Auswahl der wissenschaftlichen Literatur zum Thema „MGlu Receptors“
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Zeitschriftenartikel zum Thema "MGlu Receptors"
Chaki, Shigeyuki, Hiroyuki Koike und Kenichi Fukumoto. „Targeting of Metabotropic Glutamate Receptors for the Development of Novel Antidepressants“. Chronic Stress 3 (Januar 2019): 247054701983771. http://dx.doi.org/10.1177/2470547019837712.
Der volle Inhalt der QuelleBruno, Valeria, Giuseppe Battaglia, Agata Copani, Mara D'Onofrio, P. Di Iorio, Antonio De Blasi, Daniela Melchiorri, Peter J. Flor und Ferdinando Nicoletti. „Metabotropic Glutamate Receptor Subtypes as Targets for Neuroprotective Drugs“. Journal of Cerebral Blood Flow & Metabolism 21, Nr. 9 (September 2001): 1013–33. http://dx.doi.org/10.1097/00004647-200109000-00001.
Der volle Inhalt der QuelleMarciniak, Marcin, Barbara Chruścicka, Tomasz Lech, Grzegorz Burnat und Andrzej Pilc. „Expression of group III metabotropic glutamate receptors in the reproductive system of male mice“. Reproduction, Fertility and Development 28, Nr. 3 (2016): 369. http://dx.doi.org/10.1071/rd14132.
Der volle Inhalt der QuelleHagena, Hardy, und Denise Manahan-Vaughan. „Role of mGlu5 in Persistent Forms of Hippocampal Synaptic Plasticity and the Encoding of Spatial Experience“. Cells 11, Nr. 21 (24.10.2022): 3352. http://dx.doi.org/10.3390/cells11213352.
Der volle Inhalt der QuelleJohnson, M. P., E. S. Nisenbaum, T. H. Large, R. Emkey, M. Baez und A. E. Kingston. „Allosteric modulators of metabotropic glutamate receptors: lessons learnt from mGlu1, mGlu2 and mGlu5 potentiators and antagonists“. Biochemical Society Transactions 32, Nr. 5 (26.10.2004): 881–87. http://dx.doi.org/10.1042/bst0320881.
Der volle Inhalt der QuelleStorto, M., M. Sallese, L. Salvatore, R. Poulet, DF Condorelli, P. Dell'Albani, MF Marcello et al. „Expression of metabotropic glutamate receptors in the rat and human testis“. Journal of Endocrinology 170, Nr. 1 (01.07.2001): 71–78. http://dx.doi.org/10.1677/joe.0.1700071.
Der volle Inhalt der QuelleHofmann, Christopher S., Sheridan Carrington, Andrew N. Keller, Karen J. Gregory und Colleen M. Niswender. „Regulation and functional consequences of mGlu4 RNA editing“. RNA 27, Nr. 10 (08.07.2021): 1220–40. http://dx.doi.org/10.1261/rna.078729.121.
Der volle Inhalt der QuelleHERMANS, Emmanuel, und R. A. John CHALLISS. „Structural, signalling and regulatory properties of the group I metabotropic glutamate receptors: prototypic family C G-protein-coupled receptors“. Biochemical Journal 359, Nr. 3 (25.10.2001): 465–84. http://dx.doi.org/10.1042/bj3590465.
Der volle Inhalt der QuelleLeembruggen, Anita J. L., Yuqing Lu, Haozhe Wang, Volkan Uzungil, Thibault Renoir, Anthony J. Hannan, Lincon A. Stamp, Marlene M. Hao und Joel C. Bornstein. „Group I Metabotropic Glutamate Receptors Modulate Motility and Enteric Neural Activity in the Mouse Colon“. Biomolecules 13, Nr. 1 (09.01.2023): 139. http://dx.doi.org/10.3390/biom13010139.
Der volle Inhalt der QuelleTong, Qingchun, Raogo Ouedraogo und Annette L. Kirchgessner. „Localization and function of group III metabotropic glutamate receptors in rat pancreatic islets“. American Journal of Physiology-Endocrinology and Metabolism 282, Nr. 6 (01.06.2002): E1324—E1333. http://dx.doi.org/10.1152/ajpendo.00460.2001.
Der volle Inhalt der QuelleDissertationen zum Thema "MGlu Receptors"
Reid, Morag. „Group I mGlu receptors : desensitization properties and modulation of cerebrocortical glutamate release“. Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311428.
Der volle Inhalt der QuelleSharpe, Erica Frances. „Antinociception by systemic metabotropic glutamate receptor ligands“. Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368395.
Der volle Inhalt der QuelleBossi, Simon. „Récepteurs présynaptiques métabotropiques du glutamate : études fonctionnelles au sein du système nerveux central de rongeur à l'aide de nouveaux outils pharmacologiques“. Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS488.
Der volle Inhalt der QuelleMetabotropic glutamate receptors (mGlus) are known to modulate excitatory transmission in the Central Nervous System. Among them, those situated at the pre-synaptic level behave like autoreceptors, their activation leading to a decrease in glutamate release. Functional studies of the different mGlus have been hampered by the lack of selective pharmacological tools specifically targeting a given subgroup of these receptors. As a first step, using electrophysiological and calcium fluorometry techniques, we validated new specific pharmacological tools acting on mGlu2 (a nanobody, positive allosteric modulator, PAM) and mGlu4 (OptoGluNAM4.1, a negative allosteric modulator, NAM) on rodent hippocampal and cerebellar slices, respectively. We then used the OptoGluNAM4.1 in the cerebellar cortex to demonstrate, for the first time, the involvement of mGlu4 in a physiopathological condition: cerebellar ischemia. Using more conventional pharmacological tools, we were also able to show the existence of a dialog between mGlu4 and A1 (Adenosine type 1) receptors at the level of the synapse between parallel fibers and Purkinje cells. Whether this dialog results from functional interactions between the signaling pathways of these pre-synaptic dimeric receptors and/or is a consequence of their physical association in heterodimers is presently under study
Petersson, Marcus. „Beyond AMPA and NMDA: Slow synaptic mGlu/TRPC currents : Implications for dendritic integration“. Licentiate thesis, KTH, Computational Biology, CB, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-24833.
Der volle Inhalt der QuelleIn order to understand how the brain functions, under normal as well as pathological conditions, it is important to study the mechanisms underlying information integration. Depending on the nature of an input arriving at a synapse, different strategies may be used by the neuron to integrate and respond to the input. Naturally, if a short train of high-frequency synaptic input arrives, it may be beneficial for the neuron to be equipped with a fast mechanism that is highly sensitive to inputs on a short time scale. If, on the contrary, inputs arriving with low frequency are to be processed, it may be necessary for the neuron to possess slow mechanisms of integration. For example, in certain working memory tasks (e. g. delay-match-to-sample), sensory inputs may arrive separated by silent intervals in the range of seconds, and the subject should respond if the current input is identical to the preceeding input. It has been suggested that single neurons, due to intrinsic mechanisms outlasting the duration of input, may be able to perform such calculations. In this work, I have studied a mechanism thought to be particularly important in supporting the integration of low-frequency synaptic inputs. It is mediated by a cascade of events that starts with activation of group I metabotropic glutamate receptors (mGlu1/5), and ends with a membrane depolarization caused by a current that is mediated by canonical transient receptor potential (TRPC) ion channels. This current, denoted ITRPC, is the focus of this thesis.
A specific objective of this thesis is to study the role of ITRPC in the integration of synaptic inputs arriving at a low frequency, < 10 Hz. Our hypothesis is that, in contrast to the well-studied, rapidly decaying AMPA and NMDA currents, ITRPC is well-suited for supporting temporal summation of such synaptic input. The reason for choosing this range of frequencies is that neurons often communicate with signals (spikes) around 8 Hz, as shown by single-unit recordings in behaving animals. This is true for several regions of the brain, including the entorhinal cortex (EC) which is known to play a key role in producing working memory function and enabling long-term memory formation in the hippocampus.
Although there is strong evidence suggesting that ITRPC is important for neuronal communication, I have not encountered a systematic study of how this current contributes to synaptic integration. Since it is difficult to directly measure the electrical activity in dendritic branches using experimental techniques, I use computational modeling for this purpose. I implemented the components necessary for studying ITRPC, including a detailed model of extrasynaptic glutamate concentration, mGlu1/5 dynamics and the TRPC channel itself. I tuned the model to replicate electrophysiological in vitro data from pyramidal neurons of the rodent EC, provided by our experimental collaborator. Since we were interested in the role of ITRPC in temporal summation, a specific aim was to study how its decay time constant (τdecay) is affected by synaptic stimulus parameters.
The hypothesis described above is supported by our simulation results, as we show that synaptic inputs arriving at frequencies as low as 3 - 4 Hz can be effectively summed. We also show that τdecay increases with increasing stimulus duration and frequency, and that it is linearly dependent on the maximal glutamate concentration. Under some circumstances it was problematic to directly measure τdecay, and we then used a pair-pulse paradigm to get an indirect estimate of τdecay.
I am not aware of any computational model work taking into account the synaptically evoked ITRPC current, prior to the current study, and believe that it is the first of its kind. We suggest that ITRPC is important for slow synaptic integration, not only in the EC, but in several cortical and subcortical regions that contain mGlu1/5 and TRPC subunits, such as the prefrontal cortex. I will argue that this is further supported by studies using pharmacological blockers as well as studies on genetically modified animals.
QC 20101005
Bradley, Sophie Jane. „Regulation and pharmacological manipulation of the type 5 metabotropic glutamate (mGlu5) receptor“. Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/9391.
Der volle Inhalt der QuelleScholler, Pauline. „De la compréhension de la dynamique structurale des récepteurs mGlu au développement de nouveaux agents d’intérêt thérapeutique“. Thesis, Montpellier 1, 2013. http://www.theses.fr/2013MON13519.
Der volle Inhalt der QuelleGlutamate is the main excitatory neurotransmitter in the central nervous system. It notably acts on eight metabotropic glutamate receptors (mGluR), which are G protein coupled receptor responsible for the modulation of synaptic transmission. mGluRs are promising pharmacological targets to treat neurological, psychiatric or neurodegenerative diseases such as depression, schizophrenia or Parkinson's disease. Unfortunately, so far, no drug acting at mGluR is accessible to patients, but several molecules are in clinical trials. The main objective of my thesis has been the study of the structural dynamics of mGluR, for which the molecular mechanism allowing activation are still poorly understood. These receptors are known to form constitutive dimers, with each subunit composed of a large extracellular domain which bind glutamate and a transmembrane domain responsible for G protein activation and where synthetic allosteric modulators bind. A key step in the activation process could be the relative reorientation of the two extracellular domains in the dimer upon glutamate binding. We first developed an orthogonal labeling method of each mGlu subunits by fusion with a suicide enzyme (SNAP-/CLIP-tag) that we combined with time-resolved Förster resonance energy transfer measurements to show that in a heterologous system, mGlu subunits can associate as strict and functional heterodimers. Our experiments also revealed a specific association pattern: mGlu subunits from group I, mGlu1 and mGlu5, can associate with each other, but not with those from group II and III, which can also associate with each other. Then we improved the technology to develop the first conformational sensor to monitor mGluR activation. We were able to monitor in real time in live cells the conformational changes occurring in the mGlu receptor upon activation, and we proved that the variation in FRET signal is correlated with the activation state of the receptor. This allowed us to confirm the activation model proposed based on the crystal structures of the isolated extracellular domains, which consist of a relative movement of the dimer extracellulair domains upon activation. Moreover, this sensor makes it possible to easily discriminate between full and partial agonists, and to better understand the allosteric mechanisms occurring in the mGluR (especially the action mode of positive and negative allosteric modulators binding in the transmembrane domain). This conformational sensor strategy was further applied to study the activation of other receptors (GPCR or tyrosine kinase receptors), and to develop screening assays compatible with high-throughput formats. Finally, we developed innovative ligands acting on mGluRs using single-domain antibodies from llamas. These activating ligands seem to bind to a new site on the surface of the receptor, offering new possibilities to develop better treatment acting at mGluRs
Goyet, Elise. „Dynamique et fonction des interactions entre récepteurs du glutamate et de la dopamine“. Thesis, Montpellier, 2017. http://www.theses.fr/2017MONTT019.
Der volle Inhalt der QuelleIn some specific brain areas, synergism between glutamate and dopamine transmission is required to induce synaptic plasticity. Metabotropic glutamate receptor mGlu5 and dopamine receptor D1 are both known to control synaptic plasticity. Moreover, multiple lines of evidence converge toward the ability of G-protein coupled receptors to form dynamic heteromers thereby creating new entities with unique properties. Focusing on the hypothesis of receptor heteromerization, my PhD project aimed at investigating the molecular mechanisms underlying a functional interplay between mGlu5 and D1 receptors.To address this issue, a first part of this work consisted in improving single-cell Bioluminescent Resonance Energy Transfer (BRET) imaging, a technology enabling to study real time protein-protein interaction dynamics in living cells. Using the Nanoluciferase, an extremely bright luciferase, we characterized a faster and higher resolution single-cell BRET imaging technique with unprecedented performance in terms of temporal and spatial resolution, duration of signal stability and signal sensitivity. In the second part of this project, we showed that mGlu5 and D1 can form heteromers in heterologous expression system. The above-mentioned improvements of single-cell BRET imaging technique allowed to evidence the occurrence and the dynamics of mGlu5/D1 heteromers in cultured primary neurons. Furthermore, our results showed that the co-expression of mGlu5 and D1 receptors modifies single receptor properties to favor calcium signaling by increasing mGlu5 constitutive activity and creating a D1 agonist-induced activation of Ca2+ release from intracellular stores.These findings advance our knowledge about the molecular basis of the glutamate/dopamine functional dialogue to control neuronal communication in physiological conditions. Further investigation will help the dissection of the mGlu5/D1 heteromer specific signaling pathway with the hope of defining new therapeutics that may selectively modulate heteromer function and thus bypass undesirable side effects
Imre. „Group II metabotropic glutamate (mGlu2/3) receptors potential drug targets for the treatment of schizophrenia and anxiety? /“. [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 2006. http://irs.ub.rug.nl/ppn/297586998.
Der volle Inhalt der QuelleBrown-Wright, Sian Heledd. „Investigating metabotropic glutamate receptor 5 (mGlu5) as a novel therapeutic target in motor neuron disease (MND)“. Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/22583/.
Der volle Inhalt der QuellePhilibert, Clémentine. „Le récepteur métabotropique du glutamate mGlu2 interagit avec et transactive le récepteur tyrosine kinase TrkB : rôle dans la réponse comportementale aux antipsychotiques glutamatergiques“. Thesis, Université de Montpellier (2022-….), 2022. http://www.theses.fr/2022UMONT019.
Der volle Inhalt der QuelleSchizophrenia is a multifactorial debilitating mental disorder affecting 1 % of the world population characterized by three classes of symptoms: positive symptoms (e.g. hallucinations), negative symptoms (e.g. social isolation) and cognitive deficits (e.g. impaired working memory). Current antipsychotics such as typical and atypical antipsychotics, targeting dopamine D2 receptor and serotonin 5-HT2A receptor respectively, are able to treat efficiently the positive symptoms and partially the negative symptoms. However, antipsychotics treating efficiently the three classes of symptoms is still an unmet need. The metabotropic glutamate mGlu2 receptor (mGluR2) keeps on attracting particular attention given its implication in schizophrenia. This G protein-coupled receptor (GPCR) is the main target of a new generation of antipsychotics currently under clinical trial, treating efficiently the three class of symptoms without displaying any side effects. However, mGluR2 signaling in the brain and its pathological disturbances remain poorly characterized. Specific characterization of mGluR2 signaling in the brain was previously challenging due to a high homology of sequences with the structurally close metabotropic glutamate mGluR3 receptor, which complicated the production of specific ligands or antibodies. We have taken advantage of a single lama chain antibody (nanobody) specifically targeting mGluR2 in order to purify the endogenous receptor and its interacting proteins from mouse prefrontal cortex, a brain region known to strongly express mGluR2 but also highly disturbed in schizophrenia. This interactome was characterized by high resolution mass spectrometry and bioinformatics annotations of the gene ontologies of the candidate protein partners revealed high relevance to mGluR2 functions. One of these interactors revealed to be very attractive: the receptor tyrosine kinase TrkB. Highly significant in our AP-MS analysis, the mRNA of this rec eptor tyrosine kinase has been shown to be decreased in the brain tissue of patients with schizophrenia in comparison to control tissues. We were able to decipher that: 1) mGluR2 and TrkB interact specifically, 2) this interaction is modulated by the conformational state of both receptors, 3) mGluR2 stimulation by its agonist transactivates TrkB in cortical neurons in the prefrontal cortex, 4) the activation of TrkB leads to the modulation of the canonical activity of mGluR2 and 5) the antipsychotic-like effects of mGluR2 agonists in preclinical model of schizophrenia are mediated by TrkB for negative and cognitive deficits rescue. In summary, this reciprocal transactivation of mGluR2 and TrkB is highly promising and might have a pathophysiological influence in psychosis such as schizophrenia, but most importantly, TrkB has a pivotal role in mediating the antipsychotic-like effect of mGluR2 ligand for symptoms resisting so far to current antipsychotics
Bücher zum Thema "MGlu Receptors"
Ngomba, Richard Teke, Giuseppe Di Giovanni, Giuseppe Battaglia und Ferdinando Nicoletti, Hrsg. mGLU Receptors. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7.
Der volle Inhalt der QuelleGiovanni, Giuseppe Di, Richard Teke Ngomba, Ferdinando Nicoletti und Giuseppe Battaglia. mGLU Receptors. Humana, 2017.
Den vollen Inhalt der Quelle findenGiovanni, Giuseppe Di, Richard Teke Ngomba, Ferdinando Nicoletti und Giuseppe Battaglia. MGLU Receptors. Springer International Publishing AG, 2018.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "MGlu Receptors"
Perry, Christina J., M. Foster Olive und Andrew J. Lawrence. „mGlu5 Signaling: A Target for Addiction Therapeutics?“ In mGLU Receptors, 1–14. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_1.
Der volle Inhalt der QuelleMorin, Nicolas, und Thérèse Di Paolo. „mGlu5 Receptors in Parkinson’s Disease and MPTP-Lesioned Monkeys: Behavior and Brain Molecular Correlates“. In mGLU Receptors, 183–205. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_10.
Der volle Inhalt der Quellevan Luijtelaar, Gilles, Valerio D’Amore, Ines Santolini und Richard T. Ngomba. „Is There a Future for mGlu5-Positive Allosteric Modulators in Absence Epilepsy? A Comparison with Ethosuximide“. In mGLU Receptors, 207–24. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_11.
Der volle Inhalt der QuelleJia, Zhengping, und Graham Collingridge. „Regulation of Hippocampal mGluR-Dependent Long-Term Depression by GluA2-Dependent Cofilin-Mediated Actin Remodeling“. In mGLU Receptors, 225–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_12.
Der volle Inhalt der QuelleFerraguti, Francesco. „Metabotropic Glutamate Receptors in Amygdala Functions“. In mGLU Receptors, 241–77. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_13.
Der volle Inhalt der QuelleGuida, Francesca, Enza Palazzo, Livio Luongo, Ida Marabese, Vito de Novellis, Sabatino Maione und Francesco Rossi. „Supraspinal Metabotropic Glutamate Receptors: An Endogenous Substrate for Alleviating Chronic Pain and Related Affective Disorders“. In mGLU Receptors, 15–31. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_2.
Der volle Inhalt der QuelleGubellini, Paolo, Liliya Iskhakova, Yoland Smith und Marianne Amalric. „Metabotropic Glutamate Receptors and Parkinson’s Disease: Basic and Preclinical Neuroscience“. In mGLU Receptors, 33–57. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_3.
Der volle Inhalt der QuelleGonzález-Maeso, Javier. „Metabotropic Glutamate 2 (mGlu2) Receptors and Schizophrenia Treatment“. In mGLU Receptors, 59–78. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_4.
Der volle Inhalt der QuelleHagena, Hardy, und Denise Manahan-Vaughan. „mGlu5: A Metabotropic Glutamate Receptor at the Hub of Hippocampal Information Processing, Persistent Synaptic Plasticity, and Long-Term Memory“. In mGLU Receptors, 79–101. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_5.
Der volle Inhalt der QuelleMasilamoni, Gunasingh Jeyaraj, und Yoland Smith. „Neuroprotective Properties of Glutamate Metabotropic Glutamate Receptors in Parkinson’s Disease and Other Brain Disorders“. In mGLU Receptors, 103–27. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56170-7_6.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "MGlu Receptors"
Tayo, Lemmuel L., Alisha Marcelle C. Aquino, Andrea Matira und Reincess Valbuena. „Computational analysis of the binding interactions of omega-conotoxins on GABAb and mGlu receptors“. In ICBET 2022: 2022 12th International Conference on Biomedical Engineering and Technology. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3535694.3535717.
Der volle Inhalt der QuelleSeyedbarhagh, Mahsasadat, Arash Ahmadi und Majid Ahmadi. „Digital Realization for Ca2+ Waves Stimulated by the (mGlu5) Receptors“. In 2021 International Symposium on Signals, Circuits and Systems (ISSCS). IEEE, 2021. http://dx.doi.org/10.1109/isscs52333.2021.9497380.
Der volle Inhalt der QuelleLuessen, Deborah, Isabel Gallinger, Brenna Wolfe und P. Jeffrey Conn. „Metabotropic mGlu1Receptor Regulation of Cortical Inhibition and Cognitive Function: Implications in Adolescent Cocaine Exposure“. In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.138580.
Der volle Inhalt der QuelleLuessen, Deborah, Brenna Wolfe, Mac Meadows und P. Jeffrey Conn. „Metabotropic mGlu1Receptor Regulation of Cortical Inhibition and Cognitive Function: Implications in Adolescent Cocaine Exposure“. In ASPET 2024 Annual Meeting Abstract. American Society for Pharmacology and Experimental Therapeutics, 2024. http://dx.doi.org/10.1124/jpet.322.952900.
Der volle Inhalt der QuelleJong, Yuh-Jiin I., Steven K. Harmon und Karen O’Malley. „Intracellular metabotropic glutamate receptor 5 (mGlu5) triggers ER calcium release distinct from cell surface counterparts in striatal neurons“. In ASPET 2023 Annual Meeting Abstracts. American Society for Pharmacology and Experimental Therapeutics, 2023. http://dx.doi.org/10.1124/jpet.122.210990.
Der volle Inhalt der QuelleGelb, Tara, Sergey Pshenichkin, Hannah A. Hathaway, Ewa Grajkowska, Barry B. Wolfe und Jarda T. Wroblewski. „Abstract A15: mGlu1 Receptors and downstream signal transduction proteins as therapeutic targets for the treatment of metastatic melanoma“. In Abstracts: AACR Special Conference on Advances in Melanoma: From Biology to Therapy; September 20-23, 2014; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.mel2014-a15.
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