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frontiers in molecular neuroscience

April 6, 2021

frontiers in molecular neuroscience

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Open Access allows taxpayers to see the results . The human DEK oncogene regulates DNA damage response signaling and repair. Neurosci., 16 November 2020 The basal ganglia are involved in complex brain functions, from voluntary movement control to learning and reward processing, and they are implicated in numerous neurological and psychiatric disorders. Ever since Santiago Ramón y Cajal sketched his captivating panels of the microscopic structure of the brain with its vast diversity of neuronal morphology over a century ago, scientists have been drawn to this seemingly chaotic network of ... Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the buildup of β-amyloid plaques and neurofibrillary Tau tangles. Q1. (2019b). Instead, the full date and page number is required for a correct reference. Mol. Procedures and Policies of the Energy Research and Development Administration. The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. Manuscripts received last year. Impact Factor 5.639 | CiteScore 8.4More on impact ›, INSERM U1172 Centre de Recherche Jean Pierre Aubert, France. In Frontiers in Integrative Neuroscience we welcome in vitro or in vivo investigations across the molecular, cellular, and systems and behavioral level. DEK overexpression is correlated with the clinical features of breast cancer. Waidmann, S., Kusenda, B., Mayerhofer, J., Mechtler, K., and Jonak, C. (2014). Primary antibodies included DEK (1:100, BD Biosciences, mouse), cleaved caspase 3 (CC3; 1:400, Cell Signaling, rabbit), alpha-Tubulin (1:500; Cell Signaling, mouse), Tau-5 (total Tau, 1:100; Abcam, mouse), Tau-1 (unphosphorylated Tau, 1:200, Millipore, mouse) Phosphorylated Tau S262 (1:100; Abcam, rabbit), AT8 (S202/S205; 1:100; Invitrogen, mouse monoclonal), AT180 (T231/S235; 1:50; Invitrogen, mouse monoclonal), and clone PHF-1 (S396/S404; 1:50; Invitrogen, rabbit). (2003). ReMAPping the microtubule landscape: how phosphorylation dictates the activities of microtubule-associated proteins. Frontiers in Synaptic Neuroscience IF is increased by a factor of 2 and approximate percentage change is 73.8% when compared to preceding year 2017, which shows a rising trend The impact factor (IF) 2018 of Frontiers in Molecular Biosciences is 3.59, which is computed in 2019 as per it's definition.Frontiers in Molecular Biosciences IF is . Next, we tested the levels of potentially pathogenic levels of phosphorylated Tau. (F) Quantification of the mean number of intersections shows increased intersections for DEKsh cells compared to controls, as determined by Sholl analysis (***p < 0.001). Trends Mol. 11:280. doi: 10.1186/1479-5876-11-280, Boyle, J. P., Hettiarachchi, N. T., Wilkinson, J. The ubiquitous chromatin protein DEK alters the structure of DNA by introducing positive supercoils. A68: a major subunit of paired helical filaments and derivatized forms of normal Tau. Differentiation of a human neuroblastoma into neuron-like cells increases their susceptibility to transduction by herpesviral vectors. Support Center Support Center . Frontiers in Molecular Biosciences 影响因子:4.188 Frontiers in Molecular Neuroscience 影响因子:4.057 N. Frontiers in Nanotechnology. Social cognitive and affective neuroscience; Frontiers in neuroengineering; Insect molecular biology; Progress in biophysics and molecular biology; Axone (Dartmouth, N.S.) If you can't locate the report number then it might be better to cite the report as a book. This implicates DEK’s role in maintaining a balance of physiologically normally phosphorylated Tau; when Tau is hyperphosphorylated, it can aggregate into filaments and tangles within neurons (Lee et al., 1991; Morishima-Kawashima et al., 1995; Lim et al., 2014; Šimić et al., 2016; Alonso et al., 2018). 159, 175–183. J. Biol. Differentiation of the SH-SY5Y human neuroblastoma cell line. Also, activated p53 is found to be upregulated in AD brains and indirectly induces Tau phosphorylation in vitro (Hooper et al., 2007; Proctor and Gray, 2010). Rev. J. Transl. Glyceraldehyde caused Alzheimer’s disease-like alterations in diagnostic marker levels in SH-SY5Y human neuroblastoma cells. Cells were washed once more before the coverslips were mounted onto microscope slides using Prolong Gold antifade reagent with DAPI (Invitrogen). n/a. This book collates the contributions of a selected number of neuroscientists that are interested in the molecular, preclinical, and clinical aspects of neurotransmission research. Connexin 36 (Cx36), expressed primarily in neurons, is involved in the synchronous activity of neurons and . Here, we use an in vitro model, the SH-SY5Y cell line that can be differentiated to assume a neuronal morphology and phenotype. The spinal cord of vertebrate animals is comprised of intrinsic circuits that are capable of sensing the environment and generating complex motor behaviors. Modifications of autophagy influenced the Alzheimer-like changes in SH-SY5Y cells promoted by ultrafine black carbon. J. CiteScore Ranking. Athamneh, A. I. M., He, Y., Lamoureux, P., Fix, L., Suter, D. M., and Miller, K. E. (2017). (2020). The majority of gene therapy studies in the CNS have . Comput. doi: 10.1002/jcb.21511, Lim, S., Haque, M. M., Kim, D., Kim, D. J., and Kim, Y. K. (2014). Rep. 7:7292. doi: 10.1038/s41598-017-07402-6, Bilir, B., Kucuk, O., and Moreno, C. S. (2013). In this comparison, the ratio of pTau/Tau for sites in the projection domain (AT8, AT180) and PHF-1 was down-regulated in DEKsh cells, while S262 was modestly, but significantly, upregulated (Figures 4D–F; *p < 0.05; **p < 0.01; ***p < 0.001). doi: 10.1038/onc.2011.2, Proctor, C. J., and Gray, D. A. Wu, Q., Li, Z., Lin, H., Han, L., Liu, S., and Lin, Z. Cell Sci. (2009). Unlike scholarly journals, news papers do not usually have a volume and issue number. Given the neurite insufficiency and increased apoptosis noted in DEKsh cells, it is evident that differentiated neuronal cells experience significant amounts of cellular stress in the absence of DEK protein. A non-targeted shRNA (NTsh) was used as a control. The easiest way is to use a reference manager: Those examples are references to articles in scholarly journals and how they are supposed to appear in your bibliography. This issue of International Review of Neurobiology brings together cutting-edge research on neuromodulation. The human DEK oncogene stimulates β-catenin signaling, invasion and mammosphere formation in breast cancer. Output Styles. Find link is a tool written by Edward Betts.. Longer titles found: List of members of the National Academy of Sciences (Cellular and molecular neuroscience) (), Journal of Molecular Neuroscience () searching for Molecular neuroscience 178 found (284 total) alternate case: molecular neuroscience For a better visualisation in mobile or tablet, please turn it horizontal. Frontiers in Synaptic Neuroscience publishes rigorously peer-reviewed research that advances our understanding of the synaptic structure, function, plasticity and alterations in diseases. Arch. J. Mol. (2018). Testing Life-Hacks With ‘Citizen Science’: Does Stainless Steel Really Get Rid Of Garlic Smells? Early-onset, genetic AD is modeled widely in research but is less common in the human population. The citation style is built in and you can choose it in Settings > Citation Style or Paperpile > Citation Style in Google Docs. Specialty Chief Editors Misha Tsodyks at the Weizmann Institute of Science and Si Wu at the Beijing Normal . In 2007, a novel locus, SAX2, which is located on chromosome 17p13 and contains 3 genes, ankyrin repeat and FYVE domain-containing 1 (ANKFY1), β-arrestin 2 (ARRB2) and kinesin family member 1C (KIF1C), was linked to ARSACS. 169, 599–616. |, https://doi.org/10.3389/fnmol.2020.594319, https://www.frontiersin.org/articles/10.3389/fnmol.2020.594319/full#supplementary-material, Creative Commons Attribution License (CC BY). 418, 34–37. The role of DNA damage in AD pathogenesis is of growing interest, and several groups have provided evidence that impaired DNA damage repair is associated with the disease (Coppedè and Migliore, 2009; Shanbhag et al., 2019). The editor and reviewers' affiliations are the latest provided on their Loop research profiles and may not reflect their situation at the time of review. Qiu, L. (2017). Many biological and environmental factors are known to contribute to the risk of AD and associated dementias, including biological sex (Seshadri et al., 1997; Mazure and Swendsen, 2016), race (Chen and Zissimopoulos, 2018), vascular conditions (O’Brien and Markus, 2014), metabolic conditions (Craft, 2009), an education level (Karp et al., 2004), a history of depression (Ownby et al., 2006) and more. 9:337. doi: 10.3389/fnagi.2017.00337, Ownby, R. L., Crocco, E., Acevedo, A., John, V., and Loewenstein, D. (2006). Dev. doi: 10.1038/s41583-019-0240-3, Violet, M., Delattre, L., Tardivel, M., Sultan, A., Chauderlier, A., Caillierez, R., et al. Front. DEK-targeting DNA aptamers as therapeutics for inflammatory arthritis. 277, 24988–24994. (2014). (2011). Frontiers in Cellular Neuroscience is a leading journal in its field, publishing rigorously peer-reviewed research that advances our understanding of the cellular mechanisms underlying cell function in the nervous system across all species. . J. Oncol. We hypothesized that DEK loss in vitro would result in cellular and molecular signatures of dementia and AD. However, we observed significantly elevated levels of phosphorylation at sites S262. The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fnmol.2020.594319/full#supplementary-material. Foundation to MS and LPV. Cell counts were performed using Trypan blue exclusion and a Countess II automated cell counter (Life Technologies). The open access journal Frontiers in Molecular Neuroscience has existed since 2008. Support. Am. Neurosci.。简单的说,当您需要引用期刊Frontiers in Molecular Neuroscience时 . Frontiers' story began in 2007, with the first journal Frontiers in Neuroscience. Int. doi: 10.3760/cma.j.issn.0366-6999.2010.08.021, Keywords: tau, neurite formation, DEK, dementia—Alzheimer disease, tau phosphorylation, Citation: Greene AN, Parks LG, Solomon MB and Privette Vinnedge LM (2020) Loss of DEK Expression Induces Alzheimer’s Disease Phenotypes in Differentiated SH-SY5Y Cells. Cellular phosphorylation of tau by GSK-3β influences tau binding to microtubules and microtubule organisation. LetPub Scientific Journal Selector (2018-2021), Frontiers in Molecular Neuroscience published in 0, SWITZERLAND. AD is a debilitating global public health crisis on the rise, with still no cure and no infallible preventative measures or treatments. Hyperphosphorylation of Tau in PHF. For reports it is usually not individual people that are credited as authors, but a governmental department or agency like "U. S. Food and Drug Administration" or "National Cancer Institute". doi: 10.2174/092986708785909111, Grasemann, C., Gratias, S., Stephan, H., Schüler, A., Schramm, A., Klein-Hitpass, L., et al. 63, 556–567. Does not allow reviews to be publicly displayed, Only allows reviewers to display the journal they reviewed for. The loss of canonical Wnt signaling and β-catenin induces neuronal apoptosis (Inestrosa and Toledo, 2008). Although the pathological impact of Tau tangles vs. β-Amyloid plaques is debated, there is strong evidence to suggest that Tau hyperphosphorylation is a major factor in AD development (Giacobini and Gold, 2013; Kametani and Hasegawa, 2018; van der Kant et al., 2020). This was further exaggerated after neuronal differentiation (Figure 1C; p < 0.01). 8:14252. doi: 10.1038/ncomms14252, Mor-Vaknin, N., Kappes, F., Dick, A. E., Legendre, M., Damoc, C., Teitz-Tennenbaum, S., et al. Nat. Lancet Neurol. Also, using human postmortem brain samples we found that lower DEK protein expression in the anterior cingulate cortex was correlated with increasing dementia severity in women, but not men (O’Donovan et al., 2018). 13, 1705–1710. Res. Loop is the open research network that increases the discoverability and impact of researchers and their work. This highlights the importance of identifying novel potential mechanisms by which AD manifests in the brain to further our understanding of the disease and identify drug targets. Biochem. That's the subject of a recent study in Frontiers in Molecular Neuroscience. J. Alzheimers Dis. Molecular Neuroscience. Melanoma proliferation and chemoresistance controlled by the DEK oncogene. Neurosurg. Frontiers in Molecular Neuroscience FRONT MOL NEUROSCI ISSN. After washing with PBS, cells were permeabilized with 0.1% Triton X-100 for 5 min, then washed with PBS again. Mol. doi: 10.1016/S1474-4422(16)00067-3, Miao, J., Jing, J., Shao, Y., and Sun, H. (2020). doi: 10.1093/nar/gkr454, Khodadoust, M. S., Verhaegen, M., Kappes, F., Riveiro-Falkenbach, E., Cigudosa, J. C., Kim, D. S., et al. 30, 293–300. Neurodegener. Publications started with an inaugural Research Topic centered on molecular mechanisms of the regulation of excitatory and inhibitory synapses in the brain - also known as E-I balance. 6:52. doi: 10.1186/s40478-018-0557-6, O’Brien, J. T., and Markus, H. S. (2014). Gen. Psychiatry 63, 530–538. (2009). Category Rank; Biochemistry, Genetics and Molecular Biology - Molecular Biology . Importantly, Tau primers were designed to recognize all isoforms of Tau mRNA. Nat. Studying the relationship between DEK loss and nuclear Tau with the onset of AD pathology could provide more insight into the role of DNA damage in AD and neurodegeneration. The collection of articles ranges from molecules and mechanisms involved in regulating homeostasis and neuronal excitability to therapeutic mechanisms tailored to restore homeostatic function. Phosphorylation of Tau at different sites can alter its function. 84, 755–767. Frontiers Media SA (1997). A low-fat diet in combination with limited caloric consumption prevents activation of the brain's immune cells — called microglia — in aging mice, shows research published today in Frontiers in Molecular Neuroscience. At Frontiers, while we recognize the interest of journal-level Impact Factors, we believe these should not be used to evaluate the merit of . Alzheimers Dement. Here, we have identified DEK as a novel player in dementia and AD by showing that DEK loss could lead to hyperphosphorylated Tau accumulation and apoptosis. 05/07/2021 Oncogene 24, 6441–6449. Loop enables you to stay up-to-date with the latest discoveries and news, connect with researchers and form new collaborations. Researchers have discovered a mechanistic link between zinc, risk genes and abnormal neuronal connections in autism; Frontiers in Molecular Neuroscience . Researchers have discovered a mechanistic link between zinc, risk genes and abnormal neuronal connections in autism; Frontiers in Molecular Neuroscience . Frontiers in Molecular Neuroscience publishes rigorously peer-reviewed research that aims to identify key molecules underlying the structure, design and function of the brain across all levels. (2018). The four phosphorylation sites of interest are indicated by a black line. Indeed, we found that DEK loss in SH-SY5Y cells results in apoptosis, aberrant neurite formation, and increased total Tau expression. Mol. Alzheimer’s disease (AD) is the most common cause of dementia, accounting for 60–80% of cases (Alzheimer’s Association, 2019a). Grain boundary decohesion by impurity segregation in a nickel-sulfur system. DEK is required for homologous recombination repair of DNA breaks. This issue of TINS contains a series of specially commissioned articles illustrating some of the latest developments in molecular neuroscience, a field which is currently being revolutionized by the application of methods taken directly from molecular genetics. IF . Sex differences in Alzheimer’s disease and other dementias. Front. These sites are associated with neuronal apoptosis (Kobayashi et al., 2003) and are found to be abnormally phosphorylated in the AD brain (Schindowski et al., 2006; Neddens et al., 2018). Relation of education and occupation-based socioeconomic status to incident Alzheimer’s disease. Engl. Composed of contributions from distinguished researchers around the world, the book explores topics such as: Neuropathic itch Peripheral neuronal mechanism of itch The role of PAR-2 in neuroimmune communication and itch Mrgprs as itch ... Recent years have seen an explosion of activity in the field of biomedical imaging in an attempt to understand the behavior of the brain in healthy and disease states. Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and . Alzheimer's disease (AD) is the most common cause of dementia and is characterized by the buildup of β-amyloid plaques and neurofibrillary Tau tangles. Figure 3. Loop enables you to stay up-to-date with the latest discoveries and news, connect with researchers and form new collaborations. However, the molecular mechanisms underlying isolation-induced neuropsychiatric disorders remain elusive. RNA was extracted using the Qiagen RNeasy Mini kit and cDNA was synthesized using the QuantiTect Reverse Transcription kit (Qiagen). Here are examples of references for authored and edited books as well as book chapters. Real-time PCR analysis to determine expression levels of Tau (F, 5′-GATTGGGTCCCTGGACAATA-3′; R, 5′-GTGGTCTGTCTTGGCTTTGG-3′) and Dek (F, 5′-TGTTAAGAAAGCAGATAGCAGGACC-3′; R, 5′-ATTAAAGGTTCATCATCTGAACTATCCTC-3′) was performed using SYBR Green PCR master mix (Invitrogen) in the StepOnePlus Real-Time PCR System (Applied Biosystems). Cell. J. Frontiers in Molecular Neuroscience is an Open Access (OA) Journal. Previously, we have shown that DEK expression promotes Wnt/β-catenin signaling. This leads to decreased synaptic efficacy, cell death, and, consequently, brain atrophy in patients. DEK is overexpressed in a majority of solid tumors (Sanchez-Carbayo et al., 2003; Grasemann et al., 2005; Wu et al., 2008; Khodadoust et al., 2009; Liu et al., 2012; Privette Vinnedge et al., 2015), and is also known to be an autoantigen in autoimmune disorders such as juvenile idiopathic arthritis (Sierakowska et al., 1993; Dong et al., 2000; Mor-Vaknin et al., 2011). Connexins are transmembrane proteins that form hemichannels allowing the exchange of molecules between the extracellular space and the cell interior. doi: 10.1016/j.trci.2018.08.009, Cheung, Y.-T., Lau, W. K.-W., Yu, M.-S., Lai, C. S.-W., Yeung, S.-C., So, K.-F., et al. doi: 10.1002/anie.201913001, Hanger, D. P., Anderton, B. H., and Noble, W. (2009). Cell. Psychiatry 70, 624–630. DEK loss, or low expression of DEK, has not been widely studied, but some reports suggest that DEK loss leads to a reduced inflammatory response (Kim et al., 2015; Mor-Vaknin et al., 2017), increased DNA damage (Smith et al., 2017), and apoptosis (Smith et al., 2017). Behaviorally, this manifests as memory loss and confusion. After Denouncing ‘Fake News,’ a Catalog of Falsehoods. doi: 10.1016/j.jalz.2019.01.010. 1443, 75–88. DNA damage and cell death are observed in dementia, while β-amyloid plaques and Tau tangles are unique to AD. This year, 259 journals were listed in the category of Neurosciences in the 2016 edition of the Journal Citation Reports (JCR), of which 37 are open-access (OA).. The expression of these receptors has been detected in GBM cell lines, in ex-vivo primary tumor cells derived from GBM patients and in situ, in GBM tissue biopsies.There is a general consensus that high-grade gliomas, including GBM, express high levels of CB2. Neuronal differentiation exacerbated cell death due to DEK loss (**p < 0.01). Oncogene 34, 2325–2336. One of its very first accepted articles, before the new journal was officially accepting submissions, was a theory on the origins of autism by journal founders Kamila and Henry Markram. We found that total Tau mRNA and protein were upregulated in differentiated DEKsh cells. 103, 1283–1293. Curr. (2008). GBM tumors are known to express both major cannabinoid-specific receptors CB1 and CB2. There are two major perspectives for understanding the biology of this complicated structure.

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