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Literatura científica selecionada sobre o tema "EphrinA5"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 10 de fevereiro de 2022

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Artigos de revistas sobre o assunto "EphrinA5"

1

PRESTOZ, LAETITIA, ELLI CHATZOPOULOU, GREGORY LEMKINE, NATHALIE SPASSKY, BARBARA LEBRAS, TETSUSHI KAGAWA, KATZUHIRO IKENAKA, BERNARD ZALC e JEAN-LÉON THOMAS. "Control of axonophilic migration of oligodendrocyte precursor cells by Eph–ephrin interaction". Neuron Glia Biology 1, n.º 1 (fevereiro de 2004): 73–83. http://dx.doi.org/10.1017/s1740925x04000109.

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The migration of oligodendrocyte precursor cells (OPCs) is modulated by secreted molecules in their environment and by cell–cell and matrix–cell interactions. Here, we ask whether membrane-anchored guidance cues, such as the ephrin ligands and their Eph receptors, participate in the control of OPC migration in the optic nerve. We postulate that EphA and EphB receptors, which are expressed on axons of retinal ganglion cells, interact with ephrins on the surface of OPCs. We show the expression of ephrinA5, ephrinB 2 and ephrinB3 in the migrating OPCs of the optic nerve as well as in the diencephalic sites from where they originate. In addition, we demonstrate that coated EphB2-Fc receptors, which are specific for ephrinB2/B3 ligands, induce dramatic changes in the contact and migratory properties of OPCs, indicating that axonal EphB receptors activate ephrinB signaling in OPCs. Based on these findings, we propose that OPCs are characterized by an ephrin code, and that Eph–ephrin interactions between axons and OPCs control the distribution of OPCs in the optic axonal tracts, and the progress and arrest of their migration.

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2

Pensold, Daniel, Julia Gehrmann, Georg Pitschelatow, Asa Walberg, Kai Braunsteffer, Julia Reichard, Amin Ravaei et al. "The Expression of the Cancer-Associated lncRNA Snhg15 Is Modulated by EphrinA5-Induced Signaling". International Journal of Molecular Sciences 22, n.º 3 (29 de janeiro de 2021): 1332. http://dx.doi.org/10.3390/ijms22031332.

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The Eph receptor tyrosine kinases and their respective ephrin-ligands are an important family of membrane receptors, being involved in developmental processes such as proliferation, migration, and in the formation of brain cancer such as glioma. Intracellular signaling pathways, which are activated by Eph receptor signaling, are well characterized. In contrast, it is unknown so far whether ephrins modulate the expression of lncRNAs, which would enable the transduction of environmental stimuli into our genome through a great gene regulatory spectrum. Applying a combination of functional in vitro assays, RNA sequencing, and qPCR analysis, we found that the proliferation and migration promoting stimulation of mouse cerebellar granule cells (CB) with ephrinA5 diminishes the expression of the cancer-related lncRNA Snhg15. In a human medulloblastoma cell line (DAOY) ephrinA5 stimulation similarly reduced SNHG15 expression. Computational analysis identified triple-helix-mediated DNA-binding sites of Snhg15 in promoters of genes found up-regulated upon ephrinA5 stimulation and known to be involved in tumorigenic processes. Our findings propose a crucial role of Snhg15 downstream of ephrinA5-induced signaling in regulating gene transcription in the nucleus. These findings could be potentially relevant for the regulation of tumorigenic processes in the context of glioma.

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3

Kuang, Shao-qing, Zhi-Hong Fang, Gonzalo Lopez, Weigang Tong, Hui Yang e Guillermo Garcia-Manero. "Eph Receptor Tyrosine Kinases and Ephrin Ligands Are Epigenetically Inactivated in Acute Lymphoblastic Leukemia and Are Potential New Tumor Suppressor Genes in Human Leukemia." Blood 110, n.º 11 (16 de novembro de 2007): 2128. http://dx.doi.org/10.1182/blood.v110.11.2128.2128.

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Abstract The Eph (erythroprotein-producing hepatoma amplified sequence) family receptor tyrosine kinases and their ephrin ligands (ephrins) are involved in a variety of functions in normal cell development and cancer. We have identified several members of this family as potential targets of aberrant DNA methylation using Methylated CpG Island Amplification (MCA) / DNA promoter microarray technology. This is of importance as there are no prior reports of potential Eph receptor or Ephrin epigenetic inactivation in human leukemia. To further investigate the role of Eph receptor and ephrin family genes in leukemia, we have analyzed their DNA methylation status in a panel of 23 leukemia cell lines and 65 primary ALL patient samples. Aberrant DNA methylation of 9 of these genes (EPHA4, EPHA5, EPHA6, EPHB2, EPHB3, EPHB4, EphrinA5, Ephrin B2, and EphrinB3) was detected in multiple leukemia cell lines but not in normal samples by bisulfite pyrosequencing. In ALL patient samples, the frequencies of DNA methylation detected in the promoter regions of these genes ranged from 23% to 87% for EPHA4, EPHA5, EPHA6, EPHB2, EPHB3, EPHB4, EphrinA5, Ephrin B2, and EphrinB3. Expression analysis of 3 of these genes (EPHA5, EPHB4 and Ephrin B2) in leukemia cell lines by real-time PCR further confirmed methylation associated gene silencing. Treatment of methylated/silenced cell lines with DNA methyltransferase inhibitor 5′-aza-2′-deoxycytidine resulted in gene re-expression. Forced overexpression of EPHB4 using a lentivirus transduction system in Raji cell lines resulted in decreased cell proliferation and adhesion-independent cell growth, as well as in an increase in staurosporine induction of apoptosis. In addition, EPHB4 overexpression resulted in a significant downregulation of phosphorylated Akt pathway but had no effect on mitogen-activated protein kinase pathway. In summary, we describe for the first time the epigenetic suppression of Ephrin receptors and their ligands in human leukemia, indicating that these genes may be potential tumor suppressors in leukemia. Targeting of these pathways may result in the development of new potential therapies and biomarkers for patients with ALL.

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4

Minami, Masayoshi, Tatsuya Koyama, Yuki Wakayama, Shigetomo Fukuhara e Naoki Mochizuki. "EphrinA/EphA signal facilitates insulin-like growth factor-I–induced myogenic differentiation through suppression of the Ras/extracellular signal–regulated kinase 1/2 cascade in myoblast cell lines". Molecular Biology of the Cell 22, n.º 18 (15 de setembro de 2011): 3508–19. http://dx.doi.org/10.1091/mbc.e11-03-0183.

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Insulin-like growth factor-I (IGF-I) activates not only the phosphatidylinositol 3-kinase (PI3K)–AKT cascade that is essential for myogenic differentiation but also the extracellular signal–regulated kinase (ERK) 1/2 cascade that inhibits myogenesis. We hypothesized that there must be a signal that inhibits ERK1/2 upon cell–cell contact required for skeletal myogenesis. Cell–cell contact–induced engagement of ephrin ligands and Eph receptors leads to downregulation of the Ras-ERK1/2 pathway through p120 Ras GTPase-activating protein (p120RasGAP). We therefore investigated the significance of the ephrin/Eph signal in IGF-I–induced myogenesis. EphrinA1-Fc suppressed IGF-I–induced activation of Ras and ERK1/2, but not that of AKT, in C2C12 myoblasts, whereas ephrinB1-Fc affected neither ERK1/2 nor AKT activated by IGF-I. IGF-I–dependent myogenic differentiation of C2C12 myoblasts was potentiated by ephrinA1-Fc. In p120RasGAP-depleted cells, ephrinA1-Fc failed to suppress the Ras-ERK1/2 cascade by IGF-I and to promote IGF-I–mediated myogenesis. EphrinA1-Fc did not promote IGF-I–dependent myogenesis when the ERK1/2 was constitutively activated. Furthermore, a dominant-negative EphA receptor blunted IGF-I–induced myogenesis in C2C12 and L6 myoblasts. However, the inhibition of IGF-I–mediated myogenesis by down-regulation of ephrinA/EphA signal was canceled by inactivation of the ERK1/2 pathway. Collectively, these findings demonstrate that the ephrinA/EphA signal facilitates IGF-I–induced myogenesis by suppressing the Ras-ERK1/2 cascade through p120RasGAP in myoblast cell lines.

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5

Liu, Hui, Kavi Devraj, Kerstin Möller, Stefan Liebner, Markus Hecker e Thomas Korff. "EphrinB-mediated reverse signalling controls junctional integrity and pro-inflammatory differentiation of endothelial cells". Thrombosis and Haemostasis 112, n.º 07 (2014): 151–63. http://dx.doi.org/10.1160/th13-12-1034.

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SummaryThe EphB/ephrinB receptor-ligand system is pivotal for the development of the embryonic vasculature and for angiogenesis in the adult organism. We observed that (i) the expression of ephrinB2 and ephrinB1 is up-regulated in capillaries during inflammation, that (ii) these ligands are localised on the luminal endothelial surface, and that (iii) they interact with the ephrinB-receptor EphB2 on monocyte/macrophages. This study delineates the impact of ephrinB-mediated reverse signalling on the integrity and proinflammatory differentiation of the endothelium. To this end, in vitro analyses with human cultured endothelial cells reveal that knockdown of ephrinB2 or ephrinB1 impairs monocyte transmigration through the endothelium. While ephrinB2 but not ephrinB1 interacts with PECAM-1 (CD31) in this context, reverse signalling by ephrinB1 but not ephrinB2 elicits a c-Jun N-terminal kinase (JNK)-dependent up-regulation of E-selectin expression. Furthermore, treatment of endothelial cells with soluble EphB2 receptor bodies or EphB2-overexpressing mouse myeloma cells links ephrinB2 to PECAM-1 and induces its Src-dependent phosphorylation while diminishing Src homology phosphotyrosyl phosphatase-2 (SHP-2) activity and increasing endothelial cell permeability. We conclude that extravasation of EphB2 positive leukocyte populations is facilitated by lowering the integrity of endothelial cell junctions and enhancing the pro-inflammatory phenotype of the endothelium through activation of ephrinB ligands.

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6

Riedl, Jurgen A., Dominique T. Brandt, Eduard Batlle, Leo S. Price, Hans Clevers e Johannes L. Bos. "Down-regulation of Rap1 activity is involved in ephrinB1-induced cell contraction". Biochemical Journal 389, n.º 2 (5 de julho de 2005): 465–69. http://dx.doi.org/10.1042/bj20050048.

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Ephrins are cell surface ligands that activate Eph receptor tyrosine kinases. This ligand–receptor interaction plays a central role in the sorting of cells. We have previously shown that the ephrinB–EphB signalling pathway is also involved in the migration of intestinal precursor cells along the crypts. Using the colon cell line DLD1 expressing the EphB2 receptor, we showed that stimulation of these cells with soluble ephrinB1 results in a rapid retraction of cell extensions and a detachment of cells. On ephrinB1 stimulation, the small GTPases Rho and Ras are activated and Rap1 is inactivated. Importantly, when a constitutively active Rap1 mutant was introduced into these cells, ephrinB1-induced retraction was inhibited. From these results, we conclude that down-regulation of Rap1 is a prerequisite for ephrin-induced cell retraction in colon cells.

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7

Ghosh Moulick, Ranjita, Gregor Panaitov, Liping Du, Dirk Mayer e Andreas Offenhäusser. "Neuronal adhesion and growth on nanopatterned EA5-POPC synthetic membranes". Nanoscale 10, n.º 11 (2018): 5295–301. http://dx.doi.org/10.1039/c7nr08520f.

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8

Zhou, Xuan, Liu Xiaoli, Na Xu, Lin Li, Qisi Lu, Jinfang Zhang, Bintao Huang e Qingfeng Du. "EphrinB2/EphB4 Interaction Promotes Myeloid Leukemia Cell Invasion through RhoA-Mediated Mechanism". Blood 124, n.º 21 (6 de dezembro de 2014): 1018. http://dx.doi.org/10.1182/blood.v124.21.1018.1018.

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Abstract Background and Objective: Several studies have reported the up-regulation of EphB receptor-tyrosine kinases and ephrinB ligands in a variety of tumors, suggesting a functional relation between EphB/ephrinB signaling and tumor progression. However, how they regulate the invasiveness of myeloid leukemia cells were still unknown. Our previously study suggested that EphB4 were highly expressed in patients with extramedullary leukemia compared with patients without extramedullary leukemia, which indicated that the expression of EphB4 was related with myeloid leukemia cell invasion. To address the molecular mechanism, we aimed to characterize the role of EphB4 and ephrinB2 ligands in the interaction of myeloid leukemia cells. Methods: To clarify the question, myeloid leukemia cell lines (K562 cells and THP-1 cells) treated with clustered ephrinA1–Fc proteins, ephrinB2–Fc proteins and Fc proteins were cultured in vitro, then migration and invasion were determined by transwell assay according to different time. Pulldown western immunoblot analysis were used to detect the level of GTP-RhoA and total RhoA; the phosphorylation of EphB4 and MMP9 expression were also determined by immunoblot analysis before and after the treatment of different clustered Fc proteins. Results: The results showed that after ephrinB2–Fc stimulation, the numbers of K562 cells migrating through transwell chamber were signiﬁcantly enhanced compared to Fc proteins stimulation (1.85-fold, P=0.033), meanwhile, the numbers of K562 cells invading the matrigel also enhanced (1.46 -fold, P=0.025). However, the numbers of K562 cells migrating through transwell chamber after ephrinA1–Fc stimulation didn’t signiﬁcantly increase compared to Fc proteins stimulation (P=0.411), and the numbers of K562 cells invading the matrigel also didn’t enhanced (P=0.072) after ephrinA1–Fc stimulation. Moreover, after ephrinB2–Fc stimulation, the numbers of THP-1 cells migrating through transwell chamber were signiﬁcantly enhanced compared to Fc proteins stimulation (2.25-fold, P<0.01), meanwhile, the numbers of THP-1 cells invading the matrigel also enhanced (1.66 -fold, P<0.01). However, the numbers of THP-1 cells migrating through transwell chamber and the numbers of THP-1 cells invading the matrigel didn’t signiﬁcantly enhanced (P>0.05, P>0.05) after ephrinA1–Fc stimulation. Furthermore, EphB4 immunoprecipitation followed by immunoblotting with anti-phosphotyrosine antibody revealed that EphB4 is phosphorylated on tyrosine in K562 cells after ephrinB2–Fc stimulation. Additionally, the level of active RhoA (GTP-RhoA) and MMP9 in K562 cells were both significantly increased in response to EphB4 receptor activation with its ligand ephrin-B2-Fc ( P<0.05). Conclusions: These findings suggested that EphB4/EprinB2 signaling played an important role in myeloid leukemia cells progression by promoting their migratory ability, activating RhoA activity and increasing MMP9 expression. Our findings reveal a novel regulation of this intriguing receptor/ligand family that contributes to the cell invasiveness of myeloid leukemia cells. Disclosures No relevant conflicts of interest to declare.

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9

Wang, Ting, Jing Chen, Chuan-Xi Tang, Xiao-Yan Zhou e Dian-Shuai Gao. "Inverse Expression Levels of EphrinA3 and EphrinA5 Contribute to Dopaminergic Differentiation of Human SH-SY5Y Cells". Journal of Molecular Neuroscience 59, n.º 4 (23 de maio de 2016): 483–92. http://dx.doi.org/10.1007/s12031-016-0759-y.

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Sullivan, Chelsea S., Vishwa Mohan, Paul B. Manis, Sheryl S. Moy, Young Truong, Bryce W. Duncan e Patricia F. Maness. "Developmental Regulation of Basket Interneuron Synapses and Behavior through NCAM in Mouse Prefrontal Cortex". Cerebral Cortex 30, n.º 8 (6 de abril de 2020): 4689–707. http://dx.doi.org/10.1093/cercor/bhaa074.

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Abstract Parvalbumin (PV)-expressing basket interneurons in the prefrontal cortex (PFC) regulate pyramidal cell firing, synchrony, and network oscillations. Yet, it is unclear how their perisomatic inputs to pyramidal neurons are integrated into neural circuitry and adjusted postnatally. Neural cell adhesion molecule NCAM is expressed in a variety of cells in the PFC and cooperates with EphrinA/EphAs to regulate inhibitory synapse density. Here, analysis of a novel parvalbumin (PV)-Cre: NCAM F/F mouse mutant revealed that NCAM functions presynaptically in PV+ basket interneurons to regulate postnatal elimination of perisomatic synapses. Mutant mice exhibited an increased density of PV+ perisomatic puncta in PFC layer 2/3, while live imaging in mutant brain slices revealed fewer puncta that were dynamically eliminated. Furthermore, EphrinA5-induced growth cone collapse in PV+ interneurons in culture depended on NCAM expression. Electrophysiological recording from layer 2/3 pyramidal cells in mutant PFC slices showed a slower rise time of inhibitory synaptic currents. PV-Cre: NCAM F/F mice exhibited impairments in working memory and social behavior that may be impacted by altered PFC circuitry. These findings suggest that the density of perisomatic synapses of PV+ basket interneurons is regulated postnatally by NCAM, likely through EphrinA-dependent elimination, which is important for appropriate PFC network function and behavior.

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Mais fontes

Teses / dissertações sobre o assunto "EphrinA5"

1

Gu, Jinmo. "An NF-kappaB - EphrinA5 - Dependent Communication between NG2+ Interstitial Cells and Myoblasts Promotes Muscle Growth in Neonates". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1458152802.

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2

Kimura, Kensuke. "Pathway-specific engagement of ephrinA5-EphA4/EphA5 system of the substantia nigra pars reticulata in cocaine-induced responses". Kyoto University, 2011. http://hdl.handle.net/2433/151921.

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3

Teng, Teng. "Molecular guidance of serotonin raphe neurons during development". Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066584/document.

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Sérotonine (5-HT) neurones du mésencéphale sont nés de jour embryonnaire 10 à 12, et commencent à étendre axones, peu après la neurogenèse, tant rostrale du télencéphale et caudale du tronc cérébral. Ces projections sont très garantis, mais avec un certain degré d'organisation topographique. Dans le télencéphale, le schéma de la 5-HT innervation provenant de la dorsale (B7, B6) ou de la médiane (B5-B8) se distingue des noyaux. Cependant, il n'y a pas d'études de développement détaillées systématiques chez la souris, qui sont le modèle le plus largement utilisé, en particulier pour les études génétiques. Ces données sont importantes pour rassembler afin d'analyser les effets des mutations de la souris sur la voie moléculaire défini des neurones de la sérotonine. De plus, les molécules de guidage qui dirigent ces neurones du raphé 5-HT à différentes cibles ne sont pas connus. Nous avons effectué de nombreuses études sur l'innervation 5-HT visant à détecter la façon dont la partie dorsale et les noyaux du raphé médian sont ciblées sur des régions différentes du cerveau antérieur au cours du développement.Nous avons étudié le rôle de la signalisation ephrinA-EphA dans le ciblage sélectif. Nos résultats démontrent que l'ARNm EphA5 est exprimé sélectivement dans des sous-populations distinctes de neurones du raphé sérotonine. En particulier, EphA5 présentait le plus haut niveau dans les neurones raphé de la sérotonine dorsale (B7). Les résultats des cultures d'explants in vitro et in vivo électroporation analyses indiquent que les ligands de EphA5 (ephrinA5 et ephrinA3) agissent comme des facteurs répulsifs pour les cônes de croissance de l'axone sérotoninergique. Antérograde traçage dans le ephrinA5 - / - souris ont montré des neurones mauvais ciblage du raphé dorsal projections, y compris la projection sérotoninergique. En particulier, notre analyse de tracer les études montrent que le ciblage des dorsales et raphé médian axones à différentes couches du bulbe olfactif est modifié dans le ephrinA5 KO. Cependant, nous ne savons pas à quel stade de développement de ces altérations se produisent, en particulier si cela reflète un changement dans l'orientation des tracts croissant de fibres, ou si cela reflète la maturation de développement en retard quand axones raphé et garantissent des branches dans les régions cibles spécifiques. Nous avons profité d'une nouvelle méthode morphologique, ce qui permet d'analyser l'étiquetage immunocytochimique dans 3_D. 5-HT immunomarquage, dans la projection du cerveau sérotoninergique dans 3_D. Nos résultats montrent que les fibres sérotoninergiques projetant vers le bulbe olfactif besoin d'un calendrier spécial pour entrer la cible. Le profil d'expression de ephrinA5 suggère que ephrinA5 peut être l'un des facteurs qui modulent ce moment
In mice, serotonin (5-HT) midbrain neurons are born from embryonic day 10 to 12, and start extending axons, shortly after neurogenesis, both rostrally to the telencephalon and caudally to the brainstem. These projections are highly collateralized but with some degree of topographic organization. In the telencephalon, the pattern of 5-HT innervation arising from the dorsal (B7, B6) or the medial (B5-B8) nuclei differs. However, there are no systematic detailed developmental studies in mice, which are the most extensively used model, in particular for genetic studies. Such data are important to gather in order to analyze the effects of mouse mutations on defined molecular pathway of serotonin neurons. Moreover the guidance molecules that direct these 5-HT raphe neurons to different targets are not known. We performed several studies of 5-HT innervation aimed at detecting how the dorsal and median raphe nuclei are targeted to different forebrain regions during development. We investigated the role of ephrinA-EphA signaling in selective targeting. Our results demonstrate that EphA5 mRNA is selectively expressed in distinct subpopulation of serotonin raphe neurons. Particularly, EphA5 exhibited the highest level in dorsal raphe serotonin neurons (B7). The results of in vitro explant cultures and in vivo electroporation analyses indicated that the ligands of EphA5 (ephrinA5 and ephrinA3) act as repellent factors for the serotonergic axon growth cones. Anterograde tracing in the ephrinA5 -/- mice showed mistargeting of dorsal raphe neurons projections, including the serotonergic projection. Particularly, our analysis of tracing studies show that targeting of the dorsal and median raphe axons to different layers of the olfactory bulb is altered in the ephrinA5 KO. However we do not know at what developmental stage these alterations occur, in particular whether this reflects an alteration in the orientation of ascending fiber tracts, or whether this reflects late developmental maturation when raphe axons collateralize and branch in specific target regions. We have taken advantage a new morphological method, which allows analyzing immunocytochemical labeling in 3_D. 5-HT immunolabeling, in whole brain serotonergic projection in 3_D. Our findings show that serotonergic fibers projecting to olfactory bulb require a special timing to enter the target. The expression pattern of ephrinA5 suggests that ephrinA5 can be one of the factors that modulate this timing. Overall, our results show for the first time the implication a guidance molecule for the region-specific and time-specific targeting of serotonin raphe neurons and has implications for the anatomo-functional parsing of raphe cell groups

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4

Gerstmann, Katrin [Verfasser], Jürgen [Akademischer Betreuer] Bolz, Lennart [Akademischer Betreuer] Olsson e Karl-Friedrich [Akademischer Betreuer] Schmidt. "Der Einfluss von EphrinA5 auf die Proliferation und Identität kortikaler Vorläuferzellen während der embryonalen Neurogenese / Katrin Gerstmann. Gutachter: Jürgen Bolz ; Lennart Olsson ; Karl-Friedrich Schmidt". Jena : Thüringer Universitäts- und Landesbibliothek Jena, 2014. http://d-nb.info/1052020402/34.

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5

Reißenweber, Bettina. "Der Einfluss der Hypoxie auf die Expression und Synthese verschiedener Eph-Rezeptoren und Ephrin-Liganden beim malignen Melanom". Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-101756.

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Das maligne Melanom ist die aggressivste Form von Hautkrebs und verschiedene Familien von Rezeptortyrosinkinasen sind an der Entwicklung und der verstärkten Malignität beteiligt. Eph-Rezeptoren stellen die größte Klasse der Rezeptortyrosinkinasen dar und spielen eine wichtige Rolle bei der Tumorangiogenese und -progression. Die Genexpression und Proteinsynthese verschiedener Eph-Rezeptoren und Ephrin-Liganden ist bei vielen Tumorentitäten erhöht. Aus diesem Grund sollten sie sich als Zielproteine für die Entwicklung neuer Radiopharmaka eignen. Zudem zeigen Literaturbefunde einen Einfluss der hypoxischen Zellumgebung auf die Genexpression und die Proteinsynthese verschiedener Eph-Rezeptoren und Ephrin-Liganden. Das Ziel dieser Arbeit war es, Regulationsmechanismen bei verschiedenen Eph-Rezeptoren und Ephrin-Liganden aufzuklären, welche durch ein hypoxisches Umfeld hervorgerufen werden. Dazu wurde neben einem extrinsischen Hypoxiemodell an Monolayerzellkulturen auch ein intrinsisches Hypoxiemodell in Form von Tumorsphäroiden untersucht. Da die Genexpression und die Proteinsynthese von EphA2, EphB4, EphrinA1 und EphrinB2 laut Literatur vom Malignitätsgrad abhängig sind, wurden die metastatischen Melanomzelllinien A375, A2058 und MeWo und die prämetastatische Melanomzelllinie MEL-JUSO verwendet. Die Verifizierung der experimentellen Hypoxie erfolgte durch den etablierten Hypoxiemarker [18F]Fluormisonidazol, sowie dem Nachweis der VEGF-Genexpression unter den verwendeten Kulturbedingungen. Damit konnte die Eignung der hypoxischen Systeme gezeigt werden. Unabhängig vom Hypoxiemodell war in keiner der untersuchten Zelllinien ein Einfluss der Hypoxie auf die Genexpression und Proteinsynthese von EphA2, EphB4, EphrinA1 und EphrinB2 nachweisbar. Ein gesteigerter EphA2-Gehalt in Melanomzellen ist laut Literatur mit einer Erhöhung des Metastasierungspotentials verbunden. Um diesen Einfluss innerhalb einer Zelllinie zu untersuchen, wurden transgene A375-Zellen generiert. Mit dieser Zelllinie fanden Untersuchungen zu verschiedenen Metastasierungseigenschaften statt. Dabei wurde festgestellt, dass sich die Migration der Zellen durch den erhöhten EphA2-Gehalt verringerte, dabei war die hypoxische Umgebung ohne Einfluss. Weiterhin wurde festgestellt, dass der EphA2-Rezeptor das Adhäsionsverhalten von A375-Zellen nicht beeinflusst. Auch ein Einfluss auf das invasive Verhalten konnte nicht festgestellt werden. Eine hypoxische Umgebung war in beiden Fällen nicht von Bedeutung. Aus den Ergebnissen der vorliegenden Arbeit kann geschlussfolgert werden, dass bei den untersuchten Melanomzelllinien keine Regulation der Eph-Rezeptoren und Ephrin-Liganden durch ein hypoxisches Umfeld erfolgt. Durch die ausführliche Charakterisierung des EphA2-Rezeptors in der Arbeit kann jedoch geschlussfolgert werden, dass sich der Rezeptor als potentielles Zielmolekül für die Entwicklung neuer Radiotherapeutika und Radiodiagnostika eignet, nicht jedoch für die Detektion hypoxischer Bereiche in Tumoren. Durch die nunmehr etablierte Generierung von Sphäroiden und einer Zelllinie, welche den Rezeptor verstärkt exprimiert und synthetisiert, stehen nun Zellmodelle für die weiterführende Charakterisierung und Analyse neuer Radiodiagnostika und Radiotherapeutika auf der Basis von Inhibitoren und Antikörper gegen EphA2 zur Verfügung.

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6

Holmberg, Johan. "Ephrins off the beaten path /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-720-7.

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7

Weinges, Stefan. "Molecular dissection of ephrinB reverse signaling". Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-57408.

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Filosa, Alessandro. "Neuron-glia communication via EphA4-ephrinA3 modulates LTP through glial glutamate transport". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-116043.

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9

Rodenas-Ruano, Alma Ileana. "EphrinB3 and Eph Receptors Regulate Hippocampal Synaptic Function". Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/34.

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Resumo:

EphrinB ligands and their Eph receptor tyrosine kinases are known to regulate excitatory synaptic functions in the hippocampus. In the CA3-CA1 synapse, ephrinB ligands are localized to the post-synaptic membrane, while their cognate Eph receptors can be expressed in both pre-and post-synaptic membranes. Previous studies show that interaction of ephrinB molecules with Eph receptors leads to changes in long-term potentiation (LTP), suggesting that reverse signaling through postsynaptic ephrinBs may be required for learning and memory. Our collaborative studies demonstrate that the cytoplasmic domain of ephrinB3, and hence reverse signaling, is not required for ephrinB-dependent learning and memory tasks or for LTP of these synapses. We demonstrate that ephrinB3 null mutants show changes in several synaptic proteins including reduced levels of NMDA receptor subunits. These abnormalities are not observed in ephrinB3lacZ reverse signaling mutants, supporting an Eph receptor forward signaling role for ephrinB3 in these processes. NMDA receptors are important in regulating synaptic functions and plasticity in the adult hippocampus, and Eph receptors have been shown to cluster NMDA receptors to the cell membrane. These studies show that ephrinB3 interacts with EphA4 to regulate plasma membrane levels of NR1 in Cos-1 cells and primary hippocampal neurons. In the absence of ephrinB3, NR1 levels are decreased in synaptosomal membranes, increased in microsomal tissues, but not changed in total extracts. This suggests that ephrinB3 regulates NR1 levels through protein trafficking and not gene transcription. Analysis of protein trafficking confirmed that ephrinB3 specifically interacts with EphA4 receptor to regulate NR1 exocytosis but not endocytosis in both transfected Cos-1 cells and primary hippocampal neurons. We postulate that ephrin-Eph receptor interactions are important mediators of synaptic formation and function, in part, through their regulation of NMDA receptors in the hippocampal synapse. In addition, we find that both ephrinB3KO and ephrinB3lacZ mice show an increased number of excitatory synapses, demonstrating a cytoplasmic-dependent reverse signaling role of ephrinB3 in regulating synapse number. Together, these data suggest that ephrinB3 may act like a receptor to transduce reverse signals to regulate the number of synapses formed in the hippocampus, and that it likely acts to stimulate forward signaling through Eph receptors to modulate NMDA receptor trafficking, LTP and learning.

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Foo, Shane Siang Chin. "The role of ephrinB2 in blood vessel development". Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446850/.

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The development of the vascular network is a complex process that is controlled by precisely balanced angiogenic and anti-angiogenic factors. Several studies have established that ephrinB2 and its receptor EphB4 are important regulators of angiogenic remodelling in the embryonic vasculature. The ablation of either gene in mice leads to fatal cardiovascular defects and early lethality. As ephrinB2 is expressed in different cell types within blood vessels, specifically in arterial endothelial cells, pericytes and vascular smooth muscle cells, the function of the molecule in each cell population has remained unclear. To determine the role of ephrinB2 expression in the luminal endothelial lining of blood vessels, tissue-specific knockout mice were generated with the Cre-loxP method. The resulting mutants displayed fatal defects in the development of blood vessels and the heart that resembled the phenotype of the global ephrinB2 null mice. This demonstrated that ephrinB2 is essential in the endothelial cells and that its expression in other cell types within the cardiovascular system is not sufficient to compensate for this loss. Pericytes and vascular smooth muscle cells, so-called mural cells, are associated with the endothelium and are essential for the formation of a stable and mature vascular network. To study the role of ephrinB2 in mural cells that express progressively increasing levels of the ligand during the second half of embryonic development, a transgenic mouse line expressing Cre recombinase under the control of a fragment from the PDGFR? gene was established. This permitted the generation of mural cell-specific ephrinB2 knockouts in which the investment of pericytes and smooth muscle cells in the microvasculature was impaired so the vessel wall assembly was defective. Consequently, these mutants displayed oedema, haemorrhaging and presumably died of respiratory arrest. These findings demonstrate that ephrinB2 expression in mural cells is essential for the maturation of the microvessels but apparently not for the remodelling of the endothelium. As insufficient support by mural cells and the resulting increase in blood vessel permeability is a relevant factor in human disease, such as diabetic retinopathy and tumours, the findings presented here argue that the ligand may be a potential target for therapeutic intervention.

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Mais fontes

Livros sobre o assunto "EphrinA5"

1

Simpson, George Brown. The Mt. Ephriam Cumberland Presbyterian Church and session minutes. Utica, KY: McDowell Publications, 1987.

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2

Lusby, James Vernon. Ephriam George Copeland Hughey and some of his descendants. Houston, Tex. (11100 Braesridge #2322, Houston 77071-2132): J.V. Lusby, 1996.

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3

O'Brien, Jessie J. Four Great Grandparents of New York: Robert Miller, Letitia J. Pirrie, Emily M. Powell, Ephriam Jones. Portland, Oregon: s.n., 1987.

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4

peter of mount ephriam. kingston, jamaica: jamaica pub. house, 1985.

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5

Ikegami, Richard. Genetic integration of semaphorin and ephrin pathways regulating epidermal morphogenesis in Caenorhabditis elegans. 2004.

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6

Lin, Danny Chi Chia. Identification and characterization of mPAR-3: Potential roles in ephrin B function and in a multi-protein complex implicated in cell polarity. 2002.

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Capítulos de livros sobre o assunto "EphrinA5"

1

Salajegheh, Ali. "Erythropoietin-Producing Hepatocellular Receptors A: Ephrin A1, Ephrin A2 and Ephrin A3". In Angiogenesis in Health, Disease and Malignancy, 75–87. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_14.

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2

Allocca, Chiara, e Maria Domenica Castellone. "Ephrin Receptor A2". In Encyclopedia of Signaling Molecules, 1581–87. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101649.

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3

Allocca, Chiara, e Maria Domenica Castellone. "Ephrin Receptor A2". In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101649-1.

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4

Gomez-Soler, Maricel, e Elena B. Pasquale. "Eph Receptors and Ephrins". In Encyclopedia of Molecular Pharmacology, 1–14. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-21573-6_10045-1.

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5

Salajegheh, Ali. "Erythropoietin-Producing Hepatocellular Receptors B: Ephrin B2, Ephrin B4". In Angiogenesis in Health, Disease and Malignancy, 89–96. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28140-7_15.

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6

Gale, Nicholas W., e George D. Yancopoulos. "Ephrins and their receptors: a repulsive topic?" In Molecular Bases of Axonal Growth and Pathfinding, 227–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60905-3_8.

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7

Matsuo, Koichi. "Eph and Ephrin Interactions in Bone". In Advances in Experimental Medicine and Biology, 95–103. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1050-9_10.

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Miao, Hui, e Bingcheng Wang. "Eph/Ephrin Signaling in Postnatal Epithelial Growth". In Handbook of Growth and Growth Monitoring in Health and Disease, 2811–23. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_167.

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Ieguchi, Katsuaki, e Yoshiro Maru. "Eph/Ephrin Signaling in the Tumor Microenvironment". In Advances in Experimental Medicine and Biology, 45–56. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47189-7_3.

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Martin, T. J., E. H. Allan, P. W. M. Ho, J. H. Gooi, J. M. W. Quinn, M. T. Gillespie, V. Krasnoperov e N. A. Sims. "Communication Between EphrinB2 and EphB4 Within the Osteoblast Lineage". In Advances in Experimental Medicine and Biology, 51–60. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-1-4419-1050-9_6.

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Trabalhos de conferências sobre o assunto "EphrinA5"

1

Sreeraman Kumar, Radhika, Robert J. B. Macaulay, Hannah C. Rutherford, Natalie Barkey, Jiannong Li, Jongphil Kim, John M. Koomen e David L. Morse. "Abstract 3876: EphrinB3 and EphrinB4 receptors: potential therapeutic targets in glioblastoma". In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3876.

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2

Schlesinger, Nicole. "Abstract 1236: Ephrin signaling in medulloblastoma". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1236.

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3

Tan, Wei, Suijin Yang, David Looper, Dawn Nowlin, Zhongdong Huang, Gerrit Los e Jitesh P. Jani. "Abstract 305: EphB4 and EphrinB2 regulates ovarian cancer progression". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-305.

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4

Beauchamp, Amanda, Jill Wykosky, Akiva Mintz, Denise Gibo e Waldemar Debinski. "Abstract 1218: Investigation of the mechanism and form of ephrinA1 released from cancer cells". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1218.

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5

Tye, Karen, Xixi Luo, Elizabeth Westly, Rachael J. Klein, Justin Kline e Kenneth S. Cohen. "Abstract 395: Host ephrinB2 regulates T-cells in tumor microenvironments". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-395.

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6

Salvucci, Ombretta, Dragan Maric, Fan Zhang, Xuri Li, Mark Basik, Marguerite Buchanan e Giovanna Tosato. "Abstract 3469: EphrinB2 promotes endothelial cell survival and vascular integrity". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3469.

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Gonzalez, Oscar A., Darren Seals e Waldemar Debinski. "Abstract LB-115: EphA2/ephrinA1 system may regulate invadopodia formation of glioblastoma multiforme (GBM) cells". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-115.

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Tome, Carla M. Lema, Enzo Palma, Jill Wykoski e Waldemar Debinski. "Abstract 5465: Functional and structural characterization of the high-affinity EphA2-binding site of ephrinA1". In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5465.

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Vadivel, A., G. Rey-Parra, F. Eaton e B. Thebaud. "The Axonal Guidance Cue Ephrin Promotes Alveolar Development." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4106.

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Lee, C. H., J. M. Baek, Y. J. Choi, W. H. Yoo, M. S. Lee e J. Y. Kim. "OP0263 Claudin-11 regulates bone homeostasis via bidirectional ephb4-ephrinb2 signalling". In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3828.

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