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Academic literature on the topic 'Drebrin A'

Author: Grafiati
Published: 10 December 2022
Last updated: 30 January 2023

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Journal articles on the topic "Drebrin A"

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Chew, Catherine S., Curtis T. Okamoto, Xunsheng Chen, and Ruby Thomas. "Drebrin E2 is differentially expressed and phosphorylated in parietal cells in the gastric mucosa." American Journal of Physiology-Gastrointestinal and Liver Physiology 289, no. 2 (August 2005): G320—G331. http://dx.doi.org/10.1152/ajpgi.00002.2005.

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Developmentally regulated brain proteins (drebrins) are highly expressed in brain where they may regulate actin filament formation in dendritic spines. Recently, the drebrin E2 isoform was detected in certain epithelial cell types including the gastric parietal cell. In gastric parietal cells, activation of HCl secretion is correlated with actin filament formation and elongation within intracellular canaliculi, which are the sites of acid secretion. The aim of this study was to define the pattern of drebrin expression in gland units in the intact rabbit oxyntic gastric mucosa and to initiate approaches to define the functions of this protein in parietal cells. Drebrin E2 expression was limited entirely or almost entirely to parietal cells and depended upon the localization of parietal cells along the gland axis. Rabbit drebrin E2 was cloned and found to share 86% identity with human drebrin 1a and to possess a number of cross-species conserved protein-protein interaction and phosphorylation consensus sites. Two-dimensional Western blot and phosphoaffinity column analyses confirmed that drebrin is phosphorylated in parietal cells, and several candidate phosphorylation sites were identified by mass spectrometry. Overexpression of epitope-tagged drebrin E2 led to the formation of microspikes and F-actin-rich ring-like structures in cultured parietal cells and suppressed cAMP-dependent acid secretory responses. In Madin-Darby canine kidney cells, coexpression of epitope-tagged drebrin and the Rho family GTPase Cdc42, which induces filopodial extension, produced an additive increase in the length of microspike projections. Coexpression of dominant negative Cdc42 with drebrin E2 did not prevent drebrin-induced microspike formation. These findings suggest that 1) drebrin can induce the formation of F-actin-rich membrane projections by Cdc42-dependent and -independent mechanisms; and that 2) drebrin plays an active role in directing the secretagogue-dependent formation of F-actin-rich filaments on the parietal cell canalicular membrane. Finally, the differential distribution of drebrin in parietal cells along the gland axis suggests that drebrin E2 may be an important marker of parietal cell differentiation and functionality.
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Grintsevich, Elena E. "Effects of neuronal drebrin on actin dynamics." Biochemical Society Transactions 49, no. 2 (March 19, 2021): 685–92. http://dx.doi.org/10.1042/bst20200577.

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Drebrin is a key regulator of actin cytoskeleton in neuronal cells which is critical for synaptic plasticity, neuritogenesis, and neuronal migration. It is also known to orchestrate a cross-talk between actin and microtubules. Decreased level of drebrin is a hallmark of multiple neurodegenerative disorders such as Alzheimer's disease. Despite its established importance in health and disease, we still have a lot to learn about drebrin's interactome and its effects on cytoskeletal dynamics. This review aims to summarize the recently reported novel effects of drebrin on actin and its regulators. Here I will also reflect on the most recent progress made in understanding of the role of drebrin isoforms and posttranslational modifications on its functionality.
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Shan, Yufei, Stephen Matthew Farmer, and Susan Wray. "Drebrin regulates cytoskeleton dynamics in migrating neurons through interaction with CXCR4." Proceedings of the National Academy of Sciences 118, no. 3 (January 7, 2021): e2009493118. http://dx.doi.org/10.1073/pnas.2009493118.

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Stromal cell-derived factor-1 (SDF-1) and chemokine receptor type 4 (CXCR4) are regulators of neuronal migration (e.g., GnRH neurons, cortical neurons, and hippocampal granule cells). However, how SDF-1/CXCR4 alters cytoskeletal components remains unclear. Developmentally regulated brain protein (drebrin) stabilizes actin polymerization, interacts with microtubule plus ends, and has been proposed to directly interact with CXCR4 in T cells. The current study examined, in mice, whether CXCR4 under SDF-1 stimulation interacts with drebrin to facilitate neuronal migration. Bioinformatic prediction of protein–protein interaction highlighted binding sites between drebrin and crystallized CXCR4. In migrating GnRH neurons, drebrin, CXCR4, and the microtubule plus-end binding protein EB1 were localized close to the cell membrane. Coimmunoprecipitation (co-IP) confirmed a direct interaction between drebrin and CXCR4 using wild-type E14.5 whole head and a GnRH cell line. Analysis of drebrin knockout (DBN1 KO) mice showed delayed migration of GnRH cells into the brain. A decrease in hippocampal granule cells was also detected, and co-IP confirmed a direct interaction between drebrin and CXCR4 in PN4 hippocampi. Migration assays on primary neurons established that inhibiting drebrin (either pharmacologically or using cells from DBN1 KO mice) prevented the effects of SDF-1 on neuronal movement. Bioinformatic prediction then identified binding sites between drebrin and the microtubule plus end protein, EB1, and super-resolution microscopy revealed decreased EB1 and drebrin coexpression after drebrin inhibition. Together, these data show a mechanism by which a chemokine, via a membrane receptor, communicates with the intracellular cytoskeleton in migrating neurons during central nervous system development.
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Imamura, Kosuke, Yusuke Tomita, Ryo Sato, Tokunori Ikeda, Shinji Iyama, Takayuki Jodai, Misako Takahashi, et al. "Clinical Implications and Molecular Characterization of Drebrin-Positive, Tumor-Infiltrating Exhausted T Cells in Lung Cancer." International Journal of Molecular Sciences 23, no. 22 (November 8, 2022): 13723. http://dx.doi.org/10.3390/ijms232213723.

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T cells express an actin-binding protein, drebrin, which is recruited to the contact site between the T cells and antigen-presenting cells during the formation of immunological synapses. However, little is known about the clinical implications of drebrin-expressing, tumor-infiltrating lymphocytes (TILs). To address this issue, we evaluated 34 surgical specimens of pathological stage I–IIIA squamous cell lung cancer. The immune context of primary tumors was investigated using fluorescent multiplex immunohistochemistry. The high-speed scanning of whole-slide images was performed, and the tissue localization of TILs in the tumor cell nest and surrounding stroma was automatically profiled and quantified. Drebrin-expressing T cells were characterized using drebrin+ T cells induced in vitro and publicly available single-cell RNA sequence (scRNA-seq) database. Survival analysis using the propensity scores revealed that a high infiltration of drebrin+ TILs within the tumor cell nest was independently associated with short relapse-free survival and overall survival. Drebrin+ T cells induced in vitro co-expressed multiple exhaustion-associated molecules. The scRNA-seq analyses confirmed that the exhausted tumor-infiltrating CD8+ T cells specifically expressed drebrin. Our study suggests that drebrin-expressing T cells present an exhausted phenotype and that tumor-infiltrating drebrin+ T cells affect clinical outcomes in patients with resectable squamous cell lung cancer.
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Alvarez-Suarez, Paloma, Natalia Nowak, Anna Protasiuk-Filipunas, Hiroyuki Yamazaki, Tomasz J. Prószyński, and Marta Gawor. "Drebrin Regulates Acetylcholine Receptor Clustering and Organization of Microtubules at the Postsynaptic Machinery." International Journal of Molecular Sciences 22, no. 17 (August 30, 2021): 9387. http://dx.doi.org/10.3390/ijms22179387.

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Proper muscle function depends on the neuromuscular junctions (NMJs), which mature postnatally to complex “pretzel-like” structures, allowing for effective synaptic transmission. Postsynaptic acetylcholine receptors (AChRs) at NMJs are anchored in the actin cytoskeleton and clustered by the scaffold protein rapsyn, recruiting various actin-organizing proteins. Mechanisms driving the maturation of the postsynaptic machinery and regulating rapsyn interactions with the cytoskeleton are still poorly understood. Drebrin is an actin and microtubule cross-linker essential for the functioning of the synapses in the brain, but its role at NMJs remains elusive. We used immunohistochemistry, RNA interference, drebrin inhibitor 3,5-bis-trifluoromethyl pyrazole (BTP2) and co-immunopreciptation to explore the role of this protein at the postsynaptic machinery. We identify drebrin as a postsynaptic protein colocalizing with the AChRs both in vitro and in vivo. We also show that drebrin is enriched at synaptic podosomes. Downregulation of drebrin or blocking its interaction with actin in cultured myotubes impairs the organization of AChR clusters and the cluster-associated microtubule network. Finally, we demonstrate that drebrin interacts with rapsyn and a drebrin interactor, plus-end-tracking protein EB3. Our results reveal an interplay between drebrin and cluster-stabilizing machinery involving rapsyn, actin cytoskeleton, and microtubules.
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Keon, B. H., P. T. Jedrzejewski, D. L. Paul, and D. A. Goodenough. "Isoform specific expression of the neuronal F-actin binding protein, drebrin, in specialized cells of stomach and kidney epithelia." Journal of Cell Science 113, no. 2 (January 15, 2000): 325–36. http://dx.doi.org/10.1242/jcs.113.2.325.

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To further understand the functional role that the F-actin binding protein, drebrin (developmentally regulated brain protein), plays in the regulation of F-actin, we characterized its expression in non-neuronal cells. Using nanoelectrospray mass spectrometry methods, we initially identified drebrin in non-neuronal cultured cells. Using a drebrin-specific monoclonal antibody, we were able to detect drebrin protein in several different cell lines derived from fibroblasts, astrocytomas, and simple epithelia, but not in cell lines derived from stratified epithelia. Double-label immunofluorescence experiments of cultured cell monolayers revealed the localization of drebrin at the apical plasma membrane together with a pool of submembranous F-actin. Immunoblot analysis of mouse organs revealed that, in addition to its high levels of expression in brain, drebrin was present in stomach and to a lesser degree in kidney, colon, and urinary bladder. Drebrin protein detected in the non-brain organs migrated faster through SDS-PAGE gels, indicating that the lower molecular weight embryonic brain isoform (E2) may be the prominent isoform in these organs. RT-PCR experiments confirmed the specific expression of the E2 isoform in adult stomach, kidney, and cultured cells. In situ immunofluorescence experiments revealed a cell-type specific pattern in both stomach and kidney. In stomach, drebrin was specifically expressed in the acid-secreting parietal cells of the fundic glands, where it accumulated at the extended apical membrane of the canaliculi. In kidney, drebrin was expressed in acid-secreting type A intercalated cells, where it localized specifically to the apical plasma membrane. Drebrin was expressed as well in the distal tubule epithelial cells where the protein was concentrated at the luminal surface and present at the interdigitations of the basolateral membranes.
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Ramaswamy, Madhu, Thao Do, Mary Barden, Anthony Cruz, and Richard Siegel. "A proteomic study of early signaling events regulating the Fas-FasL Death Inducing Signaling Complex (163.20)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 163.20. http://dx.doi.org/10.4049/jimmunol.188.supp.163.20.

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Abstract Clearance of activated T cells by the Fas-FasL pathway is a critical mechanism of peripheral CD4 T cell tolerance. This process is preferentially higher in the effector subset of memory CD4+ T cells due to efficient recruitment and formation of the Fas death inducing signaling complex (DISC). In order to elucidate mechanisms of this heightened apoptosis sensitivity, we tested for differential DISC interacting proteins in Fas sensitive and Fas resistant CTCL cell lines using 2D-DIGE and Mass Spectrometry. We found several candidate proteins and invitro studies were done to confirm Fas receptor interactions through overexpression and Flourescence Energy Transfer (FRET) studies. One of these targets, Drebrin, is an actin binding protein previously found to play a role in T cell synapse formation by facilitating CXCR4 recruitment. Overexpression in 293 indicates that Drebrin interacts with Fas receptor. Further, endogenous drebrin preassociates with Fas receptor and remains associated with the Fas DISC even after Fas ligation only in Type I SKW cell line. Interestingly, Fas DISC associated Drebrin gets cleaved after Fas treatment and invitro caspase cleavage studies indicate that drebrin is a specific downstream target of caspase-8. Our studies propose Drebrin as a novel Fas interacting protein. Investigations are currently underway to study the mechanisms by which Drebrin modifies the Fas-DISC dynamics and the significance of the caspase-cleaved Drebrin in this process.
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Worth, Daniel C., Catherine N. Daly, Sara Geraldo, Fazal Oozeer, and Phillip R. Gordon-Weeks. "Drebrin contains a cryptic F-actin–bundling activity regulated by Cdk5 phosphorylation." Journal of Cell Biology 202, no. 5 (August 26, 2013): 793–806. http://dx.doi.org/10.1083/jcb.201303005.

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Drebrin is an actin filament (F-actin)–binding protein with crucial roles in neuritogenesis and synaptic plasticity. Drebrin couples dynamic microtubules to F-actin in growth cone filopodia via binding to the microtubule-binding +TIP protein EB3 and organizes F-actin in dendritic spines. Precisely how drebrin interacts with F-actin and how this is regulated is unknown. We used cellular and in vitro assays with a library of drebrin deletion constructs to map F-actin binding sites. We discovered two domains in the N-terminal half of drebrin—a coiled-coil domain and a helical domain—that independently bound to F-actin and cooperatively bundled F-actin. However, this activity was repressed by an intramolecular interaction relieved by Cdk5 phosphorylation of serine 142 located in the coiled-coil domain. Phospho-mimetic and phospho-dead mutants of serine 142 interfered with neuritogenesis and coupling of microtubules to F-actin in growth cone filopodia. These findings show that drebrin contains a cryptic F-actin–bundling activity regulated by phosphorylation and provide a mechanistic model for microtubule–F-actin coupling.
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Ginosyan, Anush A., Elena E. Grintsevich, and Emil Reisler. "Neuronal drebrin A directly interacts with mDia2 formin to inhibit actin assembly." Molecular Biology of the Cell 30, no. 5 (March 2019): 646–57. http://dx.doi.org/10.1091/mbc.e18-10-0639.

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Dendritic spines (DS) are actin-rich postsynaptic terminals of neurons that are critical for higher-order brain functions. Maturation of DS is accompanied by a change in actin architecture from linear to branched filamentous structures. Presumably, the underlying cause of this is a switch in a mode of actin assembly from formin-driven to Arp2/3-mediated via an undefined mechanism. Here we present data suggesting that neuron-specific actin-binding drebrin A may be a part of such a switch. It is well documented that DS are highly enriched in drebrin A, which is critical for their plasticity and function. At the same time, mDia2 is known to mediate the formation of filopodia-type (immature) spines. We found that neuronal drebrin A directly interacts with mDia2 formin. Drebrin inhibits formin-mediated nucleation of actin and abolishes mDia2-induced actin bundling. Using truncated protein constructs we identified the domain requirements for drebrin–mDia2 interaction. We hypothesize that accumulation of drebrin A in DS (that coincides with spine maturation) leads to inhibition of mDia2-driven actin polymerization and, therefore, may contribute to a change in actin architecture from linear to branched filaments.
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Leslie, Mitch. "Drebrin shows self-restraint." Journal of Cell Biology 202, no. 5 (August 26, 2013): 720. http://dx.doi.org/10.1083/jcb.2025iti2.

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Dissertations / Theses on the topic "Drebrin A"

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Alnafisah, Rawan Saleh Ms. "Involvement of Drebrin in Microglial Activation and Inflammation." University of Toledo Health Science Campus / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=mco1533220660007988.

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Vacca, Barbara. "Régulation du trafic des protéines de la membrane apicale dans les cellules épithéliales polarisées humaines Caco-2/TC7 : Rôle du complexe Crumbs3A et de la Drebrine E2." Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4069/document.

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Des pathologies lourdes, telles que les dystrophies de la rétine et certains cancers, impliquent une désorganisation de l'épithélium et la famille Crb, dont la protéine apicale Crumbs3 (isoformes Crb3A et Crb3B) fait partie. Les protéines transmembranaires Crb possèdent un domaine intracellulaire fortement conservé et des partenaires communs. Il est donc essentiel de comprendre comment ces protéines Crb sont régulées afin de mieux appréhender ces pathologies. Pour cela, j'ai étudié le complexe de polarité apical Crb3A (Crb3A, Pals1, PATJ) impliqué dans l'établissement et le maintien de la polarité apico-basale. Je me suis, tout d'abord, intéressée à la régulation des isoformes de Crb3 par leurs partenaires (Pals1 et PATJ), puis, à la régulation des protéines de la membrane apicale, dont Crb3A, par la Drebrine E2, un nouveau partenaire de Crb3A impliqué dans l'organisation du cytosquelette d'actine et la morphogenèse apicale. Mon travail a permis de mettre en évidence: 1) la régulation de la dynamique membranaire des isoformes de Crb3 par PATJ dans les cellules Caco-2/TC7, une lignée épithéliale intestinale humaine, mais aussi, 2) d'identifier une nouvelle fonction de la Drebrine E2 dans la régulation du trafic de plusieurs protéines de la membrane apicale dans ces cellules, dont, par exemple, la DPPIV (DiPeptidyl Peptidase IV). Dans les cellules déplétées en Drebrine E2, l'expression des protéines apicales est diminuée et leur endocytose est augmentée, puis, elles sont relocalisées dans le compartiment majeur de dégradation, le lysosome
Some serious diseases like retinal dystrophies and some cancers involve epithelial cells disorganization and the Crumbs (Crb) proteins family. The apical Crb3 (Crb3A and Cr3B isoforms) protein belongs to Crb family. The transmembrane proteins Crb have a conserved intracellular domain with common partners. It is unclear how Crb proteins are regulated by their partners and this information is required to better understand these pathologies. Here, we decided to study the apical polarity Crb3A complex (Crb3A, Pals1, PATJ) which is involved in apico-basal polarity establishment and maintenance. First, I investigated Crb3 isoforms regulation by their partners (Pals1 and PATJ). Then, I studied the regulation of apical membrane proteins, such as Crb3A, by Drebrin E2, a new partner of Crb3A which is involved in actin cytoskeleton remodeling and apical morphogenesis. During my thesis, I demonstrated: 1) the regulation of Crb3 isoforms dynamics by PATJ in Caco-2/TC7 human intestinal epithelial cells, but also, 2) a new function for Drebrin E2 in regulating the trafficking of apical membrane proteins, like DPPIV (DiPeptidyl Peptidase IV). In Drebrin E2 KD cells, apical membrane proteins expression is decreased and we observe an increased endocytosis. This leads to relocalization of the apical membrane proteins to the main degradative compartment, the lysosome. These new datas suggest a role for Drebrin E2 in the regulation of apical membrane proteins recycling pathway. The Drebrin E2 KD cells phenotype is reminiscent of the microvillar inclusions disease (MVID). Now, I am trying to investigate the link between theses pathways
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Puente, Eugenia Rojas. "Turnover and localization of the actin-binding protein Drebrin in neurons." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2016. http://dx.doi.org/10.18452/17587.

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Die vorliegende Arbeit erforscht die Regulation der Expression von Drebrin; DBN (Developmentally Regulated Brain Protein) in Neuronen. DBN ist ein Protein das Actin bindet und Actin-Filamente bündeln kann. Änderungen der Morphologie der Spines verändern die synaptische Aktivität und Plastizität – wichtigen Prozessen bei der Gedächtnisbildung und Alterung des Gehirns, sowie bei geistigen Störungen bzw. Behinderungen. DBN-Expression im Alter und in einigen neurodegenerativen Krankheiten reduziert ist. Eine schwächere Expression von DBN in Spines geht außerdem mit einem Verlust an synaptischen Verbindungen einher, einem gemeinsamen Merkmal von Alterung und neurologischen Störungen wie der Alzheimer Krankheit. Diese Befunde bildeten die Motivation und Grundlage für meine Erforschung der Produktion und Lokalisierung von DBN. In meinem Projekt, habe ich den Effekt der sequenzspezifischen S647-Phosphorylierung von DBN untersucht. Die Arbeit zeigt, dass diese post-translatorische Modifikation die Stabilität von DBN reguliert. Ich habe FUNCAT-PLA und Puro-PLA für die Visualisierung von de novo synthetisierten Proteinen in situ benutzt. Mittels hochauflösender Fluoreszenz-Hybridisierung konnte ich zeigen, dass DBN nicht nur im Zellkörper sondern auch lokal in den Spines translatiert wird. Meine Resultate bieten eine Grundlage für das Verständnis der Regulierung de DBN-Konzentration in Zellen und ermöglichen die weitere Erforschung der Rolle der S647-Phosphorylierung von DBN für die Morphologie von Spines. Die Arbeit bildet außerdem eine experimentelle Plattform für weitere Studien der Rolle von DBN für Spines, sowohl in Bezug auf Stabilität als auch der synaptischen Funktion und Stabilität.
This thesis studies the abundance of the protein Drebrin; DBN (Developmentally Regulated Brain Protein) in neurons, which is an actin-binding protein capable of bundling actin filaments. Synapses in the mammalian brain are formed on tiny protrusions, called dendritic spines. Changes in spine morphology affect synaptic activity and plasticity, which are processes underlying memory formation. DBN abundance plays an important role in regulating dendritic spine morphology. Cognitive decline and neurodegenerative conditions have been shown to be linked with a decrease in DBN levels. A weakening in the expression of this protein in spines is associated with the loss of synaptic connections, a common feature of ageing and neurological disorders such as Alzheimer''s disease. This evidence was the underlying motivation for studying the localization and turnover of DBN. I studied the effect of the site-specific S647 phosphorylation of DBN and found that such post-translational modification regulates protein stability. For the project, I established several novel techniques in our laboratory, including state-of-the-art methods such as FUNCAT-PLA and Puro-PLA for the visualization of de novo synthesized proteins in situ. My results show that DBN translation occurs not only in somata but also locally in the dendrites and spines. The same observation is true for DBN transcripts, which are present both in the soma and dendrites of neurons. These observations suggest that DBN could play an important role during synaptic plasticity. My results allow the future investigation of the potential role of site-specific phosphorylation of DBN in spine morphology. This PhD thesis represents a contribution to better understanding the regulation of DBN abundance. It also provides an experimental platform for additional investigation about the role of DBN in spine morphology, regarding its stability and its correlation with synaptic maintenance and function.
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Hardy, Holly. "Cofilin and drebrin mediated regulation of the neuronal cytoskeleton in development and disease." Thesis, University of Exeter, 2017. http://hdl.handle.net/10871/31746.

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The brain is a highly complex structure; neurons extend axons which follow precise paths to make connections with their targets. This extension is guided by a specialised and highly motile structure at the axon tip -the growth cone- which integrates guidance cues to steer the axon through the environment. Aberrant pathfinding is likely to result in developmental impairments causing disruption to brain functions underlying emotion learning and memory. Furthermore, pre-existing connections are constantly remodelled, the ability to do so declines with age, and can have huge impacts on quality of life and well-being. Examining how changes in growth cone behaviour triggered by external cues occurs is crucial for understanding processes in both development and disease. Controlled reorganisation of growth cone cytoskeletal components, such as actin filaments, generate membrane protrusions forming lamellipodia and filopodia. Filopodium formation is commonly associated with sensing the mechanical and chemical environment of the cell. Despite our understanding of the guidance choices that can be made, how filopodia transmit information at a molecular level leading to profound changes in morphology, motility and directionality remains largely unknown. Various actin-binding proteins regulate the number, stability and branching of filopodia. They may therefore have a key role in priming or abrogating the ability of the growth cone to respond to a given guidance cue. I have shown that the actin binding proteins drebrin and cofilin, whilst displaying opposing molecular activities on actin filaments, work synergistically in a temporally regulated manner. A fluorescent membrane marker combined with tagged cofilin and drebrin enabled accurate correlation of cofilin and drebrin dynamics with growth cone morphology and filopodial turnover in live neurons. In contrast to previous in vitro experiments, cofilin was found to enhance the effect of drebrin to promote filopodia formation in intact neurons, and that growth cone spread was significantly constrained when cofilin was knocked down. Importantly, this adds to our understanding of how the two actin binding proteins contribute to directed motility in neuronal growth cone filopodia during guidance. Furthermore, following acute treatment with low concentrations of the repulsive guidance cue semaphorin-3A, neuronal growth cones expressing cofilin displayed increased morphological complexity and filopodial stability. This suggests that traditional collapse signals may serve as pause signals allowing neurons to increase the surface area to sense the environment adequately and enable precise wiring decisions. Remodeling of the cytoskeleton is perturbed in a number of degenerative diseases including Alzheimer's, Huntington's, and Amyotrophic Lateral Sclerosis. These conditions are associated with widespread synaptic loss, resulting in memory loss, cognitive impairment, and movement disorders which leads to severe deterioration in quality of life for those afflicted in addition to wider negative socioeconomic impacts. How widespread synaptic loss occurs is poorly understood. One common characteristic is neuronal stress which can be initiated through different conditions such as neuroinflammation, energetic stress, glutamate excitotoxicity, and accumulation of misfolded proteins, all of which have been associated with perturbation of the actin cytoskeleton and the initiation of the cofilin-actin rod stress response. Dysfunction of the cytoskeleton can lead to the disruption of synaptic activity by blocking the delivery of elements such as organelles and proteins required for maintenance of the synapse. Modulating this stress response offers an approach to protecting the integrity of normal synaptic function. Actin interacting protein-1 is a conserved actin binding protein that enhances the filament disassembly activity of cofilin. I have discovered that AIP-1 has a potent ability to prevent the formation of cofilin rods which are thought to contribute to the neuronal dysfunction in several neurodegenerative disorders, even when they are treated with amyloid-β or subjected to metabolic stress. This is the first study to demonstrate a molecular mechanism for preventing rod formation in the presence of a neuronal stressor and has the potential to protect against rod formation by other stressors associated with disease such as inflammation and excitotoxicity. AIP-1 offers the exciting possibility of a means to reverse cofilin rod formation and the subsequent cytoskeletal pathology associated with dementia and has potential for therapeutic exploitation in human disease. Furthermore, it is the first study to demonstrate that AIP-1 localises to areas of rapid actin remodeling in neuronal growth cones. Exploiting the action of AIP-1 therefore represents an exciting and novel therapeutic avenue to tackle neurodegeneration.
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Sonego, Martina. "The role of fascin and drebrin in neuroblast migration in the postnatal brain." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-fascin-and-drebrin-in-neuroblast-migration-in-the-postnatal-brain(2a0251cb-d86a-46f0-99ad-9f2b340b6b36).html.

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After birth, stem cells in the subventricular zone (SVZ) generate neuroblasts that migrate along he rostral migratory stream (RMS) to become inerneurons in the olfactory bulb (OB). This migration is a fundamental event controlling the proper integration of new neurons in a pre-existing synaptic network. Many regulators of neuroblast migration have been identified; however, still very little is known about the intracellular molecular mechanisms controlling this process. We have investigated the function of fascin and drebin, two actin-binding proteins highly expressed by RMS neuroblasts in the postnatal mammalian brain. We show that fascin-1 ko mice display an abnormal RMS and a smaller OB. Bromodeoxyuridine labeling experiments show that lasck of fascin significantly impairs neuroblast migration, but does not affect cell proliferation. Moreover, fascin depletion alters the polarized morphology of rat neuroblasts. Protein kinase C (PKC)-dependent posphoylation of fascin on Ser39 regulates its actin-bundling function. Postnatal electroporation of phosphomimetic (S39D) or nonphosphorylatable (S39A) fascin variants followed by time-lapse imaging microscopy (FLIM) studies in rat neuroblasts reveal that the interaction between fascin and PKC can be modulated by cannabinoid signaling, which controls neuroblast migration in vivo. These findings identify fascin as a crucial regulator of neuroblast motility. We propose that a tightly regulated phospho/dephosphofascin cycle modulated by extracellular signals is required for the polarized migration of stem cell-derived neuroblasts. Depletion of drebrin using different RNAi approaches affects neuroblast morphology and impairs neuroblast migration both in vitro and in vivo. Drebrin phosphorylation on Ser142 by Cdk5 promotes actin bundling and microtubule binding. Electroporation of phosphomimetic (S142D) or non-phosphorylatable (S142A) drebrin followed by time-lapse imaging shows decreased neuroblast migration compared to control. Our findings demonstrate that drebrin is necessary for efficient neuroblast migration and suggest that its phosphorylation on Ser142 plays an important role in regulating neuroblast orientation along the RMS.
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Rehm, Kerstin [Verfasser], and Stefan [Akademischer Betreuer] Linder. "Drebrin preserves endothelial integrity by stabilizing nectin at adherens junctions / Kerstin Rehm. Betreuer: Stefan Linder." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2013. http://d-nb.info/1045024384/34.

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Vliet, Vanessa van. "Drebrin, ein Aktin-Bindeprotein, und seine Rolle in der Zell-Zell- und Zell-Matrix-Adhäsion in humanen Endothelzellen." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-98827.

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Willmes, Claudia Gisela [Verfasser]. "Investigation of hippocampal synaptic transmission and plasticity in mice deficient in the actin-binding protein Drebrin / Claudia Gisela Willmes." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1140487078/34.

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Gallrein, Christian [Verfasser]. "The actin-binding protein Drebrin and its implications for Alzheimer's Disease using the model organism C. elegans / Christian Gallrein." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1219904724/34.

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Rojas, Puente Eugenia [Verfasser], Hanspeter [Gutachter] Herzel, Britta [Gutachter] Eickholt, and Matthew [Gutachter] Larkum. "Turnover and localization of the actin-binding protein Drebrin in neurons / Eugenia Rojas Puente ; Gutachter: Hanspeter Herzel, Britta Eickholt, Matthew Larkum." Berlin : Lebenswissenschaftliche Fakultät, 2016. http://d-nb.info/1113686138/34.

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Books on the topic "Drebrin A"

1

Shirao, Tomoaki, and Yuko Sekino, eds. Drebrin. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5.

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Kunev, Trifon. Sitni drebni kato kamilcheta. Sofii͡a︡: "Stŭrshel" OOD, 1992.

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Shirao, Tomoaki, and Yuko Sekino. Drebrin: From Structure and Function to Physiological and Pathological Roles. Springer, 2017.

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Shirao, Tomoaki, and Yuko Sekino. Drebrin: From Structure and Function to Physiological and Pathological Roles. Springer, 2018.

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Shirao, Tomoaki, and Yuko Sekino. Drebrin: From Structure and Function to Physiological and Pathological Roles. Springer, 2017.

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Love and Lights: David Drebin. teNeues Publishing Company, 2018.

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Publishers, Koren. Mechilta DRebbi Yishmael. Toby Press LLC, The, 2019.

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Books, Daab. David Drebin: Love & Other Stories (Photo Bks.). daab, 2007.

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Leibson, Art. Sam Dreben: The Fighting Jew (Great West & Indian Series No 67). Westernlore Publications, 1996.

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Stroud, Barry. The Pursuit of Philosophy. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198809753.003.0003.

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This chapter reflects on a long philosophical career. According to the author, what attracted him to philosophy was in part precisely the idea that it wasn’t like getting a job or following a professional career. He thought of philosophy as something you studied just for its own sake. The author also shares his life as a graduate student at Harvard University, where he was influenced by the likes of Burton Dreben and Rogers Albritton. He went to Berkeley in 1961, and cites his erstwhile colleague Thompson Clarke as the one philosopher to whom he owes the most. The author concludes by asserting that what he and his fellow philosophers have been doing is similar to the kind of investigation undertaken by greats such as Plato, Aristotle, René Descartes, David Hume, and Immanuel Kant.
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Book chapters on the topic "Drebrin A"

1

Chen, Haiqi, Michelle W. M. Li, and C. Yan Cheng. "Drebrin and Spermatogenesis." In Advances in Experimental Medicine and Biology, 291–312. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_17.

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Shirao, Tomoaki, and Yuko Sekino. "General Introduction to Drebrin." In Advances in Experimental Medicine and Biology, 3–22. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_1.

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Takahashi, Hideto, and Yusuke Naito. "Drebrin and Spine Formation." In Advances in Experimental Medicine and Biology, 157–81. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_10.

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Ishizuka, Yuta, and Kenji Hanamura. "Drebrin in Alzheimer’s Disease." In Advances in Experimental Medicine and Biology, 203–23. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_12.

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Ludwig-Peitsch, Wiebke K. "Drebrin at Junctional Plaques." In Advances in Experimental Medicine and Biology, 313–28. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_18.

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Ludwig-Peitsch, Wiebke K. "Juxtanuclear Drebrin-Enriched Zone." In Advances in Experimental Medicine and Biology, 329–36. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_19.

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Ludwig-Peitsch, Wiebke K. "Drebrin in Renal Glomeruli." In Advances in Experimental Medicine and Biology, 337–45. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_20.

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Hayashi, Kensuke. "Cell Shape Change by Drebrin." In Advances in Experimental Medicine and Biology, 83–101. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_6.

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Sekino, Yuko, Noriko Koganezawa, Toshiyuki Mizui, and Tomoaki Shirao. "Role of Drebrin in Synaptic Plasticity." In Advances in Experimental Medicine and Biology, 183–201. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_11.

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Shirao, Tomoaki, Noriko Koganezawa, Hiroyuki Yamazaki, Kenji Hanamura, and Kazuyuki Imamura. "Localization of Drebrin: Light Microscopy Study." In Advances in Experimental Medicine and Biology, 105–18. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56550-5_7.

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Conference papers on the topic "Drebrin A"

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Xu, Shi-Qiong, Simone Buraschi, Alaide Morcavallo, Marco Genua, Tomoaki Shirao, Stephen C. Peiper, Leonard G. Gomella, Antonino Belfiore, Renato V. Iozzo, and Andrea Morrione. "Abstract 4945: A novel role for drebrin in regulating progranulin bioactivity in bladder cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4945.

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Arp, Daniel, Michael Spreitzenbarth, Malte Hübner, Hugo Gascon, and Konrad Rieck. "Drebin: Effective and Explainable Detection of Android Malware in Your Pocket." In Network and Distributed System Security Symposium. Reston, VA: Internet Society, 2014. http://dx.doi.org/10.14722/ndss.2014.23247.

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Mishra, Jyotiprakash, Sanjay K. Sahay, Hemant Rathore, and Lokesh Kumar. "Duplicates in the Drebin Dataset and Reduction in the Accuracy of the Malware Detection Models." In 2021 26th IEEE Asia-Pacific Conference on Communications (APCC). IEEE, 2021. http://dx.doi.org/10.1109/apcc49754.2021.9609892.

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Rocha, Vanderson da Silva, Diego Kreutz, Jonas Pontes, and Eduardo Feitosa. "Avaliação de Métodos de Classificação baseados em Regras de Associação para Detecção de Malwares Android." In Simpósio Brasileiro de Segurança da Informação e de Sistemas Computacionais. Sociedade Brasileira de Computação - SBC, 2022. http://dx.doi.org/10.5753/sbseg.2022.225321.

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O nosso principal objetivo e apresentar uma análise exploratória do desempenho e da viabilidade de três modelos de regras de associação existentes na literatura (CBA, CMAR, CPAR) no contexto de classificação de malwares Android. Além disso, desenvolvemos também um novo modelo de classificação baseado em regras de associação e qualidade de regras, denominado EQAR, que estende o algoritmo clássico ECLAT. Para fins de comparação dos quatro modelos, utilizamos três datasets frequentemente utilizados para o treino de modelos de detecção de malwares Android: DREBIN-215, KronoDroid Emulador e KronoDroid Dispositivo Real. Os resultados indicam que os métodos de classificação baseados em regras de associação apresentam bons resultados, entretanto, os metodos avaliados dificilmente conseguem atingir a estabilidade de métricas e os resultados numéricos alcançados por modelos de aprendizado de máquina, como RandomForest e SVM, no domínio de detecção de malwares Android.
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