Bibliografías temáticas / 158N oligodendroglial cell line

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Literatura académica sobre el tema "158N oligodendroglial cell line"

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

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

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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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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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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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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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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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Tesis sobre el tema "158N oligodendroglial cell line"

1

Padilla, Ferrer Aïda. "ADAM10 in myelination of the central nervous system : study of ADAM10 localization and development of an inducible oligodendroglial ADAM10 knock out (KOOLA10) mouse strain." Electronic Thesis or Diss., Université Paris Cité, 2022. https://wo.app.u-paris.fr/cgi-bin/WebObjects/TheseWeb.woa/wa/show?t=4270&f=41801.

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Dans le système nerveux central (SNC), les oligodendrocytes (OL) enveloppent les axones de leurs prolongements membranaires formant ainsi les gaines de myéline. La mort des OL et la perte de myéline (démyélinisation) surviennent dans les maladies démyélinisantes telles que la sclérose en plaques, pour lesquelles il n'existe pas de traitement efficace. Notre objectif est de stimuler des processus de réparation endogène via la voie ADAM10/sAPPa. Le fragment soluble sAPPa est un peptide neuroprotecteur issu du clivage de la protéine précurseur de l'amyloïde (APP) par les a-secrétases de la famill
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