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Literatura académica sobre el tema "ERK MAPK"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 13 de febrero de 2022

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Artículos de revistas sobre el tema "ERK MAPK"

Qu, Changxiu, Ji Young Park, Min Woo Yun, Qing-tao He, Fan Yang, Kiae Kim, Donghee Ham et al. "Scaffolding mechanism of arrestin-2 in the cRaf/MEK1/ERK signaling cascade". Proceedings of the National Academy of Sciences 118, n.º 37 (10 de septiembre de 2021): e2026491118. http://dx.doi.org/10.1073/pnas.2026491118.

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Arrestins were initially identified for their role in homologous desensitization and internalization of G protein–coupled receptors. Receptor-bound arrestins also initiate signaling by interacting with other signaling proteins. Arrestins scaffold MAPK signaling cascades, MAPK kinase kinase (MAP3K), MAPK kinase (MAP2K), and MAPK. In particular, arrestins facilitate ERK1/2 activation by scaffolding ERK1/2 (MAPK), MEK1 (MAP2K), and Raf (MAPK3). However, the structural mechanism underlying this scaffolding remains unknown. Here, we investigated the mechanism of arrestin-2 scaffolding of cRaf, MEK1, and ERK2 using hydrogen/deuterium exchange–mass spectrometry, tryptophan-induced bimane fluorescence quenching, and NMR. We found that basal and active arrestin-2 interacted with cRaf, while only active arrestin-2 interacted with MEK1 and ERK2. The ATP binding status of MEK1 or ERK2 affected arrestin-2 binding; ATP-bound MEK1 interacted with arrestin-2, whereas only empty ERK2 bound arrestin-2. Analysis of the binding interfaces suggested that the relative positions of cRaf, MEK1, and ERK2 on arrestin-2 likely facilitate sequential phosphorylation in the signal transduction cascade.

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Ghanaatgar-Kasbi, Sadaf, Majid Khazaei, Azam Rastgar-Moghadam, Gordon A. Ferns, Seyed Mahdi Hassanian y Amir Avan. "The Therapeutic Potential of MEK1/2 Inhibitors in the Treatment of Gynecological Cancers: Rational Strategies and Recent Progress". Current Cancer Drug Targets 20, n.º 6 (7 de julio de 2020): 417–28. http://dx.doi.org/10.2174/1568009620666200424144303.

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The mitogen-activated protein kinase (MAPK) pathway is among the key factors in numerous cellular processes involved in tumorigenesis, suggesting it as a potential therapeutic target in gynecological cancer. MAPKs connect gene expression pathways and external stimulations. They include a network consisting of Ras, Raf or MAP3K, MEK or MAP2K, ERK or MAPK. Among these, MEK is an attractive molecular target of novel cancer therapeutics as it joints upstream activators and their corresponding downstream targets. MEK inhibitors were among the first inhibitors of the MAPK pathway entering into clinical trials. Several drugs have recently been developed as MEK inhibitors. MEK1/2 inhibitors demonstrate promising efficacy and anticancer activity to treat this malignancy and captured much attention in the past decade. Here, we summarize the role of MAPK/MEK/ERK pathway in the pathogenesis of gynecological cancer, with particular emphasis on MEK inhibitors in clinical settings, including PD-0325901, Selumetinib, Cobimetinib, Refametinib, Trametinib, Pimasertib, MEK162 and WX-554 in gynecologic cancers.

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Hiratsuka, Toru, Ignacio Bordeu, Gunnar Pruessner y Fiona M. Watt. "Regulation of ERK basal and pulsatile activity control proliferation and exit from the stem cell compartment in mammalian epidermis". Proceedings of the National Academy of Sciences 117, n.º 30 (10 de julio de 2020): 17796–807. http://dx.doi.org/10.1073/pnas.2006965117.

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Fluctuation in signal transduction pathways is frequently observed during mammalian development. However, its role in regulating stem cells has not been explored. Here we tracked spatiotemporal ERK MAPK dynamics in human epidermal stem cells. While stem cells and differentiated cells were distinguished by high and low stable basal ERK activity, respectively, we also found cells with pulsatile ERK activity. Transitions from Basalhi-Pulselo(stem) to Basalhi-Pulsehi, Basalmid-Pulsehi, and Basallo-Pulselo(differentiated) cells occurred in expanding keratinocyte colonies and in response to differentiation stimuli. Pharmacological inhibition of ERK induced differentiation only when cells were in the Basalmid-Pulsehistate. Basal ERK activity and pulses were differentially regulated by DUSP10 and DUSP6, leading us to speculate that DUSP6-mediated ERK pulse down-regulation promotes initiation of differentiation, whereas DUSP10-mediated down-regulation of mean ERK activity promotes and stabilizes postcommitment differentiation. Levels of MAPK1/MAPK3 transcripts correlated with DUSP6 and DUSP10 transcripts in individual cells, suggesting that ERK activity is negatively regulated by transcriptional and posttranslational mechanisms. When cells were cultured on a topography that mimics the epidermal−dermal interface, spatial segregation of mean ERK activity and pulses was observed. In vivo imaging of mouse epidermis revealed a patterned distribution of basal cells with pulsatile ERK activity, and down-regulation was linked to the onset of differentiation. Our findings demonstrate that ERK MAPK signal fluctuations link kinase activity to stem cell dynamics.

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Usta, Diren, Romain Sigaud, Juliane L. Buhl, Florian Selt, Viktoria Marquardt, David Pauck, Stefan Pusch et al. "LGG-17. SYNERGISTIC ACTIVITY OF MAPK INHIBITOR CLASSES REVEALED BY A NOVEL CELL-BASED MAPK ACTIVITY PEDIATRIC LOW-GRADE GLIOMA ASSAY". Neuro-Oncology 22, Supplement_3 (1 de diciembre de 2020): iii369. http://dx.doi.org/10.1093/neuonc/noaa222.399.

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Abstract Pilocytic astrocytomas (PAs) and other pediatric low-grade gliomas (pLGGs) exhibit aberrant activation of the MAPK signaling pathway caused by genetic alterations, most commonly KIAA1549:BRAF fusions, BRAF V600E and NF1 mutations. In such a single-pathway disease, novel drugs targeting the MAPK pathway (MAPKi) are prime candidates for treatment. We developed an assay suitable for pre-clinical testing of MAPKi in pLGGs, aiming at the identification of novel MAPK pathway suppressing synergistic drug combinations. We generated a reporter plasmid (pDIPZ) expressing destabilized firefly luciferase driven by a MAPK-responsive ELK-1-binding element, packaged in a lentiviral vector system. We stably transfected pediatric glioma cell lines with a BRAF fusion (DKFZ-BT66) and a BRAFV600E mutation (BT-40) background, respectively. Measurement of MAPK pathway activity was performed using the luciferase reporter. pERK protein levels were detected for validation. We performed a screen of a MAPKi library and calculated Combination Indices of selected combinations. The MAPKi library screen revealed MEK inhibitors as the class inhibiting the pathway with the lowest IC50s, followed by ERK and second generation RAF inhibitors. Synergistic effects in both BRAF-fusion and BRAFV600E mutation backgrounds were observed following combination treatments with different MAPKi classes (RAFi/MEKi, > RAFi/ERKi > MEKi/ERKi). We have generated a novel reporter assay for medium- to high-throughput pre-clinical drug testing of MAPKi in pLGG cell lines. MEK, ERK and next-generation RAF inhibitors were confirmed as potential treatment approaches for KIAA1549:BRAF and BRAFV600E mutated pLGGs. Synergistic suppression of MAPK pathway activity upon combination treatments was revealed using our assay in addition.

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Wei, Xiumei, Yu Zhang, Cheng Li, Kete Ai, Kang Li, Huiying Li y Jialong Yang. "The evolutionarily conserved MAPK/Erk signaling promotes ancestral T-cell immunity in fish via c-Myc–mediated glycolysis". Journal of Biological Chemistry 295, n.º 10 (29 de enero de 2020): 3000–3016. http://dx.doi.org/10.1074/jbc.ra119.012231.

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The mitogen-activated protein kinase (MAPK) cascade is an ancient and evolutionarily conserved signaling pathway involved in numerous physiological processes. Despite great advances in understanding MAPK-mediated regulation of adaptive immune responses in mammals, its contribution to T-cell immunity in early vertebrates remains unclear. Herein, we used Nile tilapia (Oreochromis niloticus) to investigate the regulatory roles of MAPK/extracellular signal–regulated kinase (Erk) signaling in ancestral T-cell immunity of jawed fish. We found that Nile tilapia possesses an evolutionarily conserved MAPK/Erk axis that is activated through a classical three-tier kinase cascade, involving sequential phosphorylation of RAF proto-oncogene serine/threonine-protein kinase (Raf), MAPK/Erk kinase 1/2 (Mek1/2), and Erk1/2. In Nile tilapia, MAPK/Erk signaling participates in adaptive immune responses during bacterial infection. Upon T-cell activation, the MAPK/Erk axis is robustly activated, and MAPK/Erk blockade by specific inhibitors severely impairs T-cell activation. Furthermore, signals from MAPK/Erk were indispensable for primordial T cells to proliferate and exert their effector functions. Mechanistically, activation of the MAPK/Erk axis promoted glycolysis via induction of the transcriptional regulator proto-oncogene c-Myc (c-Myc), to ensure the proper activation and proliferation of fish T cells. Our results reveal the regulatory mechanisms of MAPK/Erk signaling in T-cell immunity in fish and highlight a close link between immune signals and metabolic programs. We propose that regulation of T-cell immunity by MAPK/Erk is a basic and sophisticated strategy that evolved before the emergence of the tetrapod lineage. These findings shed light on the evolution of the adaptive immune system.

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Liu, Qinghang y Polly A. Hofmann. "Protein phosphatase 2A-mediated cross-talk between p38 MAPK and ERK in apoptosis of cardiac myocytes". American Journal of Physiology-Heart and Circulatory Physiology 286, n.º 6 (junio de 2004): H2204—H2212. http://dx.doi.org/10.1152/ajpheart.01050.2003.

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Mitogen-activated protein kinases (MAPKs) play different regulatory roles in signaling oxidative stress-induced apoptosis in cardiac ventricular myocytes. The regulation and functional role of cross-talk between p38 MAPK and extracellular signal-regulated kinase (ERK) pathways were investigated in cardiac ventricular myocytes in the present study. We demonstrated that inhibition of p38 MAPK with SB-203580 and SB-239063 enhanced H2O2-stimulated ERK phosphorylation, whereas preactivation of p38 MAPK with sodium arsenite reduced H2O2-stimulated ERK phosphorylation. In addition, pretreatment of cells with the protein phosphatase 2A (PP2A) inhibitors okadaic acid and fostriecin increased basal and H2O2-stimulated ERK phosphorylation. We also found that PP2A coimmunoprecipitated with ERK and MAPK/ERK (MEK) in cardiac ventricular myocytes, and H2O2increased the ERK-associated PP2A activity that was blocked by inhibition of p38 MAPK. Finally, H2O2-induced apoptosis was attenuated by p38 MAPK or PP2A inhibition, whereas it was enhanced by MEK inhibition. Thus the present study demonstrated that p38 MAPK activation decreases H2O2-induced ERK activation through a PP2A-dependent mechanism in cardiac ventricular myocytes. This represents a novel cellular mechanism that allows for interaction of two opposing MAPK pathways and fine modulation of apoptosis during oxidative stress.

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Zhong, Bin, Kun Jiang, Danielle L. Gilvary, Pearlie K. Epling-Burnette, Connie Ritchey, Jinhong Liu, Rosalind J. Jackson, Elizabeth Hong-Geller y Sheng Wei. "Human neutrophils utilize a Rac/Cdc42-dependent MAPK pathway to direct intracellular granule mobilization toward ingested microbial pathogens". Blood 101, n.º 8 (15 de abril de 2003): 3240–48. http://dx.doi.org/10.1182/blood-2001-12-0180.

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AbstractElevated levels of mitogen-activated protein kinase/extracellular regulatory kinase (MAPK/ERK) activity are frequently found in some cancer cells. In efforts to reduce tumor growth, attempts have been made to develop cancer therapeutic agents targeting the MAPK. Here, by use of biologic, biochemical, and gene manipulation methods in human polymorphonuclear neutrophils (PMNs), we have identified a key pathway important in normal cell function involving MAPK/ERK in PMNs for growth inhibition of Candida albicans. Contact withC albicans triggered MAPK/ERK activation in PMNs within 5 minutes, and blocking of MAPK/ERK activation, either by the pharmacologic reagent PD098059 or by dominant-negative MAPK kinase (MEK) expression via vaccinia viral delivery, suppressed antimicrobial activity. Rac and Cdc42, but not Ras or Rho, were responsible for this MAPK/ERK activation. Expression of dominant-negative Rac (N17Rac) or Cdc42 (N17Cdc42) eliminated not only C albicans– mediated ERK phosphorylation but also phagocytosis and granule migration toward the ingested microbes, whereas dominant-negative Ras (N17Ras) and Rho (N19Rho) did not. PAK1 (p21-activated kinase 1) activation is induced by C albicans, suggesting that PAK1 may also be involved in the Rac1 activation of MAPK/ERK. We conclude from these data that Rac/Cdc42-dependent activation of MAPK/ERK is a critical event in the immediate phagocytic response of PMNs to microbial challenge. Therefore, use of MAPK pharmacologic inhibitors for the treatment of cancer may result in the interruption of normal neutrophil function. A balance between therapeutic outcome and undesirable side effects must be attained to achieve successful and safe anticancer therapy.

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Šrámek, Jan, Vlasta Němcová-Fürstová, Kamila Balušíková, Petr Daniel, Michael Jelínek y Jan Kovář. "Role of p38 MAPK pathway in apoptosis induction by saturated fatty acid in human pancreatic β-cells". Problems of Endocrinology 62, n.º 5 (22 de septiembre de 2016): 13–14. http://dx.doi.org/10.14341/probl201662513-14.

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Background. Pancreatic β-cells failure and apoptosis in response to chronically elevated concentrations of saturated fatty acids in blood was considered as one of the main causes of type 2 diabetes mellitus development. Although precise molecular mechanisms of this process are still unclear, there are some indications that the p38 MAPK signaling pathway could be involved.Aim, materials and methods. Therefore, we tested the role of p38 MAPK signaling pathway activation in apoptosis induction by SA in human pancreatic β-cells NES2Y. Crosstalk between p38 MAPK pathway activation and accompanying ERK pathway inhibition after SA application was also tested.Results. We have found that saturated SA at apoptosis-inducing concentration (1 mM) activated the p38 MAPK signaling pathway MKK3/6→p38 MAPK→MAPKAPK-2 and inhibited the ERK signaling pathway c-Raf→MEK1/2→ERK1/2. The inhibition of p38 MAPK expression by siRNA silencing had no significant effect on cell viability or the level of phosphorylated ERK pathway members after SA administration. The inhibition of p38 MAPK activity by the specific inhibitor SB202190 resulted in noticeable activation of ERK pathway members after SA treatment but in no significant effect on cell viability. p38 MAPK overexpression by plasmid transfection produced no significant influence on cell viability or ERK pathway activation after SA exposure. The activation of p38 MAPK by the specific activator anisomycin led to apoptosis induction similar to application of SA (PARP cleavage and caspase-7, -8, and -9 activation) and in inhibition of ERK pathway members.Conclusions. We demonstrated that apoptosis-inducing concentrations of SA activate the p38 MAPK signaling pathway and that this activation could be involved in apoptosis induction by SA in the human pancreatic β-cells NES2Y. However, this involvement does not seem to play a key role. Crosstalk between p38 MAPK pathway activation and ERK pathway inhibition in NES2Y cells seems likely. Thus, the ERK pathway inhibition by p38 MAPK activation does not also seem to be essential for SA-induced apoptosis.

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Bell-Horner, Cathy L., Akiko Dohi, Quynh Nguyen, Glenn H. Dillon y Meharvan Singh. "ERK/MAPK pathway regulates GABAA receptors". Journal of Neurobiology 66, n.º 13 (2006): 1467–74. http://dx.doi.org/10.1002/neu.20327.

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Vališ, Karel y Petr Novák. "Targeting ERK-Hippo Interplay in Cancer Therapy". International Journal of Molecular Sciences 21, n.º 9 (3 de mayo de 2020): 3236. http://dx.doi.org/10.3390/ijms21093236.

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Extracellular signal-regulated kinase (ERK) is a part of the mitogen-activated protein kinase (MAPK) signaling pathway which allows the transduction of various cellular signals to final effectors and regulation of elementary cellular processes. Deregulation of the MAPK signaling occurs under many pathological conditions including neurodegenerative disorders, metabolic syndromes and cancers. Targeted inhibition of individual kinases of the MAPK signaling pathway using synthetic compounds represents a promising way to effective anti-cancer therapy. Cross-talk of the MAPK signaling pathway with other proteins and signaling pathways have a crucial impact on clinical outcomes of targeted therapies and plays important role during development of drug resistance in cancers. We discuss cross-talk of the MAPK/ERK signaling pathway with other signaling pathways, in particular interplay with the Hippo/MST pathway. We demonstrate the mechanism of cell death induction shared between MAPK/ERK and Hippo/MST signaling pathways and discuss the potential of combination targeting of these pathways in the development of more effective anti-cancer therapies.

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Tesis sobre el tema "ERK MAPK"

Ma, Xun. "RASA3, a Key Player in Dopamine D2S Receptor-mediated MAPK Signaling". Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19775.

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The short form of dopamine D2 receptor (D2S) functions as a presynaptic autoreceptor on dopamine neurons and has an inhibitory effect on dopaminergic tone. D2-MAPKs pathway is involved in many physiological events like production of prolactin and tyrosine hydroxylase (TH) expression. However, the effect of D2S receptor signalling on MAPKs is cell type specific, and is not fully understood.A recent study in our lab has identified a Gαi-interacting ras-MAPK inhibitor RASA3. Here, we showed that RASA3 is the key effector in D2-induced inhibition of MAPK by knockdown of endogenous RASA3 in the GH4 cell using RASA3 siRNA. We have also transfected a dominant negative RASA3 to compete with the endogenous RASA3 for the binding site on Ras. Both RASA3-siRNA and dominant negative RASA3 blocked D2S-induced inhibition of MAPK activation, clearly implicating that RASA3 is a key effector in Gαi3-dependent D2S mediated MAPKs inhibition To determine whether RASA3’s inhibitory effect could be reconstituted in fibroblast cells, the effect of RASA3 on D2-mediated ERK1/2 activation in COS7 cells was tested. Our results show that both active Gαi2 (or Gαi3) and active RASA3 are required for optimal inhibition of ERK1/2 activation in fibroblast COS7 cells.

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Ovrén, Caroline. "Knockdown of the ERK pathway using siRNA in cultured chicken cardiomyocytes". Thesis, Linköpings universitet, Biologi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-104567.

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The ancient South American birds called tinamous (Tinamidae) have the smallest hearts known among birds and their cardiomyocytes have previously been shown to express significantly lower levels of the mitogen-activated protein kinase ERK compared to the more modern chicken (Gallus gallus). ERK is a well-known mediator of growth signalling in the heart, especially in hypertrophy. The aim of this project was to assess the effect of ERK knockdown on proliferation in cultured chicken cardiomyocytes. By transfecting these cells with a lipoplexed siRNA, ERK mRNA levels were knocked down to approximately half (45%, SD: 27%) compared to cells transfected with a negative control siRNA. The knockdown was coupled with a decreased proliferative response to insulin-like growth factor 1 (IGF-1) and foetal bovine serum (FBS). In conclusion, the ERK pathway was confirmed to be instrumental also in proliferative signalling. The results also support the notion that ERK itself is the rate-limiting step of this MAPK cascade. The low native expression of ERK in tinamou cardiomyocytes is expected to impose a strict limit on proliferative growth in response to various stimuli in these hearts. The genetic changes leading to higher expression levels, and with it the potential for larger hearts, in modern birds would have led to greatly increased evolutionary fitness by way of an increased aerobic scope and the ability to sustain flight.

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Valjent, Emmanuel. "La voie mapk/erk : un substrat neurobiologique de la dependance aux substances toxicomanogenes". Paris 6, 2001. http://www.theses.fr/2001PA066378.

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Le but de ce travail fut de valider un modele permettant l'etude des proprietes motivationnelles induites par le thc chez la souris puis d'evaluer le role de la voie de signalisation mapk/erk dans la mise en place des adaptations neuronales responsables des comportements addictifs du thc et de la cocaine. Les reponses motivationnelles induites par le thc ont ete evaluees dans le test de preference de place, en minimisant les effets dysphoriques induits par la premiere exposition a la drogue et/ou les consequences des proprietes pharmacocinetiques du compose. Ainsi, selon la dose et le protocole experimental utilise, le thc est capable d'induire a la fois des effets renforcants et aversifs. L'administration aigue de cocaine et de thc chez la souris, s'accompagne d'une augmentation transitoire de la phosphorylation des erks dans les cellules striatales. La liberation de dopamine constitue un evenement majeur dans l'activation des erks qui est totalement dependante de la stimulation des recepteurs d1 avec une contribution partielle des recepteurs d2. Les recepteurs nmda interviennent egalement dans l'activation des erks par ces deux substances. L'activation du facteur de transcription elk-1 et la regulation transcriptionnelle des genes precoces c-fos et zif268 en reponse a l'administration aigue de thc et de cocaine sont controlees par les voies erks. Enfin, le blocage des voies erks par un inhibiteur de mek (sl327) abolit la preference de place conditionnee induite par la cocaine et le thc ainsi que la sensibilisation locomotrice induite par une administration repetee de cocaine sans toutefois affecter les reponses comportementales aigues induites par ces deux drogues. L'activation des erks dans les cellules striatales constituerait un mecanisme commun d'action de ces drogues. En controlant une premiere vague de regulations geniques, cette voie de transduction jouerait un role majeur dans les adaptations neuronales responsables des comportements addictifs a long terme.

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Haupaix, Nicolas. "Régulation de la voie MEK/ERK par la signalisation éphrine lors du développement neural chez l'ascidie Ciona intestinalis". Phd thesis, Université Nice Sophia Antipolis, 2014. http://tel.archives-ouvertes.fr/tel-01059798.

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Durant ma thèse, j'ai participé à une étude fonctionnelle qui a démontré que p120-RasGAP, une protéine appartenant à la famille GAP (GTPase-activating protein), est le médiateur cytoplasmique de l'éphrine lors de l'atténuation d'ERK1/2. Pour confirmer cela, j'ai réalisé une expérience de co-immunoprécipitation et j'ai démontré que p120-RasGAP s'associe au récepteur de l'éphrine, Eph3, quand celui-ci est activé par un ligand éphrine. Ce résultat indique fortement que les signaux FGF et éphrine convergent au niveau de Ras et qu'ils contrôlent de manière antagoniste son activité. Dès lors, j'ai analysé les autres événements de spécification cellulaire impliquant l'antagonisme FGF/éphrine. Chez l'embryon d'ascidie, le signal FGF est décrit comme inducteur du destin neural dans les cellules ectodermiques qui, en absence du signal FGF, adoptent le destin épidermique. L'induction neurale des ascidies a lieu au stade 32 cellules et se traduit par la spécification de quatre précurseurs neuraux (ERK+) parmi les 16 cellules ectodermiques. J'ai démontré que le signal éphrine/Eph/RasGAP antagonise le signal FGF pour générer une activation d'ERK1/2 de type tout ou rien parmi les cellules ectodermiques. Enfin, en collaboration avec Philip Abitua, doctorant dans le laboratoire du Dr. Mike Levine (UC Berkeley), nous démontrons que l'antagonisme entre les signaux éphrine et FGF est impliqué dans la régionalisation antéro-postérieure de la plaque neurale

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Letourneux, Claire. "Rôles et partenaires de la protéine IEX-1 : une nouvelle cible des MAPK ERK". Paris 7, 2005. http://www.theses.fr/2005PA077150.

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Baker, Levenia A. "Investigation of prolactin induced activation of the MAPK/ERK and PI3 kinase in vivo /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1559853051&sid=7&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Sharp, Leslie L. "Studies on the role of the erk MAPK pathway in thymocyte lineage commitment decisions /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1999. http://wwwlib.umi.com/cr/ucsd/fullcit?p9944213.

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Hamilton, William. "Functional and biochemical analysis of ERK2 in mouse embryonic stem cells". Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5774.

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The ERK-MAPK pathway is a dynamic signaling module, conserved across Eukarya, and capable of processing a myriad of environmental and cellular signals. It has been implicated in controlling important cell fate decisions in many cell types and species. In mES cells, growth factor activation of the ERK-MAPK pathway is involved in the earliest stages of lineage segregation, however very little is currently known about the mechanism by which this is accomplished. Taking a loss-of-function gene targeting approach I have reexamined the relative contribution of ERK2 activity to FGF-ERK signaling. Although ERK2 depletion results in an attenuation of the combined ERK1/2 activity, this is compensated for by the hyperactivation of the remaining ERK1 isozyme. Normal ERK1/2 function can be restored to ERK2 deficient cells by transgenic expression of either ERK1 or ERK2, indicating a degree of functional redundancy between both isoforms. When subjected to the appropriate cues, lineage commitment proceeded normally in ERK2 deficient cells, however increased self-renewal was observed under standard culture conditions. Several attempts were made to further probe ERK1/2 function by siRNA depletion, and dominant negative inhibition of ERK1 in Erk2 knockout cells, however both approaches failed to provide further insight. Furthermore, taking a candidate approach, the role of Srf, a canonical target of ERK1/2 signaling, was examined. Initial experiments indicated a role for SRK in neural differentiation, however due to issues of culture adaptation and instability in several cell lines it was not possible to conclude this line of research within the time frame of this thesis. IP-MS/MS analysis identified several proteins known to interact with ERK2 and indicated an involvement in nuclear pore function through TPR as well as transcriptional and translational regulation through RSK proteins. Moreover, this study identified DUSP6 and DUSP9 as the primary induced dual specificity phosphatases that regulate ERK2 activity in mES cells. To further probe the functional significance of the ERK:p90RSK interaction I examined a mES cell line genetically depleted for PDK1, a crucial regulator of p90RSK function. This cell line exhibits no detectable p90RSK activity, however in contrast to studies in other cell lines, p90RSK activity is dispensable for mitogen-induced cFos expression in mES cells. Subsequent experiments demonstrated a requirement for PDK1 activity in either the specification or maintenance of mES cell derived neurons. Further analysis indicated that p90RSK may be involved in a negative feedback loop regulating ERK1/2 activity, and if so may represent a point whereby ERK1/2 activity can be manipulated. To examine this I determined the effect pharmacological inhibition of p90RSK has on ERK1/2 activity and self-renewal using a novel p90Rsk inhibitor, BI-D1870. Although treatment with BI-D1870 correlated with enhanced ERK1/2 phosphorylation, the offtarget effects this molecule exhibits made it impossible to draw any firm conclusions from these experiments. Overall this study has demonstrated a degree of redundancy between ERK1/2 isozymes in mES cells. It has highlighted the complex nature of ERK1/2 regulation as well as the robustness of this pathway to perturbations in ERK dose. Furthermore, it has underscored some of the common pitfalls encountered when studying differentiation phenotypes in mES cells. Although this study failed to highlight anything more than a coincidental relationship between ERK1/2 activity and self-renewal capacity of mES cells, it has helped to highlight some important behavioral characteristics of the FGF-MAPK pathway in mES cells and provide a platform for further study.

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Faure, Emilie. "Rôle de la signalisation purinergique dans la régulation de la migration des kératinocytes". Thesis, Aix-Marseille, 2012. http://www.theses.fr/2012AIXM4753/document.

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L'épiderme est un tissu stratifié, majoritairement constitué de kératinocytes qui forme la première barrière de l'organisme contre les agressions extérieures. Après blessure cutanée, la migration des kératinocytes est une phase cruciale de la cicatrisation. Le comportement des kératinocytes est placé sous le contrôle des molécules de la matrice extracellulaire ainsi que par les facteurs solubles (facteurs de croissance et cytokines..) sécrétés dans le microenvironnement. Les cellules résidentes ou recrutées sur le site de lésion libèrent également des nucléotides extracellulaires (ATP, UTP) dans l'environnement des kératinocytes. Dans ce travail de thèse, nous avons examiné l'impact des nucléotides extracellulaires et du récepteur purinergique P2Y2 sur la migration des kératinocytes et sur l'activité motogénique de deux facteurs de croissance, l'IGF-I et de l'EGF. Dans un premier temps, nous avons pu montrer que l'activation de P2Y2 et de la protéine hétérotrimérique Gαq inhibe l'activité de l'isoforme p110α de la PI3K sur des cellules stimulées par l'IGF. Cette inhibition de la voie PI3K/Akt aboutit à une perturbation de la mobilisation de la cortactine et de la formation des lamellipodes ainsi qu'une diminution de la vitesse de migration des kératinocytes. Dans un second temps, nous avons mis en évidence que l'activation de P2Y2 inhibe l'activation de la voie ERK1/2 par l'EGF en inhibant la phosphorylation des protéines MEK1/2, ERK1/2 et p90RSK. Nous avons établi que la conséquence de cette inhibition est la stabilisation des hémidesmosomes
The epidermis is a stratified tissue, mainly composed of keratinocytes, that forms the first barrier of the organism. When skin injury occurs, the epidermis structure is altered and many signalling pathways are activated in order to re-establish its homeostasis. Among these signalling pathways, the PI3K and MAPK ERK1/2 pathways play key roles by controlling keratinocyte migration and proliferation. The aim of this thesis was to analyse the regulation of these two signalling pathways by extracellular nucleotides, acting through purinergic receptors P2Y2 and the heterotrimeric Gαq protein and to evaluate the impact of this receptor on keratinocyte migration. Firstly, we showed that P2Y2 receptor activation inhibits PI3K p110α isoform and consequently alters keratinocyte cell shape and migration. Additionally, we showed that purinergic signalling activation inhibits EGF-induced ERK1/2 pathway activation by inhibiting the phosphorylation of MEK1/2, ERK1/2 and p90RSK proteins. As a consequence, P2Y2 stabilizes α6β4 integrin localisation into hemidesmosome-like structures and inhibits keratinocyte migration. The involvement of purinergic signalling pathway in regulation of different signalling events suggests that it may play a central role in regulation of cellular events that occurred during skin wound healing process. Moreover, our present data in association with those of the literature show that extracellular nucleotides can act as a double-edged sword in the regulation of cell migration: either activate or block cell migration in a striking cell-specific manner

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Rapozo, Viviane Younes. "Sinalização da MAPK/ERK na diferenciaçãao da oligodendroglia: efeitos de inibidores da MEK sobre a morfologia e distribuição de proteínas de oligodendrócitos/mielina in vitro". Universidade do Estado do Rio de Janeiro, 2009. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=9529.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico
A via de sinalização da cinase regulada por fatores extracelulares, da família das proteínas cinases ativadas por mitógenos (MAPK/ERK) é importante tanto para a sobrevivência como para a progressão da diferenciação de oligodendrócitos. Neste trabalho, a via da MAPK/ERK foi avaliada na oligodendroglia in vitro com a utilização de inibidores da MEK. A morfologia celular, assim como a distribuição de proteínas foram analisadas em diferentes estágios de maturação da oligodendroglia. Culturas primárias de oligodendrócitos foram tratadas com os inibidores da MEK PD98059 ou U0126, aos 5 ou 11dias in vitro (div), por 30min, 24 ou 48h. A oligodendroglia foi distinguida com marcadores estágio-específicos: A2B5, 23nucleotídeo cíclico 3 fosfodiesterase (CNPase) e proteína básica de mielina (MBP), e classificada de acordo com sua morfologia em diferentes estágios de desenvolvimento. O tratamento aumentou significativamente o número de células com morfologia mais imatura e diminuiu o número de células maduras. Além disso, aumentou o número de células redondas e sem prolongamentos as quais não puderam ser classificadas em nenhum dos estágios de desenvolvimento da oligodendroglia. Os efeitos mais evidentes foram observados logo após o menor tempo de tratamento. Células redondas eram positivas para CNPase e MBP, porém não foram marcadas com A2B5 ou com NG2, indicando que seriam células maduras incapazes de estender ou manter seus prolongamentos. De fato, estas mudanças foram acompanhadas por alterações na distribuição de proteínas de oligodendrócitos como a MBP e a CNPase, assim como alterações em proteínas de citoesqueleto, como actina, tubulina e na cinase de adesão focal (FAK). A MBP foi observada nas células tratadas em um padrão de distribuição desorganizado e disperso, oposto ao padrão contínuo que é observado nas células das culturas controle. Além disso, o tratamento causou uma desorganização na distribuição da CNPase, actina e tubulina. Nas células das culturas controle, estas proteínas apresentam um padrão organizado compondo as estruturas de citoqueleto semelhantes a nervuras. Após um pequeno período de tratamento (30min), actina e tubulina apresentaram o mesmo padrão de marcação puntiforme que a CNPase apresentou. O tratamento também reduziu os pontos de adesão focal demonstrados pela FAK. Com o decorrer do tratamento, após 24 e 48h, actina e tubulina aparentavam estar se reorganizando em um padrão filamentar. Estes resultados indicam um efeito importante da via da MAPK/ERK na ramificação e alongamento dos prolongamentos dos oligodendrócitos, com possíveis consequências para a formação da bainha de mielina.
The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway is important for both long-term survival and timing of the progression of oligodendrocyte differentiation. In this work, the MAPK/ERK signaling in oligodendroglia was studied in vitro by using MEK inhibitors. Cell morphology and distribution of proteins were analyzed in different stages of maturation. Primary cultures of oligodendroglia were treated with the MEK inhibitors PD98059 or U0126, at 5 or 11div for 30min, 24 or 48h. Oligodendroglial cells were distinguished by using stage specific markers: NG2 proteoglycan, A2B5, 23nucleotide-cyclic 3phosphodiesterase (CNPase) and myelin basic protein (MBP), and classified according to their morphology into different developmental stages. Treatment significantly increased the number of cells with more immature morphologies and decreased the number of mature cells. Furthermore, it increased the number of rounded cells that could not be classified into any of the oligodendroglial developmental stages. The strongest effects were usually observed shortly after treatment. Rounded cells were CNPase/MBP positive and they were not stained by anti-NG2 or A2B5, indicating that they were mature cells unable either to extend and/or to maintain their processes. In fact, these changes were accompanied by alterations in the distribution of the oligodendroglial proteins MBP and CNPase, and alterations in cytoskeleton proteins, as actin, tubulin and the focal adhesion kinase (FAK). MBP was observed in a continuous distribution in cell body and processes in control cultures. Furthermore, in treated cultures a disorganized pattern of distribution of CNPase, actin and tubulin was observed. In control cultures, these proteins compose the cytoskeleton vein-like structures. By the other side, after a short time of MEK inhibition (30min), actin and tubulin showed the same punctual pattern observed in CNPase distribution. Treatment also caused a reduction of focal adhesion sites showed by FAK. As treatment progressed, after 24 and 48h, actin and tubulin seemed to be rearranged into a filament-like pattern. These data showed an effect of the MAPK/ERK pathway on oligodendroglial branching, with possible consequences for the formation of the myelin sheath.

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Libros sobre el tema "ERK MAPK"

Kopas, Frank A. Soil survey of Cameron and Elk counties, Pennsylvania. [Washington, D.C.?]: Soil Conservation Service, 1993.

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Kopas, Frank A. Soil survey of Cameron and Elk counties, Pennsylvania. [Washington, D.C.]: The Service, 1993.

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Kopas, Frank A. Soil survey of Cameron and Elk counties, Pennsylvania. [Washington, D.C.?]: Soil Conservation Service, 1993.

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Casey, Steven y Jonathan Wright, eds. Mental Maps in the Era of Two World Wars. London: Palgrave Macmillan UK, 2008. http://dx.doi.org/10.1057/9780230227606.

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Peter, Waller. The Beeching era: Proposed--closed--survived. Hersham, Surrey: Ian Allan Publishing, 2013.

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Mental maps in the early Cold War era, 1945-1968. Basingstoke: Palgrave Macmillan, 2011.

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Casey, Steven y Jonathan Wright, eds. Mental Maps in the Early Cold War Era, 1945–68. London: Palgrave Macmillan UK, 2011. http://dx.doi.org/10.1057/9780230306066.

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Black, Jeremy. Historical atlas of Britain: The end of the middle ages to the Georgian era. Thrupp: Sutton Pub., 2000.

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Challenged territories: Cartographies of Greece and the Levant during the Ottoman era. Istanbul: Isis Press, 2010.

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Brownlow, Kevin. Behind the mask of innocence: The social problem films of the silent era. New York, N.Y: Knopf, 1990.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda et al. "MAPK Erk Kinase 3". En Encyclopedia of Signaling Molecules, 1046. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100755.

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Lotan, Tamara L. "PI3K/Akt/mTOR/PTEN and ERK/MAPK Pathways". En Molecular Pathology Library, 367–79. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-64096-9_21.

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Grossman, Rona y Ze’ev Paroush. "High-Throughput In Vitro Identification of Direct MAPK/Erk Substrates". En Methods in Molecular Biology, 127–35. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6424-6_9.

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Gómez-Soler, Maricel, Víctor Fernández-Dueñas y Francisco Ciruela. "GPCR-Mediated MAPK/ERK Cascade Activation in Mouse Striatal Slices". En Neuromethods, 465–72. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3064-7_29.

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Gómez-Soler, Maricel, Víctor Fernández-Dueñas y Francisco Ciruela. "GPCR-Mediated MAPK/ERK Cascade Activation in Mouse Striatal Slices". En Neuromethods, 541–49. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1522-5_33.

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Azzam, Diana G., Jasmine W. T. Tay, Melissa A. Greeve, Jennet M. Harvey y Jacqueline M. Bentel. "ERK/MAPK Regulation of the Androgen Responsiveness of Breast Cancer Cells". En Hormonal Carcinogenesis V, 429–35. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-69080-3_41.

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Shin, Sung-Young y Lan K. Nguyen. "Dissecting Cell-Fate Determination Through Integrated Mathematical Modeling of the ERK/MAPK Signaling Pathway". En Methods in Molecular Biology, 409–32. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-6424-6_29.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, Matthias Gaestel, Shiri Procaccia, Rony Seger, Shin Yasuda et al. "Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Regulated Kinase (ERK) Kinases 1/2 (MEK1/2)". En Encyclopedia of Signaling Molecules, 1081. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100810.

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Lee, Myon-Hee y Dong Suk Yoon. "A Phenotype-Based RNAi Screening for Ras-ERK/MAPK Signaling-Associated Stem Cell Regulators in C. elegans". En Methods in Molecular Biology, 207–21. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7108-4_15.

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Marchi, Matilde, Riccardo Parra, Mario Costa y Gian Michele Ratto. "Localization and Trafficking of Fluorescently Tagged ERK1 and ERK2". En MAP Kinase Signaling Protocols, 287–301. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-795-2_17.

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Actas de conferencias sobre el tema "ERK MAPK"

Sheikh, Abdul Q., Andrei Kogan y Daria A. Narmoneva. "Electromagnetic Field Mediates Capillary-Like Network Formation via MAPK/ERK Signaling Cascade". En ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206710.

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Abnormal angiogenesis (formation of capillaries) plays an important role in the impaired diabetic wound healing and has emerged as a new target area for therapeutic interventions. Pulsed magnetic field therapy, which was initially used for healing of bone fractures, has been recently introduced as a potential therapy to treat diabetic and chronic wounds [1], although the mechanisms responsible for improved healing are still unclear. Electromagnetic fields (EMF) have been shown to act as a directional cues in cellular responses such as migration and activations of several signal transduction cascades [2]. Recent literature delineates an important role of GHz EMF (i.e., with an oscillation period of a fraction of a nanosecond) in inducing rapid and sustained phosphorylation of mitrogen-activated kinase and extracellular-signal-regulated kinase (MAPK/ERK) [3]. Recent studies have also implicated MAP kinase in mediating the phosphorylation of Connexin-43 (Cx43) that accompanies regulation of cell-cell communication via connexin gap junctions [4]. Importantly, both MAPK/ERK pathway and Cx43 signaling are involved in the process of angiogenesis [5,6]. Therefore, the goal of this study was to test the hypothesis that high-frequency (7.5GHz) EMFs promote angiogenesis in vitro via MAPK/ERK and/or Cx43 signaling. We used a custom-built EMF exposure setup and a self-assembling peptide nanoscaffold as a controlled angiogenic microenvironment [7] to quantify the effect of EMF on capillary formation and underlying cellular responses.

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Li, Jiarui. "Ras mutations in the Erk-MAPK pathway and Cancer". En ISAIMS 2020: 2020 International Symposium on Artificial Intelligence in Medical Sciences. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3429889.3429891.

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Kim, Jin Young, Keon Uk Park, So Jin Shin, Il Seon Hwang, Eunyoung Ha y Hun-Mo Ryoo. "Abstract 2027: Carbamylated albumin increase MMP9 activity via ERK MAPK pathway". En 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.am2012-2027.

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Orzechowski, Amanda y Haidong Dong. "Abstract 5026: B7-H1 confers tumor chemoresistance by regulating MAPK/ERK activation". En Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-5026.

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Mazzotta, Mary M., Minetta C. Liu, Robert Clarke y Rebecca B. Riggins. "Abstract 4595: ERK/MAPK regulation of ERRγ in Tamoxifen resistant breast cancer". En 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.am10-4595.

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Jameson, Katherine L., Ashley M. Zehnder y Paul A. Khavari. "Abstract A49: The ERK/MAPK scaffold IQGAP1 is a tumor-selective target". En Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a49.

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Bryant, Kirsten, Sen Peng, Andrey Tikunov, Mariaelena Pierobon, Venugopal Gunda, Garima Tomar, Pankaj Singh et al. "Abstract 5492: Inhibition of ERK MAPK signaling increases pancreatic cancer dependency on autophagy". En Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5492.

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Dasgupta, Pritha, Priyanka Kulkarni, Nadeem S. Bhat, Ravi Gupta, Yutaka Hashimoto, Sharanjot Saini, Altaf A. Dar et al. "Abstract 4659: Cadmium induced malignant transformation involves activation of the Erk/MAPK pathway". En Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4659.

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Ryan, Meagan B., Ferran Fece de la Cruz, Leanne G. Ahronian, Sarah Phat, David T. Myers, Heather A. Shahzade, Catriona Hong y Ryan B. Corcoran. "Abstract B50: ERK MAPK inhibition enhances the immunogenicity of KRAS-mutant colorectal cancer". En Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-b50.

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Informes sobre el tema "ERK MAPK"

Molloway, Jamie N. y Dorrays El-Ashry. Downstream Signaling Mechanism Underlying MAPK-Induced Generation of the ERA-Negative Phenotype. Fort Belvoir, VA: Defense Technical Information Center, julio de 2002. http://dx.doi.org/10.21236/ada410214.

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Holloway, Jamie N. Downstream Signaling Mechanism Underlying MAPK-Induced Generation of the ER-Negative Phenotype. Fort Belvoir, VA: Defense Technical Information Center, julio de 2004. http://dx.doi.org/10.21236/ada430401.

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Douglas, Thomas A., Christopher A. Hiemstra, Stephanie P. Saari, Kevin L. Bjella, Seth W. Campbell, M. Torre Jorgenson, Dana R. N. Brown y Anna K. Liljedahl. Degrading Permafrost Mapped with Electrical Resistivity Tomography, Airborne Imagery and LiDAR, and Seasonal Thaw Measurements. U.S. Army Engineer Research and Development Center, julio de 2021. http://dx.doi.org/10.21079/11681/41185.

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Accurate identification of the relationships between permafrost extent and landscape patterns helps develop airborne geophysical or remote sensing tools to map permafrost in remote locations or across large areas. These tools are particularly applicable in discontinuous permafrost where climate warming or disturbances such as human development or fire can lead to rapid permafrost degradation. We linked field-based geophysical, point-scale, and imagery surveying measurements to map permafrost at five fire scars on the Tanana Flats in central Alaska. Ground-based elevation surveys, seasonal thaw-depth profiles, and electrical resistivity tomography (ERT) measurements were combined with airborne imagery and light detection and ranging (LiDAR) to identify relationships between permafrost geomorphology and elapsed time since fire disturbance. ERT was a robust technique for mapping the presence or absence of permafrost because of the marked difference in resistivity values for frozen versus unfrozen material. There was no clear relationship between elapsed time since fire and permafrost extent at our sites. The transition zone boundaries between permafrost soils and unfrozen soils in the collapse-scar bogs at our sites had complex and unpredictable morphologies, suggesting attempts to quantify the presence or absence of permafrost using aerial measurements alone could lead to incomplete results. The results from our study indicated limitations in being able to apply airborne surveying measurements at the landscape scale toward accurately estimating permafrost extent.

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Geologic map of the Elk Ridge Quadrangle, Powder River County, Montana. US Geological Survey, 1991. http://dx.doi.org/10.3133/i2140.

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