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Letteratura scientifica selezionata sul tema "Ependymin"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 3 febbraio 2022

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Articoli di riviste sul tema "Ependymin"

1

Rother, Stefan, Rupert Schmidt, Wolfgang Brysch e Karl-Hermann Schlingensiepen. "Learning-Induced Expression of Meningeal Ependymin mRNA and Demonstration of Ependymin in Neurons and Glial Cells". Journal of Neurochemistry 65, n. 4 (23 novembre 2002): 1456–64. http://dx.doi.org/10.1046/j.1471-4159.1995.65041456.x.

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2

SHASHOUA, VICTOR E. "Ependymin, a Brain Extracellular Glycoprotein, and CNS Plasticity". Annals of the New York Academy of Sciences 627, n. 1 Activity-Driv (agosto 1991): 94–114. http://dx.doi.org/10.1111/j.1749-6632.1991.tb25916.x.

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3

Adams, David S., Miki Kiyokawa, Michael E. Getman e Victor E. Shashoua. "Genes encoding giant danio and golden shiner ependymin". Neurochemical Research 21, n. 3 (marzo 1996): 377–84. http://dx.doi.org/10.1007/bf02531655.

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4

Park, Jeong Kuk, Keon Young Kim, Yeo Won Sim, Yong-In Kim, Jin Kyun Kim, Cheol Lee, Jeongran Han, Chae Un Kim, J. Eugene Lee e SangYoun Park. "Structures of three ependymin-related proteins suggest their function as a hydrophobic molecule binder". IUCrJ 6, n. 4 (20 giugno 2019): 729–39. http://dx.doi.org/10.1107/s2052252519007668.

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Abstract (sommario):

Ependymin was first discovered as a predominant protein in brain extracellular fluid in fish and was suggested to be involved in functions mostly related to learning and memory. Orthologous proteins to ependymin called ependymin-related proteins (EPDRs) have been found to exist in various tissues from sea urchins to humans, yet their functional role remains to be revealed. In this study, the structures of EPDR1 from frog, mouse and human were determined and analyzed. All of the EPDR1s fold into a dimer using a monomeric subunit that is mostly made up of two stacking antiparallel β-sheets with a curvature on one side, resulting in the formation of a deep hydrophobic pocket. All six of the cysteine residues in the monomeric subunit participate in the formation of three intramolecular disulfide bonds. Other interesting features of EPDR1 include two asparagine residues with glycosylation and a Ca2+-binding site. The EPDR1 fold is very similar to the folds of bacterial VioE and LolA/LolB, which also use a similar hydrophobic pocket for their respective functions as a hydrophobic substrate-binding enzyme and a lipoprotein carrier, respectively. A further fatty-acid binding assay using EPDR1 suggests that it indeed binds to fatty acids, presumablyviathis pocket. Additional interactome analysis of EPDR1 showed that EPDR1 interacts with insulin-like growth factor 2 receptor and flotillin proteins, which are known to be involved in protein and vesicle translocation.

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5

Anderson, Marilyn J., Chi Y. Choy e Stephen G. Waxman. "Selforganization of ependyma in regenerating teleost spinal cord: evidence from serial section reconstructions". Development 96, n. 1 (1 luglio 1986): 1–18. http://dx.doi.org/10.1242/dev.96.1.1.

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Abstract (sommario):

Multiple ependymal structures have been observed in regenerating spinal cord of the teleost Apteronotus albifrons. Evidence is presented for two modes of formation of the secondary ependymas: budding off from the primary ependyma, and de novo origin of a tube-like ependymal structure within a group of undifferentiated cells. Serial sections of regenerated cord provide evidence that undifferentiated cells not in immediate contact with the main ependymal layer can organize and differentiate into an ependymal structure in the regenerating spinal cord. These findings suggest that a significant amount of morphological organization can take place independent of the normal developmental sequence and environment.

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6

Suárez-Castillo, Edna C., e José E. García-Arrarás. "Deciphering the molecular evolution of the ependymin protein family". Developmental Biology 295, n. 1 (luglio 2006): 424. http://dx.doi.org/10.1016/j.ydbio.2006.04.304.

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7

Königstorfer, A., S. Sterrer, C. Eckerskorn, F. Lottspeich, R. Schmidt e W. Hoffmann. "Molecular Characterization of an Ependymin Precursor from Goldfish Brain". Journal of Neurochemistry 52, n. 1 (gennaio 1989): 310–12. http://dx.doi.org/10.1111/j.1471-4159.1989.tb10932.x.

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8

Adams, David S., e Victor E. Shashoua. "Cloning and sequencing the genes encoding goldfish and carp ependymin". Gene 141, n. 2 (aprile 1994): 237–41. http://dx.doi.org/10.1016/0378-1119(94)90578-9.

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9

Sterrer, S., A. Königstorfer e W. Hoffman. "Biosynthesis and expression of ependymin homologous sequences in zebrafish brain". Neuroscience 37, n. 1 (gennaio 1990): 277–84. http://dx.doi.org/10.1016/0306-4522(90)90214-o.

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10

Park, SangYoun. "De novo Phasing Xenons Observed in the Frog Ependymin-Related Protein". Crystals 10, n. 1 (10 gennaio 2020): 32. http://dx.doi.org/10.3390/cryst10010032.

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Abstract (sommario):

Pressurizing Xe or Kr noble gas into the protein crystal for de novo phasing has been one method of choice when the introduction of other heavy-atom compounds fails. One reason is because, unlike other heavy-atom compounds, their immobilized sites are mostly hydrophobic cavities. Previously, the structure of frog ependymin-related protein (EPDR) has been determined using a single wavelength anomalous diffraction (SAD) on a Xe-pressurized crystal. Since no report on the four Xe binding sites has been made, these sites are analyzed in this study. Of the four Xe atoms, three are found along the hydrophobic interfaces created by the two crystallographic symmetry mates of EPDR. One final Xe atom occupies a Ca2+-binding site of the native protein entirely stabilized by the polar atoms of the surrounding EDPR residues. We believe that this atypical Xe location is very unique and merits further study.

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Più fonti

Tesi sul tema "Ependymin"

1

Kaska, Jennifer Lynn. "Ependymin Mechanism of Action: Full Length EPN VS Peptide CMX-8933". Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0528103-102730/.

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2

Hirsch, Erica. "Telomerase activity and telomere lengths in fibroblast cells treated with ependymin peptide mimetics". Link to electronic thesis, 2005. http://www.wpi.edu/Pubs/ETD/Available/etd-050505-134911/.

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3

kapoor, varun. "Mechanism of Reversal of Alzheimerâ€™s Disease A-beta Induced Neuronal Degeneration in Cultured Human SHSY Cells Using A Neurotrophic Ependymin Mimetic". Digital WPI, 2007. https://digitalcommons.wpi.edu/etd-theses/908.

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Abstract (sommario):

"Alzheimerâ€™s disease (AD) is a neurodegenerative disorder that leads to dementia in adults. The mechanism of neurodegeneration is thought to involve the extracellular production of a highly toxic A-beta peptide that engages cell surface receptors to induce cellular oxidative stress and apoptosis, but the signal transduction pathways that lead to A-beta induced cell death are unknown. We previously showed that a human ependymin neurotrophic peptide mimetic (hEPN-1) can promote cell survival in an in vitro AD model system. This initial observation was extended in this thesis by investigating the mechanism of A-beta induced apoptosis and hEPN-1 induced survival. Immunoblots were used to assay the total cellular levels of specific caspase proteins. The results show that A-beta induced apoptosis uses an extrinsic caspase pathway involving caspases-2 and -3, and that hEPN-1 treatment can reduce those caspase levels. A caspase activity assay showed that A-beta increased caspase-3/7 activity, while hEPN-1 treatment lowered it. Moreover, in vivo studies with AD transgenic mice showed that hEPN-1 treatment increased antioxidative superoxide dismutase levels in brain. Thus, hEPN-1 holds potential as a therapeutic to treat the underlying neurodegenerative cause of AD, not merely its symptoms as with other currently approved AD drugs."

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4

Arca, Turkan. "Attempts to clone the Limulus ependymin gene, and the effects of a human ependymin peptide on human SHSY neuroblastoma cells". Link to electronic thesis, 2005. http://www.wpi.edu/Pubs/ETD/Available/etd-050405-180333/.

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5

Parikh, Suchi Vipin. "Ependymin peptide mimetics that assuage ischemic damage increase gene expression of the anti-oxidative enzyme SOD". Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0429103-132144.

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6

Saif, Sakina. "AP-1 is required for CMX-8933-induced SOD upregulation and is translocated in response to a human EPN mimetic". Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0503104-162858/.

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7

Stovall, Kirk Hiatt. "Partial restoration of cell survival by a human ependymin mimetic in an in vitro Alzheimer's disease model". Link to electronic thesis, 2006. http://www.wpi.edu/Pubs/ETD/Available/etd-082106-133513/.

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8

Kapoor, Varun. "Mechanism of reversal of Alzheimer's disease A-beta induced neuronal degeneration in cultured human SHSY cells using a neurotrophic ependymin mimetic". Link to electronic thesis, 2007. http://www.wpi.edu/Pubs/ETD/Available/etd-071607-181533/.

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9

Penninella, Donato [Verfasser]. "Corticosteroidrezeptor-abhängige Expressionsregulation des sekretorischen Zelladhäsionsmoleküls Ependymin im Hinblick auf die Gedächtnisbildung bei Teleostei / Donato Penninella". Gießen : Universitätsbibliothek, 2016. http://d-nb.info/1121474489/34.

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10

Kreul, Florian Jean-Pierre [Verfasser]. "Ultrastrukturelle Lokalisation des Glykoproteins Ependymin im Mittelhirndach (Tectum opticum) von Goldfischen und der Einfluss von Dressurversuchen / Florian Jean-Pierre Kreul". Gießen : Universitätsbibliothek, 2011. http://d-nb.info/1063110564/34.

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Libri sul tema "Ependymin"

1

Mitro, A. Ependým komorového systému lʼudského mozgu. Bratislava: VEDA, 1987.

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2

Gilbert, Mark R., e Roberta Rudà. Ependymal tumours. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199651870.003.0005.

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Abstract (sommario):

Ependymomas are uncommon central nervous system cancers that can arise in the supratentorial, infratentorial, or spinal cord region. Recently, there have been several seminal findings regarding the molecular profiles of ependymomas that have led to marked changes in the classification of this disease. In addition to the World Health Organization grading system that designates ependymomas based on histological appearance into grade I, II, or III, a new molecular classification with distinct entities within the three anatomical regions provides additional subtyping that has prognostic significance and may ultimately provide therapeutic targets. Ependymomas are typically treated with maximum safe tumour resection. Grade III tumours always require radiation treatment even with extensive resection. Radiation is also often administered to patients with grade II ependymomas. Grade I tumours typically receive radiation if there is extensive residual disease, but complete resection may be curative. Local radiation is optimal unless there is imaging or cytological evidence of dissemination in the cerebrospinal fluid. Chemotherapy is less well established although recent molecular findings may lead to subtype specific treatments.

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3

Reichenbach, Andreas, e Hartwig Wolburg. Astrocytes and Ependymal Glia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199794591.003.0004.

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This is a digitally enhanced text. Readers can also see the coverage of this topic area in the second edition of Neuroglia. The second edition of Neuroglia was first published digitally in Oxford Scholarship Online and the bibliographic details provided, if cited, will direct people to that version of the text. Readers can also see the coverage of this topic area in the ...

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4

Oksche, A., e E. M. Rodriguez. The Subcommissural Organ: An Ependymal Brain Gland. Springer, 1993.

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5

A, Oksche, Rodríguez E. M e Fernández-Llebrez P. 1954-, a cura di. The Subcommissural organ: An ependymal brain gland. Berlin: Springer-Verlag, 1993.

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6

Theeler, Brett J., e Mark R. Gilbert. Primary Central Nervous System Tumors. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0129.

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Abstract (sommario):

Ependymomas are rare primary central nervous system (CNS) tumors that are thought to arise from ependymal cells lining the ventricular system located throughout the CNS. Ependymomas occur in all age groups but are more common in the pediatric population. Ependymomas typically present as mass lesions within the ventricular system, brain or spinal cord parenchyma. As with most central nervous system tumors, pathologic evaluation is required for definitive diagnosis. Ependymomas are typically treated with a combination of surgery and radiotherapy although this varies depending on tumor location, tumor grade, patient age, extent of tumor resection, and other pretreatment factors. Recent molecular studies demonstrate molecularly defined tumor heterogeneity that appears to have a region-specific pattern. Translating the emerging molecular profiles of ependymomas into improved treatment strategies is the primary goal of ongoing research efforts.

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Capitoli di libri sul tema "Ependymin"

1

Seifert, W., H. Terlau e R. Schmidt. "A Possible Role for Ependymin in Hippocampal Plasticity". In Modulation of Synaptic Transmission and Plasticity in Nervous Systems, 249–57. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73160-0_19.

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2

Shashoua, Victor E. "The Role of Ependymin in Neuronal Plasticity and LTP". In Excitatory Amino Acids and Neuronal Plasticity, 333–45. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5769-8_37.

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3

Hasselblatt, Martin. "Ependymal Tumors". In Recent Results in Cancer Research, 51–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-31206-2_3.

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4

Fuller, Christine E. "Ependymal Tumors". In Atlas of Pediatric Brain Tumors, 53–67. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33432-5_6.

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5

Schiffer, Davide, Maria Teresa Giordana, Alessandro Mauro e Riccardo Soffietti. "Ependymal Tumors". In Brain Tumors, 228–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60529-1_11.

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6

Chougule, Meghana. "Ependymal Tumors". In Neuropathology of Brain Tumors with Radiologic Correlates, 95–120. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-7126-8_6.

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7

Lacruz, César R., Javier Saénz de Santamaría e Ricardo H. Bardales. "Ependymal Tumors". In Central Nervous System Intraoperative Cytopathology, 129–44. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98491-9_8.

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8

Fuller, Christine E., Sonia Narendra e Ioana Tolicica. "Ependymal Tumors". In Atlas of Pediatric Brain Tumors, 47–59. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1062-2_5.

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9

Lacruz, César R., Javier Sáenz de Santamaría e Ricardo H. Bardales. "Ependymal Tumors". In Central Nervous System Intraoperative Cytopathology, 97–109. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8429-5_7.

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10

Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser e Peter Strasser. "Ependymal Tumors". In Imaging Brain Diseases, 1481–511. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_60.

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Atti di convegni sul tema "Ependymin"

1

Witt, Hendrik, Martin Sill, Khalida Wani, Steve Mack, David Capper, Stephanie Heim, Pascal Johann et al. "Abstract 3094: Epigenetic classification of ependymal brain tumors across age groups". In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3094.

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2

Mettri, D., A. MALLOUHI, S. BARTSCH, G. WIDHALM, B. KIESEL e D. PRAYER. "Strukturelle und mikrostrukturelle MRT Bildgebung für die Differenzierung zwischen spinalem Ependymom und Astrozytom: Eine retrospektive Studie". In 101. Deutscher Röntgenkongress und 9. Gemeinsamer Kongress der DRG und ÖRG. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1703444.

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3

Piccirillo, Sara Grazia Maria, Inma Spiteri, Andrea Sottoriva, Anestis Touloumis, Suzan Ber, Stephen J. Price, Richard Heywood et al. "Abstract 5016: The human sub-ependymal zone harbors glioblastoma precursors and represents a distinct therapeutic target." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5016.

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