers Defective Morphological Differentiation Induced by Chemical ER Stress Inducer or PMD-Associated PLP1 Mutant Protein in FBD-102b Cells." Pathophysiology 31, no. 3 (2024): 420–35. http://dx.doi.org/10.3390/pathophysiology31030032.

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Small GTP-binding proteins of the Rab family regulate intracellular vesicle trafficking across many aspects of the transport system. Among these, Rab9 is recognized for its role in controlling the transport system not only around the trans-Golgi network but also around the late endosome. However, the specific functions across different cell types and tissues remain unclear. Here, for the first time, we report that Rab9 negatively regulates morphological changes in the FBD-102b cell line, an oligodendroglial precursor cell line undergoing morphological differentiation. The knockdown of Rab9 led
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4

Fukatsu, Shoya, Yuki Miyamoto, Yu Oka, et al. "Investigating the Protective Effects of a Citrus Flavonoid on the Retardation Morphogenesis of the Oligodendroglia-like Cell Line by Rnd2 Knockdown." Neurology International 16, no. 1 (2023): 33–61. http://dx.doi.org/10.3390/neurolint16010003.

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Recent discoveries suggest links between abnormalities in cell morphogenesis in the brain and the functional deficiency of molecules controlling signal transduction in glial cells such as oligodendroglia. Rnd2 is one such molecule and one of the Rho family monomeric GTP-binding proteins. Despite the currently known functions of Rnd2, its precise roles as it relates to cell morphogenesis and disease state remain to be elucidated. First, we showed that signaling through the loss of function of the rnd2 gene affected the regulation of oligodendroglial cell-like morphological differentiation using
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5

Sawaguchi, Sui, Rimi Suzuki, Hiroaki Oizumi, et al. "Hypomyelinating Leukodystrophy 8 (HLD8)-Associated Mutation of POLR3B Leads to Defective Oligodendroglial Morphological Differentiation Whose Effect Is Reversed by Ibuprofen." Neurology International 14, no. 1 (2022): 212–44. http://dx.doi.org/10.3390/neurolint14010018.

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POLR3B and POLR3A are the major subunits of RNA polymerase III, which synthesizes non-coding RNAs such as tRNAs and rRNAs. Nucleotide mutations of the RNA polymerase 3 subunit b (polr3b) gene are responsible for hypomyelinating leukodystrophy 8 (HLD8), which is an autosomal recessive oligodendroglial cell disease. Despite the important association between POLR3B mutation and HLD8, it remains unclear how mutated POLR3B proteins cause oligodendroglial cell abnormalities. Herein, we show that a severe HLD8-associated nonsense mutation (Arg550-to-Ter (R550X)) primarily localizes POLR3B proteins as
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6

Jin, Ying, Melanie L. McEwen, M. Said Ghandour, and Joe E. Springer. "Overexpression of XIAP Inhibits Apoptotic Cell Death in an Oligodendroglial Cell Line." Cellular and Molecular Neurobiology 24, no. 6 (2004): 853–63. http://dx.doi.org/10.1007/s10571-004-6924-9.

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7

Sawaguchi, Sui, Miki Ishida, Yuki Miyamoto, and Junji Yamauchi. "Hypomyelination Leukodystrophy 16 (HLD16)-Associated Mutation p.Asp252Asn of TMEM106B Blunts Cell Morphological Differentiation." Current Issues in Molecular Biology 46, no. 8 (2024): 8088–103. http://dx.doi.org/10.3390/cimb46080478.

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Transmembrane protein 106B (TMEM106B), which is a type II transmembrane protein, is believed to be involved in intracellular dynamics and morphogenesis in the lysosome. TMEM106B is known to be a risk factor for frontotemporal lobar degeneration and has been recently identified as the receptor needed for the entry of SARS-CoV-2, independently of angiotensin-converting enzyme 2 (ACE2). A missense mutation, p.Asp252Asn, of TMEM106B is associated with hypomyelinating leukodystrophy 16 (HLD16), which is an oligodendroglial cell-related white matter disorder causing thin myelin sheaths or myelin def
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8

Dehm, Verena, Tim Aberle, Laura Guerrero Bladé, et al. "Molecular Analysis of the Differential Activity of Sox8 and Sox10 in Oligodendroglial Cells." International Journal of Molecular Sciences 25, no. 24 (2024): 13395. https://doi.org/10.3390/ijms252413395.

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Oligodendroglial cells generate myelin sheaths in the vertebrate central nervous system to render rapid saltatory conduction possible and express the highly related Sox8, Sox9 and Sox10 transcription factors. While Sox9 and Sox10 fulfill crucial regulatory roles, Sox8 has only a limited impact on oligodendroglial development and myelination. By replacing Sox10 with Sox8 or Sox9 in the oligodendroglial Oln93 cell line, and comparing the expression profiles, we show here that Sox8 regulates the same processes as Sox10 and Sox9, but exhibits a substantially lower transcriptional activity under st
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9

Issa, Y., D. C. Watts, A. J. Duxbury, P. A. Brunton, M. B. Watson, and C. M. Waters. "Mercuric chloride: toxicity and apoptosis in a human oligodendroglial cell line MO3.13." Biomaterials 24, no. 6 (2003): 981–87. http://dx.doi.org/10.1016/s0142-9612(02)00436-2.

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10

Torii, Tomohiro, Remina Shirai, Risa Kiminami, et al. "Hypomyelinating Leukodystrophy 10 (HLD10)-Associated Mutations of PYCR2 Form Large Size Mitochondria, Inhibiting Oligodendroglial Cell Morphological Differentiation." Neurology International 14, no. 4 (2022): 1062–80. http://dx.doi.org/10.3390/neurolint14040085.

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Hypomyelinating leukodystrophy 10 (HLD10) is an autosomal recessive disease related to myelin sheaths in the central nervous system (CNS). In the CNS, myelin sheaths are derived from differentiated plasma membranes of oligodendrocytes (oligodendroglial cells) and surround neuronal axons to achieve neuronal functions. Nucleotide mutations of the pyrroline-5-carboxylate reductase 2 (PYCR2) gene are associated with HLD10, likely due to PYCR2’s loss-of-function. PYCR2 is a mitochondrial residential protein and catalyzes pyrroline-5-carboxylate to an amino acid proline. Here, we describe how each o
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11

Naffaa, Vanessa, Isabelle Hochar, Chéryane Lama, et al. "Bisphenol A Impairs Lipid Remodeling Accompanying Cell Differentiation in the Oligodendroglial Cell Line Oli-Neu." Molecules 27, no. 7 (2022): 2274. http://dx.doi.org/10.3390/molecules27072274.

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In the central nervous system, the process of myelination involves oligodendrocytes that wrap myelin around axons. Myelin sheaths are mainly composed of lipids and ensure efficient conduction of action potentials. Oligodendrocyte differentiation is an essential preliminary step to myelination which, in turn, is a key event of neurodevelopment. Bisphenol A (BPA), a ubiquitous endocrine disruptor, is suspected to disrupt this developmental process and may, thus, contribute to several neurodevelopmental disorders. In this study, we assessed the effect of BPA on oligodendrocyte differentiation thr
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12

Bello-Morales, Raquel, Marta Pérez-Hernández, María Teresa Rejas, Fuencisla Matesanz, Antonio Alcina, and José Antonio López-Guerrero. "Interaction of PLP with GFP-MAL2 in the Human Oligodendroglial Cell Line HOG." PLoS ONE 6, no. 5 (2011): e19388. http://dx.doi.org/10.1371/journal.pone.0019388.

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13

Craighead, Mark, Jessica Pole, and Catherine Waters. "Caspases mediate C2-ceramide-induced apoptosis of the human oligodendroglial cell line, MO3.13." Neuroscience Letters 278, no. 3 (2000): 125–28. http://dx.doi.org/10.1016/s0304-3940(99)00866-6.

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14

Studzinski, Diane M., Rose E. Callahan, and Joyce A. Benjamins. "Increased intracellular calcium alters myelin gene expression in the N20.1 oligodendroglial cell line." Journal of Neuroscience Research 57, no. 5 (1999): 633–42. http://dx.doi.org/10.1002/(sici)1097-4547(19990901)57:5<633::aid-jnr5>3.0.co;2-i.

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15

Mancuso, Roberta, Simone Agostini, Ivana Marventano, Ambra Hernis, Marina Saresella, and Mario Clerici. "NCAM1 is the Target of miRNA-572: Validation in the Human Oligodendroglial Cell Line." Cellular and Molecular Neurobiology 38, no. 2 (2017): 431–40. http://dx.doi.org/10.1007/s10571-017-0486-0.

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16

Horiuchi, Makoto, and Yasuhiro Tomooka. "An oligodendroglial progenitor cell line FBD-102b possibly secretes a radial glia-inducing factor." Neuroscience Research 56, no. 2 (2006): 213–19. http://dx.doi.org/10.1016/j.neures.2006.06.007.

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17

Bello-Morales, Raquel, María Fedetz, Antonio Alcina, Enrique Tabarés, and José Antonio López-Guerrero. "High susceptibility of a human oligodendroglial cell line to herpes simplex type 1 infection." Journal of Neurovirology 11, no. 2 (2005): 190–98. http://dx.doi.org/10.1080/13550280590924179.

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18

Bender, Herdis, Ziyuan Wang, Norbert Schuster, and Kerstin Krieglstein. "TIEG1 facilitates transforming growth factor-?-mediated apoptosis in the oligodendroglial cell line OLI-neu." Journal of Neuroscience Research 75, no. 3 (2004): 344–52. http://dx.doi.org/10.1002/jnr.10856.

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19

Matsumoto, Naoto, Yuki Miyamoto, Kohei Hattori, et al. "PP1C and PP2A are p70S6K Phosphatases Whose Inhibition Ameliorates HLD12-Associated Inhibition of Oligodendroglial Cell Morphological Differentiation." Biomedicines 8, no. 4 (2020): 89. http://dx.doi.org/10.3390/biomedicines8040089.

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Myelin sheaths created by oligodendroglial cells encase neuronal axons to achieve saltatory conduction and protect axons. Pelizaeus-Merzbacher disease (PMD) is a prototypic, hereditary demyelinating oligodendroglial disease of the central nervous system (CNS), and is currently known as hypomyelinating leukodystrophy 1 (HLD1). HLD12 is an autosomal recessive disorder responsible for the gene that encodes vacuolar protein sorting-associated protein 11 homolog (VPS11). VPS11 is a member of the molecular group controlling the early endosome antigen 1 (EEA1)- and Rab7-positive vesicle-mediated prot
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20

Murphy, Eric J., and Lloyd A. Horrocks. "Composition of the phospholipids and their fatty acids in the ROC-1 oligodendroglial cell line." Lipids 28, no. 1 (1993): 67–71. http://dx.doi.org/10.1007/bf02536364.

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21

Uezono, Yasuhito, Izumi Shibuya, Yoko Ueda, et al. "Adrenomedullin increases intracellular Ca2+ and inositol 1,4,5-trisphosphate in human oligodendroglial cell line KG-1C." Brain Research 786, no. 1-2 (1998): 230–34. http://dx.doi.org/10.1016/s0006-8993(97)01430-3.

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22

Studzinski, Diane M., and Joyce A. Benjamins. "Cyclic AMP differentiation of the oligodendroglial cell line N20.1 switches staurosporine-induced cell death from necrosis to apoptosis." Journal of Neuroscience Research 66, no. 4 (2001): 691–97. http://dx.doi.org/10.1002/jnr.10003.

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23

Dominicis, Alessandra, Alice Del Giovane, Matteo Torreggiani, et al. "N-Acetylaspartate Drives Oligodendroglial Differentiation via Histone Deacetylase Activation." Cells 12, no. 14 (2023): 1861. http://dx.doi.org/10.3390/cells12141861.

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An unmet clinical goal in demyelinating pathologies is to restore the myelin sheath prior to neural degeneration. N-acetylaspartate (NAA) is an acetylated derivative form of aspartate, abundant in the healthy brain but severely reduced during traumatic brain injury and in patients with neurodegenerative pathologies. How extracellular NAA variations impact the remyelination process and, thereby, the ability of oligodendrocytes to remyelinate axons remains unexplored. Here, we evaluated the remyelination properties of the oligodendroglial (OL) mouse cell line Oli-neuM under different concentrati
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24

Yoshioka, Akira, Yoko Yamaya, Shinji Saiki, Masumi Kanemoto, Genjiro Hirose, and David Pleasure. "Cyclic GMP/Cyclic GMP-Dependent Protein Kinase System Prevents Excitotoxicity in an Immortalized Oligodendroglial Cell Line." Journal of Neurochemistry 74, no. 2 (2001): 633–40. http://dx.doi.org/10.1046/j.1471-4159.2000.740633.x.

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25

Solly, S. K., P. Daubas, M. Monge, A. Dautigny, and B. Zalc. "Functional Analysis of the Mouse Myelin/Oligodendrocyte Glycoprotein Gene Promoter in the Oligodendroglial CG4 Cell Line." Journal of Neurochemistry 68, no. 4 (2002): 1705–11. http://dx.doi.org/10.1046/j.1471-4159.1997.68041705.x.

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26

Zhan, Jiangshan, Yuanxu Gao, Leo Heinig, et al. "Loss of the Novel Myelin Protein CMTM5 in Multiple Sclerosis Lesions and Its Involvement in Oligodendroglial Stress Responses." Cells 12, no. 16 (2023): 2085. http://dx.doi.org/10.3390/cells12162085.

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This study comprehensively addresses the involvement of the protein CKLF-like Marvel transmembrane domain-containing family member 5 (CMTM5) in the context of demyelination and cytodegenerative autoimmune diseases, particularly multiple Sclerosis (MS). An observed reduction in CMTM5 expression in post-mortem MS lesions prompted further investigations in both in vitro and in vivo animal models. In the cuprizone animal model, we detected a decrease in CMTM5 expression in oligodendrocytes that is absent in other members of the CMTM protein family. Our findings also confirm these results in the ex
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27

Praena, Beatriz, Raquel Bello-Morales, and José Antonio López-Guerrero. "Hsv-1 Endocytic Entry into a Human Oligodendrocytic Cell Line Is Mediated by Clathrin and Dynamin but Not Caveolin." Viruses 12, no. 7 (2020): 734. http://dx.doi.org/10.3390/v12070734.

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Endocytosis is a pathway used by viruses to enter cells that can be classified based on the proteins involved, such as dynamin, clathrin or caveolin. Although the entry of herpes simplex type 1 (HSV-1) by endocytosis has been documented in different cell types, its dependence on clathrin has not been described whereas its dependence on dynamin has been shown according to the cell line used. The present work shows how clathrin-mediated endocytosis (CME) is one way that HSV-1 infects the human oligodendroglial (HOG) cell line. Partial dynamin inhibition using dynasore revealed a relationship bet
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28

Craighead, Mark W., Priyanka Tiwari, Robert G. Keynes, and Catherine M. Waters. "Human oligodendroglial cell line, MO3.13, can be protected from apoptosis using the general caspase inhibitor zVAD-FMK." Journal of Neuroscience Research 57, no. 2 (1999): 236–43. http://dx.doi.org/10.1002/(sici)1097-4547(19990715)57:2<236::aid-jnr9>3.0.co;2-d.

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29

Uezono, Yasuhito, Ei-ichiro Nakamura, Yoko Ueda, et al. "Production of cAMP by adrenomedullin in human oligodendroglial cell line KG1C: comparison with calcitonin gene-related peptide and amylin." Molecular Brain Research 97, no. 1 (2001): 59–69. http://dx.doi.org/10.1016/s0169-328x(01)00288-1.

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30

Damato, Marina, Tristan Cardon, Maxence Wisztorski, et al. "Protein Kinase C Activation Drives a Differentiation Program in an Oligodendroglial Precursor Model through the Modulation of Specific Biological Networks." International Journal of Molecular Sciences 22, no. 10 (2021): 5245. http://dx.doi.org/10.3390/ijms22105245.

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Protein kinase C (PKC) activation induces cellular reprogramming and differentiation in various cell models. Although many effectors of PKC physiological actions have been elucidated, the molecular mechanisms regulating oligodendrocyte differentiation after PKC activation are still unclear. Here, we applied a liquid chromatography–mass spectrometry (LC–MS/MS) approach to provide a comprehensive analysis of the proteome expression changes in the MO3.13 oligodendroglial cell line after PKC activation. Our findings suggest that multiple networks that communicate and coordinate with each other may
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31

Rose, Lynn M., Susanne L. Jackevicius, and Edward A. Clark. "Monoclonal antibodies to human CD4, HNK-1, and LFA-1 surface antigens label the human oligodendroglial cell line KG-1." Journal of Neuroimmunology 16, no. 1 (1987): 147. http://dx.doi.org/10.1016/0165-5728(87)90358-4.

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32

Schuster, Norbert, Herdis Bender, Oliver G. Rössler та ін. "Transforming growth factor-β and tumor necrosis factor-α cooperate to induce apoptosis in the oligodendroglial cell line OLI-neu". Journal of Neuroscience Research 73, № 3 (2003): 324–33. http://dx.doi.org/10.1002/jnr.10666.

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33

Martínez-Pinilla, Eva, Núria Rubio-Sardón, Rafael Peláez, et al. "Neuroprotective Effect of Apolipoprotein D in Cuprizone-Induced Cell Line Models: A Potential Therapeutic Approach for Multiple Sclerosis and Demyelinating Diseases." International Journal of Molecular Sciences 22, no. 3 (2021): 1260. http://dx.doi.org/10.3390/ijms22031260.

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Apolipoprotein D (Apo D) overexpression is a general finding across neurodegenerative conditions so the role of this apolipoprotein in various neuropathologies such as multiple sclerosis (MS) has aroused a great interest in last years. However, its mode of action, as a promising compound for the development of neuroprotective drugs, is unknown. The aim of this work was to address the potential of Apo D to prevent the action of cuprizone (CPZ), a toxin widely used for developing MS models, in oligodendroglial and neuroblastoma cell lines. On one hand, immunocytochemical quantifications and gene
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34

Holzknecht, Christian, and Claudia Röhl. "Effects of Methylprednisolone and Glatiramer Acetate on Nitric Oxide Formation of Cytokine-Stimulated Cells from the Rat Oligodendroglial Cell Line OLN-93." Neuroimmunomodulation 17, no. 1 (2010): 23–30. http://dx.doi.org/10.1159/000243082.

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35

Feng, Tuancheng, Rory R. Sheng, Santiago Solé-Domènech, et al. "A role of the frontotemporal lobar degeneration risk factor TMEM106B in myelination." Brain 143, no. 7 (2020): 2255–71. http://dx.doi.org/10.1093/brain/awaa154.

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Abstract TMEM106B encodes a lysosomal membrane protein and was initially identified as a risk factor for frontotemporal lobar degeneration. Recently, a dominant D252N mutation in TMEM106B was shown to cause hypomyelinating leukodystrophy. However, how TMEM106B regulates myelination is still unclear. Here we show that TMEM106B is expressed and localized to the lysosome compartment in oligodendrocytes. TMEM106B deficiency in mice results in myelination defects with a significant reduction of protein levels of proteolipid protein (PLP) and myelin oligodendrocyte glycoprotein (MOG), the membrane p
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36

Fatatis, Alessandro, та Richard J. Miller. "Platelet-derived Growth Factor (PDGF)-induced Ca2+Signaling in the CG4 Oligodendroglial Cell Line and in Transformed Oligodendrocytes Expressing the β-PDGF Receptor". Journal of Biological Chemistry 272, № 7 (1997): 4351–58. http://dx.doi.org/10.1074/jbc.272.7.4351.

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37

Blaschuk, K. L., E. E. Frost, and C. ffrench-Constant. "The regulation of proliferation and differentiation in oligodendrocyte progenitor cells by alphaV integrins." Development 127, no. 9 (2000): 1961–69. http://dx.doi.org/10.1242/dev.127.9.1961.

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We have previously shown that oligodendrocyte progenitor cells exhibit developmental switching between alphav-associated beta integrin subunits to sequentially express alphavbeta1, alphavbeta3 and alphavbeta5 integrins during differentiation in vitro. To understand the role that alphavveta3 integrin may play in regulating oligodendrocyte progenitor cell behaviour, cells of the rat cell line, CG-4, were genetically engineered to constitutively express alphavbeta3 integrin by transfection with full-length human beta3 integrin subunit cDNA. Time-lapse videomicroscopy showed no effect of beta3 exp
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38

FIERZ, W., K. HEININGER, B. SCHAEFER, K. V. TOYKA, C. LININGTON, and H. LASSMANN. "Synergism in the Pathogenesis of EAE Induced by an MBP-Specific T-Cell Line and Monoclonal Antibodies to Galactocerebroside or a Myelin Oligodendroglial Glycoprotein." Annals of the New York Academy of Sciences 540, no. 1 Advances in N (1988): 360–63. http://dx.doi.org/10.1111/j.1749-6632.1988.tb27099.x.

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39

Alotaibi, Lena, and Amal Alqasmi. "Identification of a de novo Mutation in TMEM106B in a Saudi Child Causes Hypomyelination Leukodystrophy." Global Medical Genetics 10, no. 01 (2023): 038–41. http://dx.doi.org/10.1055/s-0043-1764370.

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AbstractHypomyelinating leukodystrophies are one of the white matter disorders caused by a lack of myelin deposition in the central nervous system (CNS). Here, we report the first case of hypomyelinating leukodystrophy in the Middle East and Saudi Arabia. This condition is caused by a mutation in the TMEM106B gene (HLD16; MIM 617964). Hypotonia, congenital nystagmus, delayed motor development, and delayed speech are the main clinical manifestations. The affected patient has mild pyramidal syndrome, a mild intellectual disability, ataxic gait, hyperreflexia, intention tremor, dysmetria, and oth
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40

Nevin, M., X. Song, S. Japoni, et al. "09 Could DLX2 regulation of neural progenitor cell fate contribute to differentiation of diffuse intrinsic pontine glioma (DIPG)?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, S3 (2018): S16. http://dx.doi.org/10.1017/cjn.2018.305.

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Introduction: Diffuse intrinsic pontine glioma (DIPG) is refractory to therapy. The identification of histone H3.1/H3.3 K27M mutations in most DIPG has provided new insights. The DLX homeobox genes are expressed in the developing forebrain. The Dlx1/Dlx2 double knockout (DKO) mouse loses tangential GABAergic interneuron migration to the neocortex. We have identified genes that encode glutamic acid decarboxylase (GAD) enzymes as direct targets of DLX1/DLX2. In DIPG patients with H3.3 K27M mutations there is decreased Dlx2 and increased expression of the myelin transcription factor, Myt1. Method
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41

Fierz, W., K. Heininger, B. Schaefer, K. V. Toyka, Ch Linington, and H. Lassmann. "Synergism in the pathogenesis of EAE induced by an MBP-specific T cell line and monoclonal antibodies to Galacto-Cerebroside or to a myelin oligodendroglial glycoprotein." Journal of Neuroimmunology 16, no. 1 (1987): 55–56. http://dx.doi.org/10.1016/0165-5728(87)90213-x.

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42

Rumsby, Martin, Keiko Ichihara-Tanaka, Terutoshi Kimura, Maria Scott, Laurie Haynes, and Takashi Muramatsu. "Bipolar undifferentiated CG-4 oligodendroglial line cells adhere, extend processes and disperse on midkine, a heparin-binding growth factor: orthovanadate and chondroitin sulphate E inhibit cell attachment." Neuroscience Research Communications 28, no. 1 (2001): 31–39. http://dx.doi.org/10.1002/1520-6769(200101/02)28:1<31::aid-nrc4>3.0.co;2-f.

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43

Silva, Maria Elena, Matías Hernández-Andrade, Nerea Abasolo, et al. "DDR1 and Its Ligand, Collagen IV, Are Involved in In Vitro Oligodendrocyte Maturation." International Journal of Molecular Sciences 24, no. 2 (2023): 1742. http://dx.doi.org/10.3390/ijms24021742.

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Discoidin domain receptor 1 (DDR1) is a tyrosine kinase receptor expressed in epithelial cells from different tissues in which collagen binding activates pleiotropic functions. In the brain, DDR1 is mainly expressed in oligodendrocytes (OLs), the function of which is unclear. Whether collagen can activate DDR1 in OLs has not been studied. Here, we assessed the expression of DDR1 during in vitro OL differentiation, including collagen IV incubation, and the capability of collagen IV to induce DDR1 phosphorylation. Experiments were performed using two in vitro models of OL differentiation: OLs de
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Glänzel, Nícolas Manzke, Belisa Parmeggiani, Mateus Grings, et al. "Myelin Disruption, Neuroinflammation, and Oxidative Stress Induced by Sulfite in the Striatum of Rats Are Mitigated by the pan-PPAR agonist Bezafibrate." Cells 12, no. 12 (2023): 1557. http://dx.doi.org/10.3390/cells12121557.

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Sulfite predominantly accumulates in the brain of patients with isolated sulfite oxidase (ISOD) and molybdenum cofactor (MoCD) deficiencies. Patients present with severe neurological symptoms and basal ganglia alterations, the pathophysiology of which is not fully established. Therapies are ineffective. To elucidate the pathomechanisms of ISOD and MoCD, we investigated the effects of intrastriatal administration of sulfite on myelin structure, neuroinflammation, and oxidative stress in rat striatum. Sulfite administration decreased FluoromyelinTM and myelin basic protein staining, suggesting m
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Smith, Graham S. T., Lopamudra Homchaudhuri, Joan M. Boggs, and George Harauz. "Classic 18.5- and 21.5-kDa Myelin Basic Protein Isoforms Associate with Cytoskeletal and SH3-Domain Proteins in the Immortalized N19-Oligodendroglial Cell Line Stimulated by Phorbol Ester and IGF-1." Neurochemical Research 37, no. 6 (2012): 1277–95. http://dx.doi.org/10.1007/s11064-011-0700-2.

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46

Agostini, Simone, Elisabetta Bolognesi, Roberta Mancuso, et al. "miR-23a-3p and miR-181a-5p modulate SNAP-25 expression." PLOS ONE 18, no. 1 (2023): e0279961. http://dx.doi.org/10.1371/journal.pone.0279961.

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SNAP-25 protein is a key protein of the SNARE complex that is involved in synaptic vesicles fusion with plasma membranes and neurotransmitter release, playing a fundamental role in neural plasticity. Recently the concentration of three specific miRNAs–miR-27b-3p, miR-181a-5p and miR-23a-3p –was found to be associated with a specific SNAP-25 polymorphism (rs363050). in silico analysis showed that all the three miRNAs target SNAP-25, but the effect of the interaction between these miRNAs and the 3’UTR of SNAP-25 mRNA is currently unknown. For this reason, we verified in vitro whether miR-27b-3p,
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47

Shahbandi, Ataollah, Saeid Atashpanjeh, Aileen Azari-Yam, Farideh Nejat, and Zohreh Habibi. "LINC-09. Coexisting glioneuronal tumor and adrenal ganglioneuroma." Neuro-Oncology 24, Supplement_1 (2022): i164. http://dx.doi.org/10.1093/neuonc/noac079.608.

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Abstract BACKGROUND: While both glial/glioneuronal neoplasia and ganglioneuroma have been reported as components of multiple primary neoplasms, no patient has been diagnosed with multiple primary neoplasms of cerebral glial/glioneuronal tumors with oligodendroglioma-like features and adrenal ganglioneuroma up to now. CASE: A previously healthy five-year-old girl was admitted with a two-week history of headaches and vomiting. Brain Magnetic resonance imaging (MRI) showed a massive heterogenous multi-cystic enhancing lesion in the right temporoparietal area with substantial vasogenic edema. The
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Schaff, Lauren R., and Ingo K. Mellinghoff. "Glioblastoma and Other Primary Brain Malignancies in Adults." JAMA 329, no. 7 (2023): 574. http://dx.doi.org/10.1001/jama.2023.0023.

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ImportanceMalignant primary brain tumors cause more than 15 000 deaths per year in the United States. The annual incidence of primary malignant brain tumors is approximately 7 per 100 000 individuals and increases with age. Five-year survival is approximately 36%.ObservationsApproximately 49% of malignant brain tumors are glioblastomas, and 30% are diffusely infiltrating lower-grade gliomas. Other malignant brain tumors include primary central nervous system (CNS) lymphoma (7%) and malignant forms of ependymomas (3%) and meningiomas (2%). Symptoms of malignant brain tumors include headache (50
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Chierto, Elena, Giulia Cristinziano, Francesca Sapone, Delphine Meffre, and Mehrnaz Jafarian-Tehrani. "ffect of Etazolate on ROS Production after tBHP-Induced Oxidative Stress in Oligodendroglial 158N Cell Line." Reactive Oxygen Species, 2020. http://dx.doi.org/10.20455/ros.2020.807.

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Kremp, Marco, Tim Aberle, Elisabeth Sock, et al. "Transcription factor Olig2 is a major downstream effector of histone demethylase Phf8 during oligodendroglial development." Glia, April 13, 2024. http://dx.doi.org/10.1002/glia.24538.

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AbstractThe plant homeodomain finger protein Phf8 is a histone demethylase implicated by mutation in mice and humans in neural crest defects and neurodevelopmental disturbances. Considering its widespread expression in cell types of the central nervous system, we set out to determine the role of Phf8 in oligodendroglial cells to clarify whether oligodendroglial defects are a possible contributing factor to Phf8‐dependent neurodevelopmental disorders. Using loss‐ and gain‐of‐function approaches in oligodendroglial cell lines and primary cell cultures, we show that Phf8 promotes the proliferatio
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